Rozprawy doktorskie: „Bradycardia”

1

Smith-White, Margaret A. Medical Sciences Faculty of Medicine UNSW. "A functional study of neuropeptide Y mediated attenuation of vagal-evoked bradycardia". Awarded by:University of New South Wales. School of Medical Sciences, 2003. http://handle.unsw.edu.au/1959.4/19090.

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In the heart, neuropeptide Y (NPY) released during stimulation of the sympathetic nerve attenuates vagal-evoked bradycardia for a prolonged period. The inhibitory action of NPY is proposed as being Y2 receptor mediated. In rat and mouse, anaesthetised with sodium pentobarbitone, the selective Y2 receptor antagonist BIIE0246 reduced the inhibition of cardiac vagal activity evoked by a Y2 agonist, N-acetyl [Leu28, 31] NPY 24-36. BIIE0246 also reduced the inhibitory effect on vagal action evoked by stimulation of the sympathetic nerve. Deletion of the receptor in Y2 receptor-knockout mice abolished all NPY mediated inhibition of cardiac vagal-evoked bradycardia. These findings strongly support the proposal that NPY released during stimulation of the sympathetic nerve acts via Y2 receptors on the vagus nerve to decrease the slowing effect on the heart evoked by vagal stimulation. Examination of the structural components within NPY, using NPY, related PP peptides and structurally altered analogs, showed proline residues in the N-terminal polyproline region of NPY were found to influence the level of presynaptic activity while residues in the PP fold region further enhanced activity. NPY fragments, as long or longer than 3-36 NPY, possessed full inhibitory activity whereas short C-terminal analogs, such as 24-36 did not. The two leucine residues in agonist N-acetyl [Leu28, 31] NPY 24-36 was found to alter the structure and enhance the amphipathic nature of the a-helix in the shortened fragment. Arginine residues in the helix were also found to be important for activity. The leucine residues in N-acetyl [Leu28, 31] NPY 24-36 are proposed to stabilise the molecule producing an over all linear conformation. Although the conformation adopted by NPY at the receptor is unknown, it is plausible to suggest that the interaction between the proline residues and the a-helix stabilise the molecule in the same way that leucine substitution does in N-acetyl [Leu28, 31] NPY 24-36. Results obtained in Y2 receptor-knockout mice infer by their faster heart rates, an inhibitory role for the receptor in regions of the brain able to effect sympathetic outflow to the heart. Therefore knowledge of the structural requirements required of agonists and antagonists for Y2 receptor activation is likely to be of practical significance in drug design for the treatment of diseases affecting both parasympathetic and sympathetic innervation of the heart.

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Ruck, Sylvia A. "Induced Bradycardia Effects on Angiogenesis, Growth and Development in Early Development in Chicken Embryos, Gallus Domesticus". Thesis, University of North Texas, 2010. https://digital.library.unt.edu/ark:/67531/metadc33199/.

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Cardiac performance, angiogenesis and growth was investigated during early chicken development. Heart rate, and thus arterial pulse pressure and cardiac output, were altered with the bradycardic drug ZD7288. Heart rates at 72 h of development of control embryos and those dosed with chicken Ringer were not different at 171 bpm. Acute and chronic application of ZD7288 caused significant bradycardia. Chronic dosing of Ringer and ZD7288 changed neither eye diameter nor development rate. Chronic dosing of ZD7288 did not significantly alter CAM vessel density close to the embryo (2, 3 and 4 mm) but at farther distances (5 and 6 mm) chronic dosing with both Ringer and ZD7288 decreased vessel density by 13 - 16%. Chronic dosing with ZD7288 also reduced body mass by 20%. Thus, lowered heart rate and cardiac output had little effect on vessel density or developmental stage, but did reduce embryo growth.

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3

Manley, Elizabeth. "Apneic Bradycardia : terrestrial and aquatic responses in man under working conditions". Thesis, Rhodes University, 1989. http://hdl.handle.net/10962/d1001838.

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The focus of this research was the reappraisal in physiological and psychophysical terms of current equivocal theories regarding the onset, course and termination of apneic bradycardia. Sixteen healthy male subjects participated in four separate testing sessions . Maximal oxygen consumption (VO₂ max) was measured on land and underwater using an identical direct, continuous progressive cycle ergometer test. On each of two other occasions subjects exercised in either environment at 50, 70 and 90% of the appropriate VO₂ max, during which time heart rate was continuously recorded. An initial apneic bout at each exercise intensity was followed by performance of the same workload without apnea for an equivalent period of time. Ratings of perceived exertion (RPE) were also monitored. While apneic bradycardia occurred at each exercise intensity studied underwater, it was apparent only at 50% VO₂ max on land. With the exception of between 50 and 90% VO₂ max on land, the mean apneic heart rates did not differ with varying exercise intensity (p<0.05); nor did the lowest heart rate recorded, although this was lower underwater than on land. Apart from 70% VO₂ max on land, apneic heart rates were lower than the equivalent values measured during exercise without apnea. Land and underwater heart rates during apneic and non-apneic conditions did not differ until 90% VO₂ max. The effects of increasing exercise intensity upon the onset of bradycardia were evident in that it occurred earlier at 50% VO₂ max underwater than at the heavier workloads, and only at 50% VO₂ max on land. The mean breath-hold duration did not differ between the land and underwater environments, nor was it affected by increasing exercise intensity. The order in which breath-holds was performed did not alter the length of apnea. Land and underwater RPE did not differ and increased with increasing exercise intensity in both environments. During apneic exercise RPE was greater than the equivalent exercise without apnea. Twelve of the original 16 subjects were divided equally into two groups on the basis of vital capacity expressed relative to body surface area. Vital capacity was measured during the first laboratory session. Neither the mean heart rate response to apneic exercise at 50% V0₂ max in both environments, nor the lowest heart rates recorded differed between groups, prompting the conclusion that lung volume did not affect apneic bradycardia. Despite a longer breath-hold duration for Group A (large relative lung volume) than Group B (small relative lung volume), the onset point of bradycardia was the same for either group when expressed relative to total breath-hold duration

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4

Subramanian, Melanie. "Relative Bradycardia With Hypertension in Traumatic Brain Injury: A Marker for Mortality?" Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:17295909.

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Traumatic brain injury (TBI) is a leading cause of death in patients under 45 years of age. Hypertension has been shown to be associated with increased mortality in patients with moderate to severe traumatic brain injury (TBI). Furthermore, it is known that relative bradycardia is associated with increased mortality in hypotensive patients. We conducted a study to evaluate the relationship of initial heart rate (HR) with outcome in hypertensive TBI patients. This was a retrospective study of adult patients with moderate to severe blunt TBI (GCS <13) that presented to a Level I trauma center (2001-2011). Patients with hypertension, defined as an initial emergency department systolic blood pressure (SBP) ≥140 mmHg, were included in the analysis. The primary outcome was in-hospital mortality. Logistic regression analysis was used to control for age, injury severity, midline shift >5mm, pupil reflexes, hyperosmolar therapy, and blood transfusion. Secondary outcomes, including Glasgow Outcome Scale scores, were also analyzed. Of 490 patients with moderate to severe TBI, 53 patients were excluded. Of the remaining 437 patients, 223 (51%) presented with hypertension. Total in-hospital mortality was 31% in this group and the initial HR was significantly lower in the group that died (86±26 vs. 96±23; p=0.009). Bradycardia (HR≤60) upon presentation, which was identified in 21 (9%) patients, was associated with increased mortality (71% in HR≤60 vs. 27% in HR>60; p<0.001). Logistic regression identified bradycardia as an independent predictor of mortality (odds ratio 4.82; 95% confidence interval 1.36-17.10; p=0.015). Further subgroup analysis of relative bradycardia failed to identify HR between 60 and 90 as a predictor of mortality (p=0.113), although HR≤60 remained significant (p=0.006). The combination of initial hypertension and bradycardia in moderate to severe blunt TBI patients is associated with increased mortality.

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5

St-Hilaire, Marie. "Chémoréflexes laryngés induits par l'acide, l'eau vs le salin chez les agneaux nouveau-nés durant le sommeil calme". Mémoire, Université de Sherbrooke, 2004. http://savoirs.usherbrooke.ca/handle/11143/3789.

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Mise en contexte : Les chémoréflexes laryngés (CRI) sont déclenchés suite au contact entre un liquide et la muqueuse laryngée. Chez un organisme mature, ces CRL sont responsables de mécanismes de protection des voies aériennes inférieures (VAI) tels que déglutitions, toux et réaction d'éveil afin d'éviter l'aspiration. Par contre, chez un organisme immature comme c'est le cas chez les nouveau-nés, ces CRL associent apnée, bradycardie, laryngospasme, hypertension et redistribution du débit sanguin. En période néonatale, ces CRL, déclenchés en réponse à un reflux gastro-oesophagien acide, sont tenus responsables d'apnées du prématuré, de malaises graves du nourrisson (ALTE) et probablement de quelques cas de mort subite du nourrisson (MSN). Malgré leur pertinence clinique évidente, la revue de la littérature permet de constater que de nombreuses questions persistent concernant les CRL, principalement parce que les conditions expérimentales des études antérieures ne reflètent pas ce qui est vu en clinique. Ainsi, les CRL ont été étudiés le plus souvent en utilisant des modèles anesthésiés, en utilisant l'eau distillée, en se servant d'une trachéotomie pour l'injection des solutions et finalement en ne prenant pas en compte les stades de conscience. Une meilleure compréhension des CRL, en particulier déclenchés par des solutions acides, est donc nécessaire. But du projet : Le but de ce travail est d'étudier les CRL chez l'agneau nouveau-né sans sédation en réponse à l'acide, en comparaison à l'eau distillée et au salin durant le sommeil calme.

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Mateos, Juan Carlos Pachon. "Estudo comparativo dos parâmetros eletrofisiológicos da estimulação endocárdica septal com a estimulação cardíaca endocárdica convencional". Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/98/98131/tde-12062012-074413/.

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Fundamento: A estimulação endocárdica convencional do ventrículo direito em ápice ou na região subtricuspídea ocasiona grande alargamento do QRS e importante dessincronização do miocárdio comprometendo a função ventricular. Com o surgimento da estimulação bifocal do VD e com a necessidade de estimulação cardíaca menos deletéria, a estimulação septal do VD tem sido cada vez mais utilizada. Eventualmente têm sido relatados limiares de estimulação mais altos e ondas R menores na estimulação septal. Objetivo: Comparar os parâmetros eletrofisiológicos das estimulações apical e septal, no mesmo paciente, para verificar se existem diferenças que possam interferir na escolha do ponto de estimulação. Este não é um estudo de ressincronização, porém tem o objetivo de contribuir na busca de uma estimulação ventricular monofocal menos deletéria. Casuística e métodos: Estudo prospectivo controlado. Foram incluídos 25 pacientes, com 67,2 ± 9 anos, 10 (40%) mulheres, 15 (60%) homens, com indicações clássicas de marca-passo por bradiarritmias. As etiologias foram Degenerativa em 9 (36%), Insuficiência coronária em 8 (32%), Doença de Chagas em 7 (28%), e Valvopatia em 1 (4%) pacientes. Foram utilizados eletrodos de fixação ativa tanto no ápice e região subtricuspídea, como no septo IVD. Foram medidos e comparados os limiares de comando, impedância e onda R uni e bipolares no momento do implante (medida direta) e após seis meses de evolução (medida por telemetria). Resultados: No implante, as médias dos limiares de comando septais x apicais foram respectivamente 0,73 x 0,74V (unipolar) e 0,73 x 0,78V (bipolar). As médias das ondas R septais x apicais foram 10 x 9,9mV (unipolar) e 12,3 x 12,4mV (bipolar). As médias das impedâncias septais x apicais foram 579 x 621? (unipolar) e 611 x 629? (bipolar). Todas as diferenças entre parâmetros septais e apicais com teste t-pareado bicaudal foram não significativas (p > 0,1). Após seis meses do implante, as médias dos limiares de comando septais x apicais foram respectivamente 0,5 x 0,72V (unipolar) e 0,71 x 0,87V (bipolar). As médias das ondas R septais x apicais foram 11,4 x 9,5mV (unipolar) e 12 x 11,2mV (bipolar). As médias das impedâncias septais x apicais foram 423 x 426? (unipolar) e 578 x 550? (bipolar). As diferenças entre parâmetros septais e apicais após 6 meses com teste t-pareado bicaudal foram não significativas (p > 0,05), exceto quanto às médias dos limiares de estimulação unipolares septal x apical (p=0,02) com menores limiares septais. 27, Conclusão: Este estudo mostrou que não existem diferenças expressivas entre parâmetros eletrofisiológicos de estimulação septal e apical, quando comparadas no mesmo paciente. Estes dados sugerem que em relação aos parâmetros de estimulação não há restrições para a escolha da estimulação septal em ventrículo direito. Este estudo não tem o objetivo de testar a ressincronização ventricular, porém contribui na escolha de uma estimulação monofocal ventricular direita mais fisiológica e menos deletéria.
Background: The conventional endocardial pacing in right ventricular apex or subtricuspid area causes significant QRS enlargement and important left ventricular desynchronization with ventricular function damage. By the introduction of RV bifocal pacing and the need of a less deleterious ventricular stimulation right ventricular septal pacing has been increasingly used. However, despite rare, some authors have reported high pacing thresholds and low R wave in septal pacing. Objective: To compare the electrophysiological parameters of the apical and septal stimulation in the same patient, seeking for any difference that could affect the choice of the pacing point. This is not a resynchronization study however it has the aim to search for for a better monofocal ventricular pacing. Materials and methods: Prospective controlled study of 25 symptomatic patients (67.2 ± 9 years old, 10 [40%] female, 15 [60%] male) having permanent atrial fibrillation with high degree AV block and classical pacemaker indication. The etiologies were 9 (36%) aging, 8 (32%) coronary disease, 7 (28%) Chagas disease and 1 (4%) valvar cardiopathy. There were used active fixation leads both in septal and in apical locations. The generators were Biotronik Philos II DR and Entovis DR. There were measured and compared pacing thresholds, impedance and R wave uni and bipolar during implantation (direct measurement) and after six months of follow-up (telemetry measurement). Results: During implantation, the septal vs apical mean pacing threshold were respectively 0.73 vs 0.74V (unipolar) and 0.73 vs 0.78V (bipolar). Mean R wave septal vs apical were 10 vs 9.9 mV (unipolar) and 12.3 vs 12.4mV (bipolar). The mean impedance septal vs apical were 579 vs 621? (unipolar) and 611vs 629? (bipolar). All septal vs apical comparisons were non-significant (p > 0.1, two-tailed paired t-test). After six months the mean pacing threshold septal vs apical were respectively 0.5 vs 0.72V (unipolar) and 0.71 vs 0.87V (bipolar). The mean R wave septal vs apical were 11.4 vs 9.5mV (unipolar) and 11.2 vs 12mV (bipolar). The mean impedance septal vs apical were 423 vs 426? (unipolar) and 578 vs 550? (bipolar). Only the unipolar septal vs apical mean threshold had significant difference (p = 0.02) with lower septal value. Conclusion: This study showed no significant difference between electrophysiological septal and apical pacing parameters when the 29 comparison is done in the same patient. By this way there are no restrictions for the right ventricular septal pacing. Despite being a non-resynchronization study it may contribute for chosen a less deleterious right ventricular monofocal pacing.

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7

Lindholm, Peter. "Severe hypoxemia during apnea in humans : influence of cardiovascular responses /". Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-314-7/.

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Mosca, Nancy Walsh. "Holding premature infants during gavage feeding: Effect on apnea, bradycardia, oxygenation, gastric residual, gastrin, and behavioral state". Case Western Reserve University School of Graduate Studies / OhioLINK, 1995. http://rave.ohiolink.edu/etdc/view?acc_num=case1057766341.

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Montazeri, Ghahjaverestan Nasim. "Early detection of cardiac arrhythmia based on Bayesian methods from ECG data". Thesis, Rennes 1, 2015. http://www.theses.fr/2015REN1S061/document.

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L'apnée est une complication fréquente chez les nouveaux-nés prématurés. L'un des problèmes les plus fréquents est l'épisode d'apnée bradycardie dont la répétition influence de manière négative le développement de l'enfant. C'est pourquoi les enfants prématurés sont surveillés en continu par un système de monitoring. Depuis la mise en place de ce système, l'espérance de vie et le pronostic de vie des prématurés ont été considérablement améliorés et ainsi la mortalité réduite. En effet, les avancées technologiques en électronique, informatique et télécommunications ont conduit à l'élaboration de systèmes multivoies de monitoring néonatal de plus en plus performants. L'un des principaux signaux exploités dans ces systèmes est l'électrocardiogramme (ECG). Toutefois, même si l'analyse de l'ECG a évolué au fil des années, l'ensemble des informations qu'il fournit n'est pas encore totalement exploité dans les processus de décision, notamment en monitoring en Unité de Soins Intensifs en Néonatalogie (USIN). L'objectif principal de cette thèse est d'améliorer la prise en compte des dynamiques multi-dimensionnelles en proposant de nouvelles approches basées sur un formalisme bayésien, pour la détection précoce des apnées bradycardies chez le nouveau-né prématuré. Aussi, dans cette thèse, nous proposons deux approches bayésiennes, basées sur les caractéristiques de signaux biologiques en vue de la détection précoce de l'apnée bradycardie des nouveaux-nés prématurés. Tout d'abord avec l'approche de Markov caché, nous proposons deux extensions du Modèle de Markov Caché (MMC) classique. La première, qui s'appelle Modèle de Markov Caché Couplé (MMCC), créé une chaîne de Markov à chaque dimension de l'observation et établit un couplage entre les chaînes. La seconde, qui s'appelle Modèle Semi-Markov Caché Couplé (MSMCC), combine les caractéristiques du modèle de MSMC avec le mécanisme de couplage entre canaux. Pour les deux nouveaux modèles (MMCC et MSMCC), les algorithmes récursifs basées sur la version classique de Forward-Backward sont introduits pour résoudre les problèmes d'apprentissage et d'inférence dans le cas couplé. En plus des modèles de Markov, nous proposons deux approches passées sur les filtres de Kalman pour la détection d'apnée. La première utilise les modifications de la morphologie du complexe QRS et est inspirée du modèle générateur de McSharry, déjà utilisé en couplant avec un filtre de Kalman étendu dans le but de détecter des changements subtils de l'ECG, échantillon par échantillon. La deuxième utilise deux modèles AR (l'un pour le processus normal et l'autre pour le processus de bradycardie). Les modèles AR sont appliqués sur la série RR, alors que le filtre de Kalman suit l'évolution des paramètres du modèle AR et fournit une mesure de probabilité des deux processus concurrents
Apnea-bradycardia episodes (breathing pauses associated with a significant fall in heart rate) are the most common disease in preterm infants. Consequences associated with apnea-bradycardia episodes involve a compromise in oxygenation and tissue perfusion, a poor neuromotor prognosis at childhood and a predisposing factor to sudden-death syndrome in preterm newborns. It is therefore important that these episodes are recognized (early detected or predicted if possible), to start an appropriate treatment and to prevent the associated risks. In this thesis, we propose two Bayesian Network (BN) approaches (Markovian and Switching Kalman Filter) for the early detection of apnea bradycardia events on preterm infants, using different features extracted from electrocardiographic (ECG) recordings. Concerning the Markovian approach, we propose new frameworks for two generalizations of the classical Hidden Markov Model (HMM). The first framework, Coupled Hidden Markov Model (CHMM), is accomplished by assigning a Markov chain (channel) to each dimension of observation and establishing a coupling among channels. The second framework, Coupled Hidden semi Markov Model (CHMM), combines the characteristics of Hidden semi Markov Model (HSMM) with the above-mentioned coupling concept. For each framework, we present appropriate recursions in order to use modified Forward-Backward (FB) algorithms to solve the learning and inference problems. The proposed learning algorithm is based on Maximum Likelihood (ML) criteria. Moreover, we propose two new switching Kalman Filter (SKF) based algorithms, called wave-based and R-based, to present an index for bradycardia detection from ECG. The wave-based algorithm is established based on McSarry's dynamical model for ECG beat generation which is used in an Extended Kalman filter algorithm in order to detect subtle changes in ECG sample by sample. We also propose a new SKF algorithm to model normal beats and those with bradycardia by two different AR processes

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Wung, Shu-Fen. "Bradyarrhythmias: Clinical Presentation, Diagnosis, and Management". W B SAUNDERS CO-ELSEVIER INC, 2016. http://hdl.handle.net/10150/621215.

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Bradyarrhythmias are common clinical findings consisting of physiologic and pathologic conditions (sinus node dysfunction and atrioventricular [AV] conduction disturbances). Bradyarrhythmias can be benign, requiring no treatment; however, acute unstable bradycardia can lead to cardiac arrest. In patients with confirmed or suspected bradycardia, a thorough history and physical examination should include possible causes of sinoatrial node dysfunction or AV block. Management of bradycardia is based on the severity of symptoms, the underlying causes, presence of potentially reversible causes, presence of adverse signs, and risk of progression to asystole. Pharmacologic therapy and/or pacing are used to manage unstable or symptomatic bradyarrhythmias.

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Yang, Fan. "Amylin mediates brainstem control of heart rate in the diving reflex". Diss., Temple University Libraries, 2012. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/193415.

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Pharmacology
Ph.D.
Amylin, or islet amyloid polypeptide is a 37-amino acid member of the calcitonin peptide family. Amylin role in the brainstem and its function in regulating heart rates is unknown. The diving reflex is a powerful autonomic reflex, however no neuropeptides have been described to modulate its function. In this thesis study, amylin expression in the brainstem involving pathways between the trigeminal ganglion and the nucleus ambiguus was visualized and characterized using immunohistochemistry. Its functional role in slowing heart rate and also its involvement in the diving reflex were elucidated using stereotaxic microinjection, whole-cel patch-clamp, and a rat diving model. Immunohistochemical and tract tracing studies in rats revealed amylin expression in trigeminal ganglion cells, which also contained vesicular glutamate transporter 2 positive. With respect to the brainstem, amylin containing fibers were discovered in spinal trigeminal tracts. These fibers curved dorsally toward choline acetyltransferase immunoreactive neurons of the nucleus ambiguus, suggesting that amylin may synapse to parasympathetic preganglionic neurons in the nucleus ambiguus. Microinjection of fluorogold to the nucleus ambiguus retrogradely labeled a population of trigeminal ganglion neurons; some of which also contained amylin. In urethane-anesthetized rats, stereotaxic microinjections of amylin to the nucleus ambiguus caused a dose-dependent bradycardia that was reversibly attenuated by microinjections of the selective amylin receptor antagonist, salmon calcitonin (8-32) (sCT (8-32)) or AC187, and abolished by bilateral vagotomy. In an anesthetized rat diving model, diving bradycardia was attenuated by glutamate receptor antagonists CNQX and AP5, and was further suppressed by AC187. Whole-cel patch-clamp recordings from cardiac preganglionic vagal neurons revealed that amylin depolarizes neurons while decreasing conductance. Amylin also resulted in a reduction in whole cell currents, consistent with the decrease in conductance. Amylin is also found to increase excitability of neurons. In the presence of TTX, spontaneous currents in cardiac preganglionic vagal neurons were observed to decrease in frequency in response to amylin while amplitude remained constant, signifying that amylin reduces presynaptic activity at cardiac preganglionic vagal neurons. Finally, evoked synaptic currents revealed that amylin decreases evoked currents, further demonstrating that amylin depolarization and increase in excitability of cardiac preganglionic vagal neurons is also associated with simultaneous inhibition of presynaptic transmission. Our study has demonstrated for the first time that the bradycardia elicited by the diving reflex is mediated by amylin from trigeminal ganglion cells projecting to cardiac preganglionic neurons in the nucleus ambiguus. Additionally, amylin results in the depolarization and increased excitability of cardiac preganglionic vagal neurons while inhibiting presynaptic transmission.
Temple University--Theses

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Furtado, Fabiola Fialho. "Efeitos cardiovasculares induzidos por um novo doador de óxido nítrico, o nitrato tetrahidrofurfurílico (NTHF), em ratos". Universidade Federal da Paraíba, 2014. http://tede.biblioteca.ufpb.br:8080/handle/tede/6808.

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Previous studies have show that the organic nitrate tetrahydrofurfuryl (NTHF) induces vasorelaxation in mesenteric artery rings with involvement of the NO-sGC-PKG pathway. This study evaluated the action of NTHF on cardiovascular parameters in spontaneously hypertensive (SHR) and Wistar Kyoto (WKY) rats, investigating: the nitric oxide (NO) release, acute toxicity, the NTHF effect on blood pressure and heart rate, its vasorelaxant effect and its ability to induce tolerance. NTHF increased NO levels in rat aortic smooth muscle cells (SMC) and cardiomyocites. In acute toxicity studies, a high single dose from NTHF showed low toxicity. In normotensive animals, NTHF induced hypotension after oral administration of NTHF, and bradycardic and hypotensive effects following administration of this nitrate. These results were similar that found using nitroglycerine (NTG). In addition, these effects were not altered by pretreatment with hexamethonium, a ganglionic blocker. However the treatment with methylene blue, a sGC inhibitor, promoted attenuation of both hypotensive and bradycardic effects, suggesting the involvement of the sGC pathway in these effects. In mesenteric artery rings from SHR and WKY rats precontracted with phenylephrine, NTHF induced concentration dependent vasodilatation in both intact and removed endothelium. This result suggests that the vasorelaxant effect is an endothelium derived relaxation factors (EDRFs) independent mechanism. Furthermore, in the presence of NO° scavenging (PTIO) or ODQ, a sGC inhibitor, the vasorelaxation induced by NTHF was decreased, indicating the involvement of NO-sGC pathway in this response in both SHR and WKY. In the presence of cyanamide, an aldehyde dehydrogenase (mtALDH) inhibitor, the vasorelaxant effect was diminished, suggesting that NTHF is metabolized by this enzyme. After exposure to depolarizing agent KCl, the nitrate effect was significantly attenuated, a characteristic of substances which acts by K+ channels activation. This effect was confirmed after using tetraetylamonium (TEA), a K+ channels inhibitor. In normotensive rats treated with NTHF, the acute administration of NTHF promoted bradycardia and hypotension were are not changed in relation to which those observed in vehicle-treated animals, suggesting that organic nitrate did not induce in vivo tolerance. In vitro tolerance was evaluated in both mesenteric artery rings from animals pretreated with NTHF as well as rings previously exposed to isolated concentrations of NTHF. The vasorelaxant effect was not modified by pretreatment or exposure to NTHF, unlike that observed with NTG. In rings treated with NTG, the effect induced by NTHF was not modified, indicating that NTHF did not promote in vitro tolerance. The results demonstrated that NTHF promoted hypotensive and bradycardic effects in both SHR and WKY rats, with involvement of sGC enzyme; NTHF induced a vasorelaxant effect with participation of NO-sGC-PKG pathway and K+ channels. These effects seem to be mediated by NO release from cardiomyocites and SMC. Finally this study will help to advance the field towards clinical trials, since NTHF caused low toxicity and this nitrate was devoid of in vivo and in vitro tolerance.
Estudos anteriores demonstraram que o nitrato orgânico tetra-hidrofurfurílico (NTHF), promoveu efeito vasorrelaxante em artéria mesentérica de ratos normotensos, com envolvimento da via NO-sGC-PKG. O objetivo deste trabalho foi avaliar os efeitos cardiovasculares induzidos pelo NTHF em ratos espontaneamente hipertensos (SHR) e normotensos Wistar Kyoto (WKY), investigando: a liberação de óxido nítrico (NO), a toxicidade aguda, o efeito do NTHF sobre pressão arterial (PA) e frequência cardíaca (FC), o efeito vasodilatador desse composto, além de sua capacidade em induzir tolerância. Em células musculares lisas vasculares (CMLV) de aorta de rato e cardiomiócitos, NTHF promoveu aumento dos níveis de NO. Na avaliação da toxicidade aguda, NTHF foi administrado por via oral numa dose elevada, e nestas condições o nitrato orgânico apresentou baixa toxicidade. Em animais normotensos, NTHF promoveu hipotensão quando administrado por via oral e efeito hipotensor e bradicárdico após a administração intravenosa, semelhante ao observado pelo gliceril trinitrato (GTN). Este efeito não foi alterado pelo prétratamento com hexametônio, um bloqueador nicotínico ganglionar. Porém, o tratamento com azul de metileno, inibidor da enzima ciclase de guanilil solúvel (sGC), promoveu diminuição da resposta, indicando a participação da sGC nos efeitos hipotensor e bradicárdico. Em animais WKY e SHR NTHF promoveu efeito hipotensor e bradicárdico. Em anéis de artéria mesentérica de ratos SHR e WKY, pré-contraídos com fenilefrina, NTHF promoveu vasodilatação concentraçãodependente, com endotélio vascular intacto ou removido, sugerindo um efeito independente da liberação dos fatores relaxantes derivados do endotélio (EDRFs). Na presença do sequestrador de NO radicalar (PTIO) ou do inibidor seletivo da sGC (ODQ), o efeito vasorrelaxante do NTHF foi atenuado, indicando a participação da via NO-sGC tanto em SHR quanto WKY. Na presença de cianamida, um inibidor da enzima aldeído desidrogenase mitocondrial (mtALDH), o efeito vasorrelaxante foi atenuado, indicando que o nitrato é metabolizado por esta enzima. Após a exposição ao agente despolarizante KCl e após adição de tetraetilamônio (TEA), inibidor de canais para K+, o efeito do NTHF foi diminuído. Em animais normotensos prétratados com NTHF, a administração aguda de NTHF hipotensão e bradicardia, comparáveis às observadas no grupo controle, sugerindo que o NTHF não induz tolerância in vivo. A tolerância in vitro foi avaliada em artéria mesentérica de animais tratados previamente com NTHF, quando previamente expostos a concentrações isoladas do nitrato. O efeito vasorrelaxante não foi modificado pelo tratamento ou exposição prévia ao NTHF. Efeito contrário ao obtido com GTN. Em anéis prétratados com GTN, o efeito induzido pelo NTHF não foi modificado, sugerindo que o nitrato em estudo não promove tolerância in vitro. Os resultados demonstram que o NTHF promoveu efeito hipotensor e bradicárdico em animais normotensos e hipertensos, com envolvimento da enzima sGC; apresentou efeito vasorrelaxante, com participação da via NO-sGC-PKG e também de canais para K+. Esses efeitos parecem ser mediados por meio da liberação de NO tanto em CMLV quanto em cardiomiócitos. Por fim, NTHF evidencia um potencial clínico por apresentar baixa toxicidade e não induzir tolerância in vivo e in vitro

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Williamson, Allan John. "Cardiovascular effects of a low and a high dose of fentanyl in the isoflurane anesthetized dog: the influence of the anesthetic-sparing effect and the correction of bradycardia". Thesis, Virginia Tech, 2017. http://hdl.handle.net/10919/86614.

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Fentanyl has historically been used to reduce inhalant anesthetic requirements in the dog, with the end goal of reducing detrimental cardiovascular effects seen with their use. While fentanyl has been investigated in this context with the older agent enflurane, this agent is no longer in common use. In the current literature, no studies exist that compare the effects of low and high doses of fentanyl on cardiovascular function in dogs anesthetized with isoflurane. In previous literature, a high dose of fentanyl improved cardiovascular function in enflurane anesthetized dogs only following correction of bradycardia associated with its use. The objective of this study was to evaluate the effect of two doses of fentanyl on isoflurane requirement in the dog, followed by an evaluation of cardiovascular function in the isoflurane-anesthetized dog at equivalent depth of anesthesia. The hypothesis was that fentanyl would reduce inhalant requirements in a dose dependent fashion, and that cardiovascular function would increase with fentanyl administration only following correction of bradycardia. A total of 8 healthy adult male beagle dogs were enrolled in this study, which was performed in a randomized cross-over design. Minimum Alveolar Concentration (MAC) was determined in these dogs via a 30 mA electric stimulation both before and after administration of a low (loading dose 30 µg/kg, continuous rate infusion (CRI) of 0.2 µg/kg/minute) or high (loading dose 90 µg/kg, CRI 0.8 µg/kg/min) dose of fentanyl. A 7-day washout was observed between experimental days. Following MAC determination, in a subsequent anesthetic episode animals were placed at a MAC multiple of 1.3 and cardiovascular and blood gas parameters were evaluated before and after each fentanyl dose in the presence and absence of bradycardia. Fentanyl decreased MAC in a dose-dependent fashion (p < 0.001), with the low dose reducing MAC by about 42% and the high dose by about 77%. MAC reduction, however, did not translate into improvement in cardiovascular function, with a significant reduction in cardiac index and oxygen delivery noted with both doses (p < 0.01) that was not different between treatments. Normal mean arterial pressures were maintained with both treatments despite these effects. Only with the high dose, however, correction of bradycardia caused an increase in both cardiac index and oxygen delivery (p < 0.02) when compared to isoflurane alone. In clinically healthy dogs, administration of a high dose of fentanyl increased cardiac function following correction of bradycardia, but a decrease was observed when bradycardia went uncorrected. Further studies are needed in order to evaluate these effects in clinical patients.
Master of Science

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Sunti, Daniele Martinez de. "Efeitos da abolição da bradicardia reflexa nas respostas cardiorrespiratórias de tambaqui, Colossoma macropomum (Cuvier, 1818), em hipóxia severa: vagotomia versus inibição farmacológica". Universidade Federal de São Carlos, 2013. https://repositorio.ufscar.br/handle/ufscar/1358.

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Hypoxic bradycardia is a reflex response to hypoxia observed in most fish species studied so far. This reflex is initiated by the stimulation of O2 chemoreceptors and induced by an increase in the inhibitory vagal tonus. Despite of being well described and characterized, the hypothesis that hypoxic bradycardia improves the O2 transference from the ventilatory water to the gills still remain to be proved. The utilization of different methods to inhibit hypoxic bradycardia (vagotomy and atropinization) may have contributed to generate different cardiorespiratory responses, making this issue even more controversial. In this study the cardiorespiratory variables (heart frequency fH, metabolic rate - VO2 , O2 extraction from the ventilatory current EO2, gill ventilation - VG , breathing frequency fR, and ventilatory requirement - VG / VO2 ) were measured in the tambaqui, Colossoma macropomum, under normoxia and after 40 min of exposure to severe hypoxia (20 mmHg) and the 3 subsequent hours of recovery. Each fish was subjected to this protocol before (Control group), after atropine administration (A group) and after vagotomy (V group). Under hypoxia the fish of control group displayed the characteristic hypoxic bradycardia (reduction of 56% in fH) with hyperventilation (increases of 96% in fR and 650% in VG ). This hyperventilation was probably responsible by the decrease in EO2 (65%) and, consequently, in the VO2 (62%), resulting in an increase of 1800% in the VG / VO2 . The beginning of the recovery period was characterized by an elevated VO2 (~200% above the normoxic values) accompanied by tachycardia (50.6 bpm) and gradual recovery of EO2, fR, VT and VG . Atropine and vagotomy elevated the fH in normoxia (from 32.0 ± 1.7 to 77.8 ± 4.1 and 80.6 ± 5.8 bpm), indicating a high basal vagal tone. In these two groups the fH remained constant during the experimental time course. This evidenced that the post-hypoxia tachycardia probably occurred as a consequence of a reduction in the cholinergic tonus. The groups control, atropinized and vagotomized did not show significant differences in EO2, VO2 and the other respiratory variables analyzed in any protocol. This results point out that hypoxic bradycardia does not improve the O2 transference to the gills, independently of the method employed to abolish the bradycardic reflex. Therefore, other hypotheses on the hypoxic bradycardia must be investigated in this species.
A bradicardia hipóxica é uma resposta reflexa à hipóxia presente na maioria dos teleósteos. Este reflexo é induzido por um aumento no tônus vagal inibitório e iniciado pela estimulação de quimiorreceptores de oxigênio (O2). Apesar de muito descrita e bem caracterizada, a hipótese de que esta redução na frequência cardíaca (fH) melhore a transferência de O2 pelas brânquias ainda não foi comprovada. A utilização de diferentes métodos para inibir a bradicardia hipóxica (vagotomia e atropinização) pode ter contribuído para gerar respostas cardiorrespiratórias diversas e tornar esta questão ainda mais controversa. Neste trabalho foram avaliadas as variáveis cardiorrespiratórias (fH; taxa metabólica VO2 ; extração de O2 da corrente ventilatória EO2; ventilação branquial VG ; frequência respiratória fR; volume ventilatório VT e necessidade ventilatória VG / VO2 ) do tambaqui, Colossoma macropomum, em normóxia, após 40 min de hipóxia severa (20 mmHg) e durante 3 h de recuperação subsequente. Cada animal foi submetido a este protocolo antes (Ctr), após administração de atropina (A) e após vagotomia (V). Em hipóxia os animais Ctr apresentaram a característica bradicardia hipóxica (redução de 56% na fH) com aumentos na fR (~96 %) e VT (~275 %) elevando muito a VG (~650 %). Esta alta VG , provavelmente foi responsável pela queda significativa na EO2 (65%), consequentemente reduzindo a VO2 (62 %) e aumentando muito a VG / VO2 (1800 %) em hipóxia. O início do período de recuperação do grupo Ctr foi caracterizado por elevada VO2 (~200 % acima dos valores de normóxia), acompanhada de taquicardia (50,6 bpm) e recuperação gradual da EO2, fR, VT e VG . A atropina e a vagotomia elevaram a fH em normóxia (de 32,0 ± 1,7 para 77,8 ± 4,1 e 80,6 ± 5,8 bpm) indicando um alto tônus vagal de repouso, sendo que nestes dois grupos a fH permaneceu constante em todos os tempos experimentais evidenciando que a taquicardia póshipóxia foi, provavelmente, consequência de uma redução no tônus colinérgico. Na EO2, VO2 e demais parâmetros respiratórios analisados não houve diferenças entre os grupos Ctr, A e V, em nenhum momento do protocolo. Estes resultados demonstram que a bradicardia hipóxica, possivelmente, não melhora a transferência de O2 pelas brânquias de tambaqui independente do método de abolição do reflexo bradicárdico. Portanto, outras hipóteses sobre a função da bradicardia hipóxica, como na proteção do miocárdio, devem ser investigadas nesta espécie.

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Silva, Maria do Socorro de França. "Avaliação dos efeitos do 2-nitrato-1,3- dibutoxipropano (NDBP) sobre o sistema cardiovascular". Universidade Federal da Paraíba, 2012. http://tede.biblioteca.ufpb.br:8080/handle/tede/6741.

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Previous studies have shown that the 2-nitrate-1,3-dibuthoxypropan (NDBP), an organic nitrate synthesized from glycerin, induced vasorelaxation in mesenteric artery of rats through activation of the NO-cGMP-PKG pathway and K+ channels, in addition, caused hypotension and bradycardia in normotensive conscious rats. The current research aimed to investigate the effects of the NDBP on cardiovascular system in rats, evaluating the NO release in rat smooth muscle cell culture, the ability of NDBP to induce tolerance to vasodilatation and the effect of the acute administration of the compound on autonomic control of blood pressure and heart rate of normotensive and hypertensive rats, using in vitro and in vivo approaches. For biochemical determination aortic rat smooth muscle cell culture (ARSMC) was used and the pharmacological experiments were developed using Wistar rats or spontaneously hypertensive (SHR) and normotensive Wistar Kyoto (WKY) rats. The NDBP caused concentration-dependent increases in NO levels in ARSMC. In addition, NDBP produced no change in the vasorelaxation induced by the NDBP when the rings were pre-incubated with the NDBP (10 μM or 100 μM), suggesting that the NDBP did not induce tolerance. In vivo experiments, SHR rats were significantly hypertensive compared with WKY rats. The acute administration of the NDBP (1, 5, 10, 15 and 20 mg/kg, i.v.) caused a biphasic response: hypotension and bradycardia followed by hypertension and tachycardia in WKY and SHR rats. The blockade of muscarinic receptors with atropine (2 mg/kg) blunted the bradycardia induced by NDBP (15 mg/kg) and reduced the hypotension in WKY and SHR. However, the pressor response to the compound was potentiated. Furthermore, vagotomy almost abolished the bradycardia in WKY and SHR. Moreover, hexamethonium (30 mg/kg), a nicotinic ganglionic blocker, reduced both bradycardia and pressor response in WKY and SHR. The administration of methylene blue (4 mg/kg), a soluble guanylyl cyclase (sGC) blocker, attenuated the hypotension and bradycardia induced by the NDBP (15 mg/kg) in WKY. Similar event occurred in SHR animals. In conclusion, the NDBP releases NO in ARSMC, and was unable to induce tolerance to its vasorelaxant effect, however, the cardiovascular effects of NDBP are mainly mediated by the central action of the compound, resulting in changes on autonomic function of spontaneously hypertensive and normotensive rats.
Relatos prévios demonstraram que o 2-nitrato-1,3-dibutoxipropano (NDBP), um nitrato orgânico sintetizado a partir da glicerina, induziu vasodilatação em anéis de artéria mesentérica cranial isolada de rato mediante a ativação da via NO-GMPc- PKG, bem como dos canais para K+ e, adicionalmente, causou hipotensão e bradicardia em ratos normotensos não-anestesiados. O estudo atual teve como objetivo investigar os efeitos do NDBP sobre o sistema cardiovascular em ratos, avaliando a liberação de NO eliciada pelo NDBP em células musculares lisas vasculares, a capacidade do NDBP induzir tolerância ao vasorrelaxamento e o efeito da administração aguda do composto sobre o controle autonômico de animais normotensos e hipertensos, por meio de abordagens in vitro e in vivo. Nos experimentos bioquímicos foi utilizada a cultura de células musculares lisas de aorta de rato (CMLAR) e, nos experimentos farmacológicos foram utilizados ratos Wistar ou ratos espontaneamente hipertensos (SHR) e normotensos Wistar Kyoto (WKY). Foi observado que o NDBP causou um aumento concentração-dependente nos níveis de NO em CMLAR. Além disso, não houve alteração no efeito vasodilatador do NDBP quando os anéis de artéria mesentérica foram previamente expostos ao NDBP, nas concentrações de 10 μM ou 100 μM, sugerindo que o nitrato orgânico em estudo não induziu tolerância. Nos experimentos in vivo, foi constatado que a pressão média basal dos animais espontaneamente hipertensos foi significantemente maior que a do grupo normotenso. A administração aguda do NDBP (1, 5, 10, 15 e 20 mg/kg, i.v.) induziu uma resposta bifásica: hipotensão e bradicardia seguidas de hipertensão e taquicardia, em ratos SHR e WKY. O bloqueio dos receptores muscarínicos pela atropina (2 mg/kg) atenuou a bradicardia induzida pelo NDBP (15 mg/kg), reduzindo também a hipotensão em WKY e SHR. Entretanto, a resposta pressora ao composto foi potencializada. A secção bilateral do nervo vago praticamente aboliu a bradicardia em WKY e SHR. Adicionalmente o hexametônio (30 mg/kg), um bloqueador nicotínico ganglionar, reduziu tanto a bradicardia quanto a resposta pressora em ambos os grupos. A administração do azul de metileno (4 mg/kg), um bloqueador da ciclase de guanilil solúvel (CGs), atenuou as repostas hipotensora e bradicárdica induzida pelo NDBP (15 mg/kg) em ratos WKY. Evento similar aconteceu nos animais SHR. Esses resultados sugerem que o NDBP libera NO em CMLAR, sendo incapaz de induzir tolerância ao seu efeito vasorrelaxante, entretanto, os efeitos cardiovasculares do NDBP são mediados, principalmente, pela ação central do composto, resultando em alterações na função autonômica de ratos normotensos e espontaneamente hipertensos.

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Souza, Kleber Oliveira de. "Estimulação cardíaca artificial septal versus estimulação apical: estudo comparativo dos parâmetros ecocardiográficos de sincronia cardíaca". Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/98/98131/tde-06092018-150600/.

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INTRODUÇÃO: A estimulação cardíaca artificial convencional em ponta do ventrículo direito é o tratamento de eleição para os quadros de bradicardia severa, contudo, apesar de excelente para corrigir a frequência cardíaca, favorece o surgimento de dissincronia ventricular mecânica, podendo agravar ou originar insuficiência cardíaca. Neste contexto, desde a década de 90 são utilizadas no Instituto Dante Pazzanese as estimulações septal (ou para-Hissiana) e bifocal de ventrículo direito (septal e apical). Postula-se que a estimulação em posição septal teria melhores resultados tanto em termos clínicos quanto às medidas elétricas e ecocardiográficas de função sistólica quando comparada à posição apical. Esta nova estimulação ainda não foi amplamente testada frente à estimulação convencional com as novas tecnologias de avaliação da sincronia cardíaca. MÉTODOS: Pacientes portadores de fibrilação atrial permanente, sem possibilidade de estimulação atrial, com disfunção sistólica leve ou moderada e bradicardia com indicação de marca-passo definitivo foram submetidos à implante de marca-passo bifocal de ventrículo direito com eletrodos em posição septal e apical em todos os casos. Os pacientes foram randomizados para estimulação unifocal por dois meses e a seguir submetidos à crossover no ponto de estimulação cardíaca. Após cada período de estimulação eram realizados eletrocardiograma e ecocardiograma transtorácico bidimensional com avaliação de parâmetros de sincronia do miocárdio ventricular. RESULTADOS: Foram incluídos 25 pacientes em cada grupo de estimulação na análise final do estudo. A estimulação em posição septal demonstrou uma menor duração do QRS estimulado (153 ± 12 ms vs. 174 ± 16 ms, p < 0,001) e melhor fração de ejeção do ventrículo esquerdo (44 ± 9% vs. 40 ± 8%, p < 0,001) quando comparada com a posição apical. A classe funcional (NYHA) também foi menor com a estimulação septal (1,8 ± 0,6 vs. 2,2 ± 0,7, p < 0,001). A avaliação da sincronia cardíaca evidenciou menos dissincronia interventricular (p < 0,001) e intraventricular com a estimulação septal (Septal to posterior delay: 33,1 ± 28,7 vs. 80,7 ± 46,2 ms, p < 0,001; Índice de Yu: 33,4 ± 8,6 ms vs. 50,2 ± 14,0 ms, p < 0,001; Strain radial: 78,8 ± 57,1 ms vs. 137,2 ± 50,2 ms, p < 0,001). CONCLUSÃO: A avaliação intrapaciente mostrou que, em comparação com a estimulação apical convencional, a estimulação em posição septal esteve associada à menor dissincronia cardíaca medida pela ecocardiografia, o que pode estar relacionado à melhor função sistólica do ventrículo esquerdo e consequentemente melhores resultados clínicos observados.
INTRODUCTION: Conventional artificial cardiac pacing in the right ventricle apex is the treatment of choice for severe bradycardia. Although it is excellent for correcting heart rate, it favors the onset of electromechanical ventricular dyssynchrony, which may aggravate or even lead to heart failure. In this context, the Septal (or para-Hissian) and bifocal (septal and apical) stimulation were used since the 90\'s in the Dante Pazzanese Institute. It was observed that the septal stimulation could have better results both in clinical terms and in the electrical and echocardiographic measurements of systolic function when compared to the apical stimulation. This new stimulation has not been yet extensively tested against conventional one with the new technologies of cardiac synchrony evaluation. METHODS: Patients with permanent atrial fibrillation, without possibility of atrial stimulation, with mild or moderate systolic dysfunction and bradycardia with indication of pacemaker were submitted to implantation of bifocal pacemaker in the right ventricle with electrodes in a septal and apical position in all cases. The patients were randomized to unifocal stimulation for two months and then underwent crossover, changing the point of cardiac stimulation. After each stimulation period, electrocardiogram and two-dimensional transthoracic echocardiography were performed with evaluation of ventricular myocardial synchrony parameters. RESULTS: Twenty-five patients were included in each stimulation group in the final analysis of the study. Septal pacing demonstrated a shorter duration of the QRS (153 ± 12 ms vs. 174 ± 16 ms, p < 0.001) and a better left ventricular ejection fraction (44 ± 9% vs. 40 ± 8%, p < 0.001) when compared to the apical position. NYHA functional class was also lower with septal pacing (1.8 ± 0.6 vs. 2.2 ± 0.7, p < 0.001). The cardiac synchrony evaluation showed less interventricular (p < 0.001) and intraventricular dyssynchrony with septal pacing (Septal to posterior delay: 33.1 ± 28.7 vs. 80.7 ± 46.2 ms, p < 0.001; Yu index: 33.4 ± 8.6 ms vs. 50.2 ± 14.0 ms, p < 0.001; Radial strain: 78.8 ± 57.1 ms vs. 137.2 ± 50.2 ms, p < 0.001). CONCLUSION: The intrapatient comparision showed that, compared to the apical conventional stimulation, the septal pacing was associated with lower cardiac dyssynchrony measured by echocardiography, which may be related to the better left ventricular systolic function and consequently better clinical results observed.

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FERRARO, GENEVIEVE. "Bradycardie sinusale spontanee : interet de la denervation pharmacologique". Angers, 1990. http://www.theses.fr/1990ANGE1078.

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Belão, Thiago de Campos. "Respostas cardiorrespiratórias do teleósteo de respiração aérea, Clarias gariepinus, exposto à hipóxia gradual". Universidade Federal de São Carlos, 2010. https://repositorio.ufscar.br/handle/ufscar/1325.

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Air-breathing fish are classified as obligatory (when breathing obligatory atmospheric air independently of the water O2 tension) or facultative air-breather (using an air breathing organ ABO -, when theirs gills are not able to extract all O2 necessary to maintain the aerobic mechanisms under hypoxic conditions). The catfish, Clarias gariepinus, is airbreathing fish that shows modifications on the gill lamella, forming a ventilatory fan, and on the 2o e 4o gill arches, forming an arborescent organ. These structures form the ABO of this specie.The objectives of the present study were: 1. To determine if C. gariepinus is an obligatory or a facultative air breather. 2. To analyze the cardio-respiratory responses ( VO2 - metabolic rate; VG - gill ventilation; VT ventilatory volume; fR respiratory frequency; EO2 O2 extraction from the ventilatory current; fH- heart frequency) in response to progressive hypoxia. 3. To verify if the critical O2 tension (PcO2) of this specie is correlated with the O2 uptake from the atmospheric air.To classify the air-breathing mode of C. Gariepinus, the fish (Wt ~ 350 g; n = 7) were maintained in normoxia during 24 hours without access to air. The fR maintained constant during all the experiment and there was no mortality, indicating that C. gariepinus is a facultative air-breather. To analyze the cardio-respiratory responses to progressive hypoxia, VO2 , EO2, fR, VT, VG , EO2 and fH were recorded under the following water O2 tensions(PwO2): 100, 70, 50 e 30 mmHg. Fish maintained a constant VO2 until the PcO2 (~ 55 mmHg), below which VO2 decreased significantly. This decreasing was followed with the significant reduction of EO2 in PinspO2 of 62,7 ± 1,30 mmHg reaching values of 19,6 ± 1,9 % in severe hypoxia. The VG and the VT increased progressively until PinspO2 of 28,0 ± 0,5 mmHg, reaching highest values of, respectively, 1545,7 ± 63,5 mLH2O.kg-1.min-1, 33,9 ± 0,8 mLH2O.Kg-1.resp-1 e 57,2 ± 1,4 resp.min-1. The fH reduced progressively from 43,4 ± 0,4 bpm, in normóxia, arriving significant values just above the PcO2 and reaching minimum values (19,2 ± 3,0 bpm) in severe hypoxia. Under progressive hypoxia (100, 70, 50, 30 e 20 mmHg) and with the access to the atmospheric air, C. gariepinus (Wt ~ 610 g; n = 9) presented a 5-fold increase in the air-breathing frequency (fRA). A bradycardia was observed just before the air breath and a tachycardia just after.Concluding, C. gariepinus is a continuous facultative air-breathing fish that regulate the 2 O V until the PcO2 of ~54 mmHg. Below this tension fish increase the VG mainly due to a larger increase of VT (lower metabolic cost of VG ). The hypoxic pre-air breath bradycardia is characteristic of aquatic breathers while the post-air breath tachycardia is typical of air respirators. The fRA increased proportionally with the progressive hypoxia, mainly just above the PcO2. These results show that C. gariepinus is adapted to survive at hypoxic habitats and that this species show a higher dependence of the atmospheric air than the others facultative air-breathing fishes.
Peixes de respiração aérea são classificados como respiradores aéreos obrigatórios (aqueles que respiram ar atmosférico independente das tensões de O2 da água) ou facultativos (aqueles que usam o órgão de respiração aérea ABO quando as brânquias não conseguem extrair a quantidade de O2 necessário para manter o metabolismo aeróbico em condições hipóxicas). O bagre-africano, Clarias gariepinus, é um peixe de respiração aérea que apresenta modificações na lamela branquial, formando um leque ventilatório, e, nos 2os e 4os arcos branquiais, os órgãos arborescentes. Estas últimas estruturas formam o ABO desta espécie.Os objetivos do presente estudo foram: 1. Determinar se C. gariepinus é um respirador aéreo facultativo ou obrigatório. 2. Analisar as respostas cardiorrespiratórias ( VO2 - taxa metabólica; EO2 - extração de O2 da corrente ventilatória; VG - ventilação branquial; VT - volume ventilatório; fR - frequência respiratória; fH- frequência cardíaca) em resposta a hipóxia gradual. 3. Verificar se a tensão crítica de O2 (PcO2) desta espécie está relacionada com a tomada de O2 do ar atmosférico.Para classificar a modalidade da respiração aérea de C. gariepinus, os peixes (Wt ~ 350 g; n = 7) foram mantidos em normóxia durante 24 h sem acesso ao ar atmosférico. A fR manteve-se constante durante todo o experimento e não houve mortalidade, indicando que C. gariepinus é um respirador aéreo facultativo. Para analisar as respostas cardiorrespiratórias em normóxia (controle) e hipóxia gradual, a VO2 , EO2, fR, VT, V G e fH foram registradas durante as seguintes tensões de O2 (PwO2): 100, 70, 50 e 30 mmHg. Os peixes mantiveram VO2 constante até a PcO2 (~ 55 mmHg), abaixo da qual a VO2 decresceu significativamente. Esta diminuição da VO2 foi acompanhada da diminuição significativa da EO2 em PinspO2 de 62,7 ± 1,30 mmHg atingindo valores de 19,6 ± 1,9 %, em hipóxia severa. A VG , VT e fR aumentaram progressivamente até a PinspO2 de 28,0 ± 0,5 mmHg, chegando a valores máximos de, respectivamente, 1545,7 ± 63,5 mLH2O.kg-1.min-1, 33,9 ± 0,8 mLH2O.Kg-1.resp-1 e 57,2 ± 1,4 resp.min-1. A fH diminui progressivamente de 43,4 ± 0,4 bpm, em normóxia, até alcançar valores significativos próximos a PcO2 e valores mínimos em hipóxia severa (19,2 ± 3,0 bpm). Em experimentos de hipóxia gradual (100, 70, 50, 30, 20 e 10 mmHg) com acesso ao ar atmosférico, C. gariepinus aumentou aproximadamente 5x a frequência de respiração aérea (fRA). Em cada tensão hipóxica ocorreu uma bradicardia pré-RA seguido de taquicardia significativa pós-RA (típico de respiração aérea); a fR manteve-se praticamente constante (~ 32 resp.min-1) até as duas últimas PwO2 (20 e 10 mmHg), nas quais a fR diminuiu para 23,0 ± 1,18 resp.min-1.Finalmente, C. gariepinus é um peixe de respiração aérea facultativa contínua que regula a VO2 até a PcO2 de ~ 55 mmHg. Abaixo desta tensão o animal aumenta a VG devido principalmente a um pronunciado aumento na VT (diminuição do custo metabólico da VG ). A bradicardia hipóxica pré-RA é uma característica de respiradores aquáticos, enquanto a taquicardia hipóxica pós-RA é típica de respiradores aéreos. A fRA aumentou proporcionalmente com a hipóxia gradual, principalmente próximo a PcO2. Tais resultados demonstram que C. gariepinus está adaptado a sobreviver em habitats hipóxicos e demonstra uma maior dependência do ar atmosférico do que outros respiradores bimodais facultativos.

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Bičiště, Jan. "Umělá aorta pro demonstraci činnosti intraaortální balonkové kontrapulzace". Master's thesis, Vysoké učení technické v Brně. Fakulta elektrotechniky a komunikačních technologií, 2009. http://www.nusl.cz/ntk/nusl-218047.

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This dissertation work describes design and construction of simulated aorta device intended to demonstrate performance of the intra-aortal balloon catheter (IAB), and to test reaction of the contra-pulsation pump during simulated cardiac output in conditions of tachycardia, bradycardia and arrhythmia. The major part of the device is transparent plastic tube. The pressure pulses (waves) are generated inside this plastic tube to simulate real cardiac output. These pressure pulses are generated by step motor with membrane. The step motor is controlled by programmable control system AMiNi-E. Individual pressure pulses simulate cardiac output in conditions of tachycardia, bradycardia and arrhythmia. Required simulated cardiac output is selected by control switches. Generated pressure pulses are read by pressure sensor and are transferred to the control system of the configuration computer. Read data can be displayed as graphs in program Microsoft Excel. The intra-aortal balloon catheter (IAB) is inserted inside the aorta and is connected with contra-pulsation pump which on pressure pulse is responding.

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Montiel, Christophe Amiouni Elias. "Apnée sportive influence des techniques de compensation sur la bradycardie d'immersion /". [S.l.] : [s.n.], 2006. http://theses.univ-nantes.fr/thesemed/MEDmontiel.pdf.

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Traboulsie, Achraf. "Etude de la spécificité pharmacologique et de l'impact physiologique des canaux T". Montpellier 1, 2006. http://www.theses.fr/2006MON13513.

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Les canaux calciques à bas seuil d'activation ou de type T (canaux T) sont impliqués dans plusieurs fonctions physiologiques telles que l'activité pacemaker cardiaque, l'excitabilité neuronale, la sécrétion, la fécondation. . . Le courant calcique correspondant est caractérisé par une activation et une inactivation transitoire (T), une déactivation lente et une faible conductance. Trois sous-unités codant pour les canaux T ont été récemment clonées : α1G, α1H et α1I. Ces canaux n'ont malheureusement pas une pharmacologie spécifique. L'objectif de ma thèse a été de caractériser le rôle de canaux T cardiaques et d'étudier la pharmacologie de ces canaux. La première partie des résultats correspond à l'étude du rôle de la sous-unité α1G cardiaque grâce à une souris knock-out pour α1G. Nous avons montré que ces souris présentaient une bradycardie et un ralentissement de la conduction atrio-ventriculaire par un approche d'électrophysiologie cellulaire (cellules isolées du sinus et de l'oreillette), d'électrophysiologie in vivo (ECG sur animaux anesthésiés et enregistrements télémétriques) et moléculaire. Ces résultats démontrent l'implication de la sous-unité α1G dans la genèse et la conduction du rythme cardiaque. La deuxième partie de la thèse concerne l'étude pharmacologique des canaux T. La fluoxétine (Prozac ®) inhibe les 3 sous-unités de canaux T avec la même affinité. Elle se fixe et maintient le canal T dans l'état inactivé. Le zinc est un bloqueur plus spécifique de la sous-unité α1H. Il se fixe préférentiellement sur l'état inactivé du canal. L'efonidipine (isomère R -), qui appartient à la famille des dihydropyridines, inhibe plus spécifiquement les canaux T que les canaux L. Dans son ensemble, ces travaux contribuent à une meilleure compréhension du rôle physiologique et des propriétés pharmacologiques des canaux T.

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ROUGEOT, VERONIQUE. "Bradycardies et arrets cardiaques au cours des crises d'epilepsie". Université Louis Pasteur (Strasbourg) (1971-2008), 1992. http://www.theses.fr/1992STR1M101.

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MESSAGER, PASCALE. "De la stimulation cardiaque temporaire non invasive en urgence : dix exemples d'utilisation au centre hospitalier de senlis". Amiens, 1993. http://www.theses.fr/1993AMIEM049.

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Leoni, Anne-Laure Escande Denis. "Modèles murins en rythmologie expérimentale". [S.l.] : [s.n.], 2006. http://castore.univ-nantes.fr/castore/GetOAIRef?idDoc=38466.

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Azevedo, Luciene Ferreira. "Adaptações autonômicas e cardiovasculares em atletas de alto rendimento: influência da modalidade e periodização do treinamento físico". Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/5/5131/tde-01122011-151729/.

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INTRODUÇÃO: O treinamento físico provoca adaptações cardiovasculares, sendo que maiores adaptações estruturais cardíacas são observadas em atletas de elite, que realizam treinamento físico de alta intensidade com o objetivo de aumento no rendimento. Além disto, atletas apresentam diminuição da frequência cardíaca de repouso, embora os mecanismos que explicam a bradicardia em atletas ainda são controversos. O nível das adaptações pode variar e fatores como o tipo de modalidade esportiva, tempo e nível de treinamento físico podem contribuir para tal variação. Desta forma, o objetivo deste estudo foi investigar a influência de modalidades esportivas (ciclismo, corrida de longa distância e remo) e da periodização do treinamento físico nas adaptações estruturais e funcionais, autonômicas e não autonômicas cardíacas e vasculares em atletas de elite no repouso, na inclinação ortostática e nas 24 horas. MÉTODOS: Neste estudo experimental longitudinal prospectivo foram avaliados 13 ciclistas, 13 corredores e 11 remadores de elite, saudáveis (entre 20 e 36 anos; masculino), engajados em treinamento físico competitivo, em 2 períodos de treinamento: período básico-PB e período competitivo-PC. Avaliação da capacidade funcional máxima foi feita por teste cardiorrespiratório. Adaptações estruturais cardíacas foram avaliadas por meio do ecocardiograma bidimensional com doppler. Frequência cardíaca intrínseca foi estudada por meio do duplo bloqueio farmacológico (atropina 0,04 mg/kg e esmolol 500 g/kg, i.v.). Frequência cardíaca e pressão arterial foram registradas continuamente no repouso e no teste de inclinação ortostática por meio de ECG e monitor de pressão arterial, respectivamente (500Hz). A variabilidade da frequência cardíaca e pressão arterial foram analisadas pelo método auto-regressivo. Frequência cardíaca e pressão arterial de 24 horas foram aquisitadas pelo Holter e Mapa, respectivamente. Avaliação da sensibilidade barorreflexa espontânea foi calculada pelo método da sequência. Os dados foram apresentados como mediana e variação interquartil. RESULTADOS: Remadores apresentaram maior VO2max que os corredores no PC (p<0,04). Ciclistas e remadores apresentaram maior VO2max no PC comparado ao PB (p<0,05). Corredores apresentaram maiores diâmetros diastólicos do ventrículo esquerdo que ciclistas (p<0,06) e remadores (p<0,01) no PB. Corredores e ciclistas apresentaram maiores diâmetros diastólicos do ventrículo esquerdo que remadores (p<0,004) no PC. Corredores apresentaram maiores índices de massa do ventrículo esquerdo que ciclistas (p<0,04) no PB e ciclistas maiores que remadores (p<0,03) no PC. Ciclistas foram os únicos atletas que apresentaram a reversão do remodelamento cardíaco no PB (p<0,04). No repouso, corredores mostraram menor frequência cardíaca que ciclistas no PC ciclistas = 50(45/55), corredores = 44(43/47), remadores = 44(43/53)bpm, p<0,03]. Corredores e remadores mostraram maior efeito vagal [ciclistas = 41(36/46), corredores = 55(48/59), remadores = 50(42/66)bpm, p=0,03] e maior frequência cardíaca intrínseca ciclistas = 84(82/87), corredores = 92(87/94), remadores = 96(85/101)bpm, p=0,03] que ciclistas no PC. Remadores tinham maior frequência cardíaca intrínseca que ciclistas no PB ciclistas = 88(86/92), corredores = 91(82/99), remadores = 95(90/101)bpm, p=0,03]. PC comparado ao PB diminuiu o efeito vagal 41(36/46) vs. 48(43/51)bpm, p<0,05] e frequência cardíaca intrínseca 84(82/87) vs. 88(86/92), p<0,05] dos ciclistas. No teste de inclinação, corredores mostraram menor aumento da frequência cardíaca que ciclistas no PB ciclistas = 64(49/73), corredores = 46(43/55), remadores = 53(42/77)%, p<0,05]. Nem a modalidade ou período de treinamento físico influenciaram os índices de variabilidade da frequência cardíaca no repouso ou na inclinação ortostática. A modalidade esportiva e o período de treinamento físico influenciaram a pressão arterial e sua variabilidade, no repouso e na inclinação ortostática. Remadores apresentaram menor sensibilidade barorreflexa espontânea que corredores no PC (p=0,03). Tanto a modalidade quanto o período de treinamento físico influenciaram a resposta da frequência cardíaca de 24 horas, sua variabilidade e a resposta da pressão arterial de 24 horas. CONCLUSÃO: Tanto a modalidade esportiva quanto o período de treinamento físico influenciaram nas adaptações estruturais cardíacas, intrínsecas e autonômicas cardíacas e vasculares. Entretanto a modalidade esportiva parece influenciar mais expressivamente essas adaptações
INTRODUCTION: Physical exercise training provokes cardiovascular adaptations and the highest structural cardiac adaptations are observed in elite athletes who perform high intensity training with the objective of increasing their physical performance. Besides, athlete shows decrease on resting heart rate. However, the mechanisms that explain the bradycardia in athletes are still controversial. The level of these adaptations may vary and some factors as the type of sport modality, time and level of physical training can contribute to such different responses. Thus, the aim of this study was to investigate the influence of sport modalities (cycling, long distane runner and rower) and physical training periodization on cardiac structural and functional, cardiac autonomic and non-autonomic and vascular adaptations in elite athletes at rest, tilt table test and within 24 hours. METHODS: In this prospective longitudinal experimental study, 13 cyclists, 13 runners and 11 rowers, healthy (20 to 36 years old; male), engaged in competitive training were evaluated in 2 periods of training: basic period BP and competitive period -CP. Maximal functional capacity was evaluated by cardiopulmonary test. Cardiac structural adaptations were evaluated by two-dimensional echocardiography with doppler. Intrinsic heart rate was studied by means of double pharmacological blockade (atropine 0.04 mg/kg and esmolol 500 g/kg, iv.). Heart rate and blood pressure were recorded continuously at rest and tilt table test by means of ECG and arterial blood pressure monitor, respectively (500Hz). The heart rate and blood pressure variabilities were analyzed by autoregressive method. Heart rate and blood pressure within 24 hours were recorded using Holter and blood pressure ambulatory monitor, respectivamente. Spontaneous baroreflex sensitivity was calculated using the sequence method. The data were presented as median and interquartile range. RESULTS: Rowers showed higher VO2max than runners at CP (p<0.04). Cyclists and rowers showed higher VO2max at CP compared to BP (p<0.05). Runners presented higher left ventricular diastolic diameters than cyclists (p<0.06) and rowers (p<0.01) at BP. Runners and cyclists presented higher left ventricular diastolic diameters than rowers (p<0.004) at CP. Runners showed higher left ventricular mass index than cyclistas (p<0.04) at BP and cyclists higher than rowers (p<0.03) at CP. Cyclists were the only athletes who had a reversal of cardiac remodeling at BP (p<0.04). At rest, runners showed lower heart rate than cyclists at CP cyclists = 50(45/55), runners = 44(43/47), rowers = 44(43/53)bpm, p<0.03]. Runners and rowers showed higher vagal effect [cyclists = 41(36/46), runners = 55(48/59), rowers = 50(42/66)bpm, p=0.03] and higher intrinsic heart rate cyclists = 84(82/87), runners = 92(87/94), rowers = 96(85/101)bpm, p=0,03] than cyclists at CP. Rowers had higher intrinsic herat rate than cyclists at BP cyclists = 88(86/92), runners = 91(82/99), rowers = 95(90/101)bpm, p=0.03]. CP compared with BP decreased the vagal effect 41(36/46) vs. 48(43/51)bpm, p<0.05] and intrinsic heart rate 84(82/87) vs. 88(86/92), p<0.05] of cyclists. At tilt table test, runners showed smaller increase in heart rate than cyclists at BP cyclists = 64(49/73), runners = 46(43/55), rowers = 53(42/77)%, p<0.05]. Neither the sport modality or the training period influenced the indices of heart rate variability at rest and tilt test. The sport modality and the training period influenced the blood pressure and its variability at rest and tilt test. Rowers showed lower spontaneous baroreflex sensitivity than runners at CP (p=0.03). Both the sport modality and the training period influenced the heart rate response in 24 hours, its variability and blood pressure response in 24 hours. CONCLUSION: Both Sport modality and physical training period influenced the cardiac structural, intrinsic and autonomic adaptations as well the vascular adaptations. However, the sport modality seems to influence more significantly these adaptations

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Altuve, Miguel. "Détection multivariée des épisodes d'apnée-bradycardie chez le prématuré par modèles semi-markovien cachés". Rennes 1, 2011. http://www.theses.fr/2011REN1S053.

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Cette thèse a comme domaine applicatif la détection précoce des événements d'apnée-bradycardie (AB) chez le prématuré. Après avoir situé l'importance sur le plan clinique de la détection des AB, une démarche méthodologique est proposée. Elle s'appuie sur un processus de fouille de données qui inclut le nettoyage et l'extraction de caractéristiques. Au chapitre 3, une méthode originale à base d'algorithmes évolutionnaires, pour optimiser des seuils et fenêtres d'analyse, est proposée pour adapter les algorithmes de traitement du signal ECG aux caractéristiques spécifiques du prématuré, très différentes de l'EGC de l'adulte. Au chapitre 4, une approche semi-Markovienne est adaptée pour la modélisation des dynamiques et plusieurs améliorations sont proposées : hétérogénéité des modèles, adaptation au traitement en ligne, optimisation de la gamme dynamique, extension de l'observabilité. Au chapitre 5, ces propositions sont exploitées dans des expériences de classification et de détection en ligne, tant sur signaux simulés que réels. Les résultats mettent bien en exergue l'intérêt de prendre en compte la dynamique des signaux. Ils soulignent également qu'avec un prétraitement approprié tel que la quantification des observations, l'introduction du retard entre les observables, un gain notable en performance peut être observé
This dissertation studies the early detection of apnea-bradycardia (AB) events in preterm infants. After defining the importance of AB detection from a clinical point of view, a methodological approach is proposed. It relies on a data mining process that includes data cleansing and feature extraction. In chapter 3, a novel method based on evolutionary algorithms, for optimizing the thresholds and the analysis windows, is proposed to adapt the algorithms of the ECG signal to the specific characteristics of preterm infants, very different from the EGC of adult. In chapter 4, a semi-Markovian approach is adapted for modeling of dynamics and several improvements are proposed : heterogeneous models, adaptation to online processing, optimization of experiments, are reported on simulated and read signals. They clearly highlight the importance of considering the dynamic of the signals. They also emphasize that with a suitable pre-treatment such as the quantification of observations and the introduction of delay between the observable, a significant gain in performance can be observed

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Leoni, Anne-Laure. "Modèles murins en rythmologie expérimentale". Nantes, 2006. http://archive.bu.univ-nantes.fr/pollux/show.action?id=538b454d-5553-4cc8-8af0-c8f22d052097.

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L’activité électrique cardiaque prend naissance dans le nœud sinusal et se propage au myocarde contractile grâce au tissu de conduction. Le travail exposé dans cette thèse démontre le rôle de deux sous-unités de canaux ioniques dans l’automatisme des cellules sinusales et la conduction de l’influx électrique dans le cœur, grâce à l’utilisation de modèles murins. Le premier confirme in vivo l’hypothèse selon laquelle le canal calcique de type T, Cav3. 1, participe à l’automatisme du nœud sinusal et démontre son implication dans la conduction auriculo-ventriculaire (AV) de l’influx électrique. Dans un second, l’invalidation du canal sodique Nav1. 5 (Scn5a+/-) conduit à une dysfonction sinusale, des troubles de conduction AV et intra-ventriculaires identiques à ceux observés chez des patients porteurs de mutations du gène SCN5A. Ce modèle reproduit fidèlement l’hétérogénéité phénotypique existant chez les patients, suggérant l’importance de gènes modulateurs ou de l’environnement dans le phénotype des maladies génétiques. Enfin, la modulation du rythme constituant un enjeu majeur en thérapeutique cardiaque, nous avons montré que l’inhibition chronique des canaux pacemaker HCN induisait un remodelage ionique sinusal mais avait peu d’effet sur l’expression des canaux ioniques dans le ventricule chez la souris
Cardiac impulse originates from the sinus node and propagates through the cardiac conduction system to depolarise atrial and ventricular myocardium. The work exposed herein reveals the implications of two ion channel subunits in sinus node automaticity and in cardiac electrical conduction by the use of mouse models. The first model confirms the hypothesis implicating the calcium channel subunit Cav3. 1 in sinus node automaticity, and shows its implication in atrioventricular (AV) conduction. The second model shows that heterozygous invalidation of Nav1. 5 sodium channel subunit (Scn5a+/- mice) induces sinus node dysfunction, impaired AV conduction and delayed intramyocardial conduction. These cardiac abnormalities are similar to the phenotype observed in patients with SCN5A mutations. Moreover, Scn5a+/- mice showed phenotype heterogeneity, just as in patients, revealing the importance of modulator genes or environment in the phenotype of genetic disorders. Finally, as cardiac rhythm modulation is of major interest in cardiac therapeutics, we have shown that chronic inhibition of HCN channels induces a complex ionic remodelling in the sinus node, but has little impact on ion channel expression in the mouse ventricle

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Beuchée, Alain. "Intérêt de l'analyse de la variabilité du rythme cardiaque en néonatalogie : comportement des systèmes de régulation cardiovasculaire dans le syndrome apnée/bradycardie du nouveau-né". Rennes 1, 2005. http://www.theses.fr/2005REN1B090.

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Sont présentés les résultats d'études expérimentales de modulation ou stimulation du système nerveux autonome de façon à reproduire les mécanismes potentiellement impliqués dans la survenue de bradycardies chez le nouveau-né. Le comportement du système nerveux autonome et de la fréquence cardiaque a été analysé en situation de stress chez l'animal immature. Il a été mis en évidence une relation causale entre une stimulation sympato-vagale et l'aspect "complexe" le l'organisation spatiale des RR successifs, l'augmentation de LF et HF, et la baisse de LF/HF en "miroir" de l'augmentation de RR. Ce mode d'adaptation est apparu être de type mature et se conserver entre espèce. Les études menées chez le nouveau-né humain ont été de type corrélationnel. Elles ont permis de caractériser des populations de nouveau-nés prématurés souffrant d'apnées-bradycardies fréquentes en fonction du comportement de leur fréquence cardiaque et en particulier d'observer une corrélation entre la diminution de l'entropie de RR et la survenue d'un sepsis chez ces nouveau-nés. Un outil de détection précoce des bradycardies, basé sur un seuil relatif et adaptatif au rythme de base a été également développé. L'étude de la variabilité du rythme cardiaque a donc permis d'apprécier l'état d'équilibre et les perturbations des systèmes de régulation cardiovasculaires. Ces outils d'analyse ont été ensuite utilisés pour détecter précocement la survenue de bradycardies et reconnaître les états pathologiques qui leur sont associés. Mais il n'a pas été possible de décrire un profil évolutif caractéristique à l'approche des bradycardies, ni de déterminer si l'état d'équiilibre préalable influençait la survenue et l'importance des bradycardies.

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GORJUX, SYLVIANE. "Etude des fratries de mort subite du nourrisson par triple exploration : holter, phmetrie oesophagienne, polygraphie du sommeil ; a propos de 175 cas". Aix-Marseille 2, 1994. http://www.theses.fr/1994AIX20153.

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Chung, You Chong Antony. "Normalisation de la fréquence cardiaque et de la conduction auriculo-ventriculaire dans des modèles de bradycardie congénitale par l'inhibition pharmacologique du courant IkACh". Thesis, Montpellier, 2019. http://www.theses.fr/2019MONTT002/document.

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Correction de la bradycardie et des troubles de conduction dans des modèles de dysfonction congénitale de l’automatisme cardiaque par l’inhibition pharmacologique du courant IKAChLa dysfonction du nœud sinusal (DNS) est l’une des principales pathologies de l’automatisme cardiaque. La DNS désigne une multitude de troubles caractérisées par l’incapacité du nœud sinusal (SAN) à générer ou à conduire l’impulsion cardiaque. La seule thérapie actuellement disponible pour la DNS est l’implantation d’un pacemaker électronique. Des études épidémiologiques prévoient un besoin croissant d’implantation de pacemaker électroniques au cours des 50 prochaines années à cause du vieillissement de la population. Le développement des thérapies innovantes pour la DNS est donc un enjeu médical et sociétal important. L’inhibition pharmacologique du courant potassique activé par l’acétylcholine (IKACh) pourrait constituer une nouvelle option thérapeutique pour traiter la DNS.Nous avons donc testé l’inhibition du courant IKACh par un peptide de venin d’abeille, la Tertiapine-Q, pour corriger le DNS et le dysfonctionnement de la conduction chez des souris modèle de pathologies cardiaque humaine en particulier les souris portant l’inactivation des canaux L Cav1.3 (Cav1.3-/-), les souris portant simultanément l’ablation de Cav1.3 et des canaux de type-T Cav3.1 (Cav1.3-/-/Cav3.1-/-), les souris porteuses de la perte de fonction des canaux f- (HCN4-CNBD) et les souris haplo-suffisantes Nav1.5 (Scn5a+/-).Nous avons enregistré par télémétrie, l’ECG, chez ces modèles murins avant et après l’administration de différentes doses de Tertiapine-Q.L’inhibition du courant IKACh par la Tertiapine-Q prévient des dysfonctions sinusales et améliore la conduction dans ces modèles de bradycardie congénitale suggérant la possibilité d’un développement d’un ciblage pharmacologique d’IKACh afin de parvenir à corriger la DNS et les troubles de la conduction
Inhibition of KACh channels by the bee venom peptide tertiapin-Q rescues inherited cardiac conduction defects, sino-atrial bradycardia, and atrioventricular block in models of congenital dysfunctionSinus node dysfunction (SND) is a widespread disease of heart automaticity. SND refers to a multitude of sinus node (SAN) disorders characterized by failure to generate or conduct the cardiac impulse. The only currently available therapy for chronic SND is the implantation of an electronic pacemaker. Epidemiological studies forecast an increasing need for pacemaker implantation during the next 50 years, with the ageing of the population. It is thus an important medical and societal issue, to develop innovative therapies for SND. Pharmacologic inhibition of the G-protein activated K+ current (IKACh) could be a new therapeutic option to treat bradycardia and SND associated with other cardiac pathologies.We tested whether inhibition of IKAch by the peptide Tertiapin-Q could rescue SND and conduction dysfunction in Cav1.3-/- mice carrying concurrent ablation of L-type Cav1.3 and T-type Cav3.1 channels (Cav1.3-/-/Cav3.1-/-), mice carrying loss-of-function of f-channels (HCN4-CNBD) and Nav1.5 haploinsufficient (Scn5a+/-) mice.We employed telemetric ECG recordings of heart rate (HR), SAN pacemaking and AV dysfunction in mice before and after administration of different doses of Tertiapin-Q.Tertiapin-Q significantly improves the HR of Cav1.3-/-, Cav1.3-/-/Cav3.1-/-, and HCN4-CNBD from doses of 0.1 to 5 mg/kg. HRs of Tertiapin-Q-treated mice were similar to those recorded in untreated wild-type mice. Tertiapin-Q also improved cardiac conduction of Scn5a+/- mice by 24%.Pharmacological inhibition of IKAch by Tertiapin-Q prevents SAN dysfunction and improves conduction in three models of congenital bradycardia suggesting the possibility of pharmacologic development of IKACh targeting to manage SND and conduction disease, to delay or replace the implantation of an electronic pacemaker

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31

Alaoui, Katim. "Contribution à l'étude des effets cardiovasculaires des agonistes dopaminergiques et de leurs mécanismes d'action chez le rat". Bordeaux 2, 1989. http://www.theses.fr/1989BOR2B002.

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32

Lahlou, Saad Mohamed. "Étude fonctionnelle de l'hypersensibilité du système dopaminergique spinal chez le rat vigile". Université Joseph Fourier (Grenoble), 1990. http://www.theses.fr/1990GRE18008.

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33

Toader, Emil-Codrut. "Activation parasympathique centrale mise en évidence par enregistrement des motoneurones cardiaques vagaux chez le rat". Lyon 1, 2008. http://tel.archives-ouvertes.fr/docs/00/29/10/46/PDF/ToaderE_08.pdf.

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L’innervation parasympathique du cœur est responsable de la régulation à court terme de la pression artérielle (PA), par le biais du contrôle battement par battement de la fréquence cardiaque. Une diminution de l’activité vagale est considérée comme indice de mauvais pronostic. La projection vagale du noyau ambigu sur le cœur constitue un chemin commun pour le baroréflexe cardiaque et le chemoreflexe de von Bezold Jarisch (BJ). Des mises au point récentes des techniques d’enregistrement extracellulaire des motoneurones cardiaques vagaux (CVM) chez le rat ont rendu un peu plus aisé l’exploration de ces deux réflexes. Ceci permet une meilleure compréhension des mécanismes et de sites d’action. 1) Un agoniste α-2 adrénergique, la clonidine, hypotenseur central, agit sur la régulation à court-terme de la PA. Le présent travail a montré une augmentation de l’activité unitaire des CVMs, et de la pente du baroréflexe cardiaque au niveau central (relation PA-CVM) quand la clonidine est administrée systémiquement, en dose croissante (10-100µg/kg i. V. ). Une analyse approfondie de l’activité des neurones a révélé un nouveau mécanisme d’action de la clonidine via des décharges rapides (« doublet »). 2) Une peptide natriuretique de type B (BNP), utilisée dans le traitement de l’insuffisance cardiaque, a augmenté significativement la bradycardie et l’activité des CVMs lors de l’activation du réflexe BJ. La bradycardie, proportionnelle à l’activation vagale, fait conclure par logique soustractive que le site d’action du BNP est sur le bras afférent du réflexe. Une activation parasympathique centrale représenterait une solution dans le traitement des problèmes cardiovasculaires
The parasympathetic supply to the heart is responsible for the short-term regulation of blood pressure (BP), by controlling the heart rate (HR) on a beat-by-beat basis. Decreased cardiac vagal activity is considered an index of poor outcome. The vagal projection of the nucleus ambiguus on the heart is the common pathway for different cardiac reflexes, like the cardiac baroreflex and the von Bezold-Jarisch (BJ) chemoreflex. Recent advances in extracellular recording methods of cardiac vagal motoneurons (CVM) in rat made easier the exploring of these two reflexes. Thus, a better understanding of the mechanisms and sites of action of two drugs could be achieved. 1). An α-2 adrenergic agonist, clonidine, a central hypotensive, influences the short-term regulation of BP. The present work shows an increase of the activity of CVM, together with the slope of the cardiac baroreflex at central level (BP-CVM relationship) when clonidine is administered systemically, in cumulative doses (10-100µg/kg i. V. ). A deeper analysis of the CVM activity revealed a possible new mechanism of action of clonidine by fast firing (“doublet”). 2). B-type natriuretic peptide (BNP), used in the treatment of the heart failure, increased significantly the bradycardia and the CVM activity during the activation of the BJ reflex. The bradycardia is proportional to the vagal activation. This proves, by subtractive logic, that the BNP site of action is on the afferent arm of the reflex. Cardiac vagal activation is a solution in the treatment of cardiovascular disorders

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34

Lopes, Paulo Ricardo. "Efeitos cardiovasculares induzidos pela administração crônica de ativador da enzima conversora de angiotensina 2 associada ao exercício aeróbio em ratos espontaneamente hipertensos". Universidade Federal de Goiás, 2016. http://repositorio.bc.ufg.br/tede/handle/tede/8114.

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Physical training has been cited as an effective non-pharmacological treatment in the control of metabolic syndrome and cardiovascular diseases. In addition, the diminazene aceturate (DIZE) is a potential therapeutic tool which enhances the catalytic effect of ACE2 of the renin-angiotensin system and, as a final product, can increase the concentrations of angiotensin (1-7). In turn, angiotensin (1-7) is able to interact with MAS receptor and promote opposite effects to the vasoconstrictor, proliferative and hypertrophic axis of ANG II (ACE-ANG II AT1-) promoting vasodilator, antiproliferative and anti-hypertrophic effects. However, little is known about the association between exercise and antihypertensive drugs. This study sought to determine the effects of aerobic training on a treadmill associated with DIZE administration on cardiovascular parameters in spontaneously hypertensive rats (SHR). Therefore, SHR rats at 12 weeks of age were used. One group was underwent to eight weeks of training on a treadmill (T). Another group remained without physical activity (S). On the last 15 days of training, the animals were redistributed into four groups: S and T animals receiving DIZE (1 mg / kg, i.g.; D1) or distilled water (vehicle; V) by gavage. Tail plethysmography was performed throughout the treatment. At the end of the treatment, the animals were anesthetized 2-3% halotana (Cristália Ltda, Brazil) and surgery cannulation (femoral artery and vein) and implant ECG electrode were performed. After 24 hours, the animals were subjected to the PAP, MAP, ECG and HR records before and after pharmacological stimulation to obtain the baroreflex index (BI; Phenylephrine 2 mg / kg) and double autonomic blockade (Atropine 4 mg / kg; metoprolol 2 mg / kg). We observed that aerobic training is not effective in causing hypotension in the trained animals (T, from 196.3 ± 3.0 to 198.7 mm Hg ± 2.3 mm Hg; Figure 5A) compared to sedentary group (S: from 195.9 ± 3.2 to 197.5 ± 4.6 mm Hg; Figure 5A). However, we can observe bradycardia in the trained group compared to the sedentary group, since the first two weeks (T: n = 15, 370.2 ± 4.7 vs. S: n = 15, 388.1 ± 5.1 bpm; p <0.05) until the end of the training (T: 367.0 ± 3.8 vs. S: 395.8 ± 6.1 mmHg, p <0.05). In all, after treatment with DIZE it was observed a decrease in the SBP of the trained group that received DIZE in relation to the trained group receiving vehicle (T + D1 n = 6 186.4 ± 5.5 vs. T + V n = 9 199.4 ± 4.2 mmHg, p <0.05). However, there was no significant difference between both groups sedentary (S + V: n = 8, 198.2 ± 4.9 vs. S + D1: n = 7, 185.0 ± 6.0 mmHg) and, between sedentary and trained groups that received treatment with DIZE (S + D1: 185.0 ± 6.0 vs. T D1 +: 186.4 ± 5.5 mmHg). Moreover, we observed reduction in SBP of the trained group that received DIZE against the trained group receiving vehicle (T + D1: n = 6, 186.4 ± 5.5 vs. T + V: n = 9, 199.4 ± 4.2 mmHg, p <0.05). However, there was no significant difference in this parameter between both sedentary groups (S + V: n = 8, 198.2 ± 4.9 vs. S + D1: n = 7, 185.0 ± 6.0 mmHg). It was evidenced improvement of IB in T + D1 animals (-1.15 ± 0.16 02 bpm / mmHg, p <0.05) when compared to other groups (S + V: -0.70 ± 0.03; S + D1: -0.77 ± 0.02; T + V: -0.98 ± 0.02 bpm / mm Hg). We also observed an reduction in IHR rats T + D1 (bpm 334.8 ± 4.8; p <0.05) compared with T + V (353.5 ± 7.4 beats per minute) or S + D1 (353.7 ± 7.4 beats per minute) groups. Together the results demonstrate that physical exercise on a treadmill was effective in promoting rest bradycardia. Furthermore the association of physical training and DIZE potentiate bradycardia, reduced SBP and intrinsic HR and even improved baroreflex sensitivity in SHR. Finally, it is concluded that the association of physical activity with the activator of angiotensin-converting enzyme 2 improves the cardiovascular system in SHR.
O treinamento físico tem sido apontado como um tratamento não farmacológico coadjuvante no controle de doenças cardiovasculares, dentre as quais destacamos a Hipertensão Arterial. Por outro lado, o aceturato de diminazeno (DIZE) é um fármaco capaz de potencializar o efeito catalítico da enzima conversora de angiotensina 2 (ECA2) do sistema renina-angiotensina e como produto final aumentar as concentrações de Angiotensina (1-7) (ANG (1-7)). Por sua vez, a ANG (1-7) é capaz de interagir com receptor MAS promovendo efeitos vasodilatador, antiproliferativo e anti-hipertrófico. Entretanto, pouco se sabe sobre a associação entre exercício físico e fármacos anti-hipertensivos. O presente estudo procurou determinar os efeitos do treinamento aeróbico em esteira rolante associada à administração de DIZE sobre parâmetros cardiovasculares em ratos espontaneamente hipertensos (SHR). Para tanto, foram utilizados machos SHR com 12 semanas de idade. Um grupo foi submetido a oito semanas de treinamento em esteira (T). Outro grupo permaneceu sem atividade física (S). Nos últimos 15 dias de treinamento, os animais foram redistribuídos em quatro grupos, onde animais S e T receberam Dize (1 mg / kg; i.g.; D1) ou água destilada (veículo; V) por gavagem. Foi realizada pletismografia de cauda durante todo tratamento. Ao final do tratamento, os animais foram anestesiados com halotana 2-3% (Cristália Ltda, Brasil) e submetidos à cirurgia de canulação (artéria e veia femorais) e implante de eletrodo de eletrocardiograma (ECG). Após 24 horas, os animais foram submetidos ao registro de pressão arterial pulsátil (PAP), pressão arterial média (PAM), ECG e frequência cardíaca (FC) antes e após estimulação farmacológica para obtenção do índice baroreflexo (IB; Fenilefrina 2 μg / Kg) e duplo bloqueio autonômico (Atropina 4 mg / Kg; Metropolol 2 mg / Kg). Por fim, os animais foram eutanasiados e decapitados para a extração do coração. Observamos que o treinamento aeróbio não foi eficaz em promover hipotensão nos animais treinados (T; de 196,3 ± 3,0 mm Hg para 198,7 ± 2,3 mm Hg; Figura 5A) em comparação com o grupo sedentário (S: de 195,9 ± 3,2 para 197,5 ± 4,6 mm Hg; Figura 5A). Entretanto, podemos observar bradicardia no grupo treinado em relação ao grupo sedentário, desde as duas primeiras semanas (T: n=15, 370,2 ± 4,7 vs. S: n=15, 388,1 ± 5,1 bpm; p<0,05) até o termino do treinamento (T: 367,0 ± 3,8 vs. S: 395,8 ± 6,1 mmHg; p<0,05). Além disso, observamos redução dos valores de PAS do grupo treinado que recebeu DIZE em relação ao grupo treinado que recebeu veículo (T+D1: n=6, 186,4 ± 5,5 vs. T+V: n=9, 199,4 ± 4,2 mmHg; p<0,05). Entretanto, não houve diferença significativa desse parâmetro entre ambos os grupos sedentários (S+V: n=8, 198,2 ± 4,9 vs. S+D1: n=7, 185,0 ± 6,0 mmHg). Evidenciamos também redução do IB de ratos T+D1 (-1,15 ± 0,16 02 bpm /mmHg; p<0,05) quando comparados aos demais grupos (S+V: -0,70 ± 0,03; S+D1: -0,77 ± 0,02; T+V: -0,98 ± 0,02 bpm / mmHg). Observamos ainda uma redução da FC intrínseca dos ratos T+D1 (334,8 ± 4,8 bpm; p<0,05) quando comparados com os ratos T+V (353,5 ± 7,4 bpm) ou com os ratos S+D1 (353,7 ± 7,4 bpm). Em conjunto os resultados apresentados demonstram que o exercício físico em esteira foi efetivo em promover bradicardia de repouso. Ademais a associação do treinamento com o DIZE potencializou a bradicardia, reduziu a PAS e a FC intrínseca e ainda melhorou a sensibilidade baroreflexa em SHR. Por fim, conclui-se que a associação do exercício físico com o ativador da enzima conversora de angiotensina 2 melhora o sistema cardiovascular em SHR.

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35

Netzer, Florence. "Contrôle des réflexes cardiovasculaires pendant la réaction de défense : rôle du noyau cunéiformis et des neurones sérotoninergiques bulbaires". Paris 5, 2009. http://www.theses.fr/2009PA05P645.

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L’homéostasie cardiovasculaire est maintenue par un ensemble de réflexes (le baroréflexe, le réflexe de Bezold-Jarisch et le chémoréflexe) qui induisent une bradycardie, modulées en fonction des conditions environnementales. En effet, les conduites de fuite ou d’attaque, déclenchées en réponse à certains stimuli stressant (la réaction de défense), s’accompagnent d’une inhibition de la bradycardie du baroréflexe. Chez le rat anesthésié, nous avons montré que la bradycardie du réflexe de Bezold-Jarisch et du chémoréflexe étaient aussi inhibées pendant la réaction de défense, cette inhibition étant sous-tendue par l’activation des récepteurs 5-HT3, NK1 et GABAA localisés dans le noyau du tractus solitaire (NTS). Nos travaux ont permit de d’identifier les neurones sérotoninergiques de la région B3 (Raphé magnus et Noyaux latéraux paragigantocellulaires) comme la source de sérotonine libérée dans le NTS pendant la réaction de défense et activant les récepteurs 5-HT3 à l’origine de l’inhibition des bardycardies réflexes. Enfin nous avons montré, pour la première fois, que le Noyau Cunéiformis (Cnf) participait à l’inhibition des bradycardies réflexes pendant la réaction de défense. Puis par une approche neuroanatomique et pharmacologique nous avons identifié les projections activatrices directes du Cnf sur une structure clé de la réaction de défense, la colonne dorsolatérale de la substance grise périaqueductale
The cardiovascular reflexes are regulatory mechanism devoted to maintain constant blood pressure. During the stress reactions the cardiovagal component of the reflexes are inhibited. Activation of the dorsolateral periaqueductal grey (dlPAG) induces the defence reaction and the inhibition of the reflex bradycardia thought activation of the 5-HT3, NK1 and GABAA receptors in the NTS. Our experiment showed that the B3 group was the origin of serotonin released in the NTS during the defence reaction. We found that the nucleus cuneiformis (Cnf) is involved in this cardiac reflex modulation following the same pathway. In addition we found massive afferents from the Cnf reached the dlPAG

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36

Toader, Emil. "Activation parasympathique centrale mise en évidence par enregistrement des motoneurones cardiaques vagaux chez le rat". Phd thesis, Université Claude Bernard - Lyon I, 2008. http://tel.archives-ouvertes.fr/tel-00291046.

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L'innervation parasympathique du cœur est responsable de la régulation à court terme de la pression artérielle (PA), par le biais du contrôle battement par battement de la fréquence cardiaque. Une diminution de l'activité vagale est considérée comme indice de mauvais pronostic. La projection vagale du noyau ambigu sur le cœur constitue un chemin commun pour le baroréflexe cardiaque et le chemoreflexe de von Bezold Jarisch (BJ). Des mises au point récentes des techniques d'enregistrement extracellulaire des motoneurones cardiaques vagaux (CVM) chez le rat ont rendu un peu plus aisé l'exploration de ces deux réflexes. Ceci permet une meilleure compréhension des mécanismes et de sites d'action. 1) Un agoniste α-2 adrénergique, la clonidine, hypotenseur central, agit sur la régulation à court-terme de la PA. Le présent travail a montré une augmentation de l'activité unitaire des CVMs, et de la pente du baroréflexe cardiaque au niveau central (relation PA-CVM) quand la clonidine est administrée systémiquement, en dose croissante (10-100µg/kg i.v.). Une analyse approfondie de l'activité des neurones a révélé un nouveau mécanisme d'action de la clonidine via des décharges rapides (« doublet »). 2) Une peptide natriuretique de type B (BNP), utilisée dans le traitement de l'insuffisance cardiaque, a augmenté significativement la bradycardie et l'activité des CVMs lors de l'activation du réflexe BJ. La bradycardie, proportionnelle à l'activation vagale, fait conclure par logique soustractive que le site d'action du BNP est sur le bras afférent du réflexe. Une activation parasympathique centrale représenterait une solution dans le traitement des problèmes cardiovasculaires.

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37

(6861473), Hung-Chun Lin. "Incidence of Bradycardia, Hypotension, Bradycardia with Hypotension and Their Risk Factors in Dogs Undergoing General Anesthesia". Thesis, 2019.

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Background: Bradycardia and hypotension are complications commonly occurring during general anesthesia in small animals. Intraoperative hypotension has been found to be associated with adverse postoperative consequences.

Objectives: The objectives of his study were first, to determine the incidence of bradycardia, hypotension, and bradycardia with hypotension in dogs undergoing general anesthesia, and second, to identify the risk factors associated with these three complications. The third objective was to evaluate the relationship between these three intraoperative complications and the recovery quality in these dogs.

Methods and Materials: A retrospective cohort study was performed using anesthetic records from 250 dogs undergoing general anesthesia between May 23, 2018 and October 1, 2018 at the Purdue University Veterinary Teaching Hospital. Intraoperative bradycardia was defined as heart rate < 60 beats/min for at least two consecutive readings at 5 minutes apart. Hypotension was defined as mean arterial pressure (MAP) < 60 mmHg or a systolic arterial pressure (SAP) < 80 mmHg for at least two consecutive readings. A univariate analysis followed by multiple logistic regression was performed to build the model for bradycardia, hypotension, and bradycardia with hypotension. The relationships between the three complications and the recovery quality were analyzed using the Pearson’s chi-square test.

Results: The study found that out of the 250 dogs, 114 (45.6%) developed bradycardia, 113 (45.2%) developed hypotension, and 32 (12.8%) dogs developed bradycardia with hypotension. The use of dexmedetomidine-based tranquilizers/sedatives, longer duration of anesthesia, and subjection to orthopedic and neurologic surgical procedures were all identified as risk factors for the dogs to develop bradycardia. The use of acepromazine-based tranquilizers/sedatives, young and old age dogs, and dogs subjected to neurologic surgery were associated with the development of intraoperative hypotension. When the length of the anesthesia increased, the chance for developing bradycardia with hypotension increased. There was no significant association between these intraoperative complications and the recovery quality.

Conclusions: We found a high incidence of bradycardia or hypotension while a much lower incidence of bradycardia with hypotension in the anesthetized dogs. The risk factors for bradycardia were the use of dexmedetomidine-based tranquilizers/sedatives, the longer duration of anesthesia, and the performance of orthopedic surgery and neurosurgery. The risk factors for hypotension included the use of acepromazine-based tranquilizers/sedatives, the older or younger age of dogs, and the performance of neurosurgery. The risk factor for bradycardia with hypotension was the longer duration of anesthesia. While these adverse events developed intraoperatively, we could not identify a direct influence of these complications on the recovery quality.

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Hsueh, Chia-Hsiang, i 薛嘉祥. "Genetic Analysis of Patients with Bradycardia". Thesis, 2004. http://ndltd.ncl.edu.tw/handle/83932089035115407324.

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碩士
國立臺灣大學
藥理學研究所
92
Background Cardiac bradyarrhythmia is commonly seen in elderly people. It causes symptoms of fatigue, dizzness, fainting, or even sudden death. Pathological bradycardia is usually caused by sick sinus syndrome and/or AV block. Familial sick sinus syndrome and AV block have been reported. Genetic influence on bradycardia has also been confirmed in twin studies. It is generally believed that there are some genetic factors contributing to the pathogenesis of bradyarrhythmias.. Patients and Methods In this report, we performed an association study to search for possible genetic factors causing bradycardias. We analyzed single nucleotide polymorphisms (SNPs) or mutations in ion channels genes and other genes using polymerase chain reaction (PCR) and restriction fragment length polymorphism(RFLP). These genes include beta 1 adrenergic receptor (ADRB1 A231G), funny current (HCN2 C1239G), inward rectifying potassium channel 3.4(KCNJ5 C104T), connexin 40 (Cx40 A71G, Cx40 G-44A) and cardiac sodium channel (SCN5A A1673G, SCN5A C3266T, SCN5A G4219A and SCN5A C3890T) and low voltage activated calcium channel 3.2 (CACNA1H G5207C) . We enrolled 264 patients with an average age of 72.5±12.7 years and the control group was matched to the cases regarding to age and gender one by one. Results We found that the allele frequency of SCN5A A1673G and CX 40G-44A was significantly lower in cases than in controls (p = 0.034, 0.046 respectively) while other SNPs (including ADRB1 A231G, HCN2 C1239G, KCNJ5 C104T, Cx40 A71G, and SCN5A C3266T) did not show significant difference between cases and controls. In haplotype analysis for Cx40, we found the incidence of CX40(-44A,71A) was significantly lower in cases while the incidence of CX40(-44G,71G) was significantly higher in cases( p=0.009 and 0.003 respectively). In subgroup comparison, we found that the incidence of CX40 ( -44A,71A) was significantly lower in patients with AV block（p＝0.01）, while the incidence of CX40(-44G,71G) was significantly higher in patients with sick sinus syndrome（p＝0.003）. MDR analysis showed that there was no significant gene interactions among the SNPs. Conclusion SCN5A A1673G allele was protective against the occurrence of bradycardia. CX40(-44A,71A) and CX40(-44G,71G) was associatiated with AV block and sick sinus syndrome respectively. For CX40 gene, the incidence of (-44A,71A) haplotype was significant lower in cases while the incidence of (-44G,71G) haplotype was significant higher in cases. There was no association between bradycardia and ADRB1 A231G, HCN2 C1239G, KCNJ5 C104T, SCN5A C3266T. Our investigation demonstrated possible genetic factors contributing to the pathogenesis of bradyarrhythmia.

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Smith-White, Margaret A. "A functional study of neuropeptide Y mediated attenuation of vagal-evoked bradycardia /". 2003. http://www.library.unsw.edu.au/~thesis/adt-NUN/public/adt-NUN20031028.105649/index.html.

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"Computational Challenges in Non-parametric Prediction of Bradycardia in Preterm Infants". Master's thesis, 2020. http://hdl.handle.net/2286/R.I.63054.

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abstract: Infants born before 37 weeks of pregnancy are considered to be preterm. Typically, preterm infants have to be strictly monitored since they are highly susceptible to health problems like hypoxemia (low blood oxygen level), apnea, respiratory issues, cardiac problems, neurological problems as well as an increased chance of long-term health issues such as cerebral palsy, asthma and sudden infant death syndrome. One of the leading health complications in preterm infants is bradycardia - which is defined as the slower than expected heart rate, generally beating lower than 60 beats per minute. Bradycardia is often accompanied by low oxygen levels and can cause additional long term health problems in the premature infant.The implementation of a non-parametric method to predict the onset of brady- cardia is presented. This method assumes no prior knowledge of the data and uses kernel density estimation to predict the future onset of bradycardia events. The data is preprocessed, and then analyzed to detect the peaks in the ECG signals, following which different kernels are implemented to estimate the shared underlying distribu- tion of the data. The performance of the algorithm is evaluated using various metrics and the computational challenges and methods to overcome them are also discussed. It is observed that the performance of the algorithm with regards to the kernels used are consistent with the theoretical performance of the kernel as presented in a previous work. The theoretical approach has also been automated in this work and the various implementation challenges have been addressed.
Dissertation/Thesis
Masters Thesis Electrical Engineering 2020

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Sievers, Jule [Verfasser]. "Effect of four different nasal ventilation and CPAP systems on bradycardia and desaturation events in preterm infants / vorgelegt von Jule Sievers". 2008. http://d-nb.info/994121962/34.

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Cadete, Rúben Alexandre Monteiro Pereira Parreira. "Impact of the Lockdown for COVID19 in the Urgent Pacemaker Implantations". Master's thesis, 2021. http://hdl.handle.net/10316/98432.

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Trabalho Final do Mestrado Integrado em Medicina apresentado à Faculdade de Medicina
Introduction: COVID-19 was first considered a pandemic on the 11th of March of 2020 by the World Health Organization. Its impact comprised, not only the direct consequences of the disease, but also a decrease in the follow-up and interventions of patients with cardiovascular (CV) disease. In Portugal, the consequences of this complex paradigm shift on emergent pacemaker implantation rates during and after this pandemic is largely unknown. Methods: In this retrospective observational study, we included 180 patients who had a pacemaker intervention after presenting to the Emergency Department in the 2020 “lockdown” and “post-lockdown” periods and homologous 2019 periods. We compared the 4 time periods: 1) March 18, 2020 to May 17, 2020 (lockdown); 2) May 19 to July 17, 2020 (post-lockdown); 3) and 4) homologous periods from the year before; we then looked for changes that could be explained by the pandemic.Results: Urgent pacemaker implantation rates during “lockdown” was lower than the homologous period (-23.7%), and cases in “post-lockdown” were significantly increased (+106.9% vs “lockdown”; +13.2% vs May-July 2019). There was a tendency for an increase in hypotension at presentation during “lockdown” (p=0.0544), as well as a significantly higher proportion of patients with bradycardia in the “post-lockdown” phase (p=0.017), compared to the corresponding phases of 2019.When comparing lockdown and post-lockdown periods, there was a tendency for a higher number of temporary pacemaker need (3.4% vs 16.7%; p=0.076). Patients admitted during lockdown were 7.57 times more likely to present with hypotension/shock (odds ratio (OR) 7.57; p=0.013).No patients were admitted to the emergency department during lockdown for anomalies detected on ambulatory tests (Holter, electrocardiogram or implanted loop recorder).Conclusion: Our data shows that COVID-19 pandemic had a real impact on urgent pacemaker implantation. During lockdown, urgent implantation rates declined, and clinical presentation was generally more severe, with a greater number of patients presenting with hypotension/shock. In addition, there appears to exist a lockdown effect on post-lockdown emergent pacemaker implantations, with higher admission rates and more severe presentations. Patients with bradyarrhythmias are at particular risk for severe complications and should seek medical care regardless of the state of the pandemic.
Introdução: A COVID-19 foi primeiro considerada pandemia a 11 de março de 2020 pela Organização Mundial de Saúde. O seu impacto resulta, não apenas das consequências diretas da doença, mas também de uma diminuição do seguimento e intervenção em doentes com doença cardiovascular. Em Portugal, as consequências desta mudança de paradigma nas implantações urgentes de pacemaker durante e depois desta pandemia são largamente desconhecidas.Métodos: Neste estudo observacional retrospetivo, incluímos 180 pacientes que tiveram um pacemaker implantado após apresentação no serviço de urgências no período de “confinamento” e “desconfinamento” de 2020 e nos períodos homólogos de 2019. Comparámos os 4 períodos de tempo: 1) 18 de março de 2020 a 17 de maio de 2020 (“confinamento”); 2) 19 de maio a 17 de julho de 2020 (“desconfinamento”); 3) e 4) períodos homólogos do ano anterior; procurámos depois avaliar alterações explicáveis pela pandemia.Resultados: Implantações urgentes de pacemakers durante o “confinamento” foi inferior ao do período homólogo (-23.7%), e casos durante o “desconfinamento” aumentaram significativamente (+106.9% vs “confinamento”; +13.2% vs maio-julho 2019). Houve uma tendência para uma maior proporção de doentes com hipotensão à apresentação durante o “confinamento” (p=0.0544), assim como uma proporção significativamente maior de doentes com bradicardia na fase de “desconfinamento” (p=0.017), comparativamente às fases correspondentes de 2019. Ao comparar os períodos de “confinamento” e de “desconfinamento”, verificou-se uma tendência para uma maior necessidade de uso de pacemakers temporários na fase de desconfinamento (3.4% vs 16.7%; p=0.076, respectivamente). Os doentes admitidos durante o “confinamento” apresentaram 7.57 vezes mais hipotensão/choque na admissão (odds ratio (OR) 7.57; p=0.013).Não houve doentes admitidos nas urgências durante o “confinamento” por anomalias detetadas em exames em ambulatório (Holter, eletrocardiograma, ou gravador implantável).Conclusão: Os nossos dados mostram que a pandemia por COVID-19 teve um impacto real nas implantações urgentes de pacemaker. Durante o “confinamento”, a taxa de implantações urgentes de pacemaker diminuiu e a apresentação clínica foi no geral mais grave, com um maior número de doentes admitidos com hipotensão/choque. Adicionalmente, parece haver um “efeito de confinamento” nas implantações urgentes de pacemakers na fase de “desconfinamento”, com maior número de admissões e maior gravidade de apresentação. Os doentes com bradiarritmias têm um risco particular de complicações graves e devem procurar os cuidados de saúde independentemente de estados pandémicos.

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Tanguay, Jeremie. "Identifications des interactions des inhibiteurs connus des canaux HCNs". Thesis, 2018. http://hdl.handle.net/1866/24378.

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Les canaux activés par l’hyperpolarisation et sensibles aux nucléotides cycliques (hy- perpolarization cyclic nucleotide-gated channel; HCN) ont un rôle dans la régulation du rythme cardiaque ainsi que dans la transmission des influx nerveux. De nombreuses pathologies sont causées par un disfonctionnement de ces canaux. A ce jour, Ivabradine représente la seule molécule utilisée comme médicament, mais malgré sa spécificité en- vers les canaux HCNs, elle n’est pas sélective entre les isoformes de la famille HCN. Dans le but d’identifier une molécule plus adéquate pour le traitement qu’Ivabradine, nous avons analysé l’interaction entre les canaux HCNs et 9 bloqueurs connus garce à l’arrimage moléculaire. Cette analyse nous a permis d’identifier les résidus nécessaires pour la liaison des ligands. On observe aussi qu’Ivabradine ne forme aucune liaison so- lide avec les canaux HCNs mais ne fait que bloquer le passage par sa présence tout comme ses dérivées Zatebradine et Cilobradine. Les ligands de plus petites tailles quant à eux, se logent dans une cavité hydrophobe et forme des liaisons stable avec les pro- téines. Nos résultats semblent suggérer que le blocage par Ivabradine est plus efficace, mais que les liaisons stables des petits ligands possèdent un potentiel plus grand vers une meilleure affinité. Par contre, les interactions observées suggèrent que la spécificité envers les isoformes proviendrait des cinétiques des canaux et des dépendances d’états des ligands plutôt que des interactions identifiées. Pour finir, l’arrimage des ligands sur la conformation fermé du canal HCN1 suggère qu’il existerait une conformation fermée- liée non connue puisqu’aucun ligand n’a pu accéder au pore.
HCN channels have a role in regulating heart rate as well as in the transmission of nerve impulses. Many pathologies are caused by a malfunction of these channels. To date, Ivabradine is the only molecule used as a drug, but despite its specificity for HCN chan- nels, it is not selective between the isoforms of the HCN family. In order to identify a molecule more suitable for the treatment than ivabradine, we analyzed the interaction between HCN family and 9 known blockers using docking. This analysis allowed us to identify the necessary residuals for ligand binding. It is also observed that ivabradine forms no solid bond with the HCN channels but only blocks the passage by its pres- ence, the same was observed for its derivatives Zatebradine and Cilobradine. Ligands of smaller size, for their part, are lodged in a hydrophobic cavity and form stable bonds with the proteins. Our results seem to suggest that blocking with Ivabradine is more effi- cient but that the stable bonds of small ligands have a greater potential for better affinity. However, the observed interactions suggest that the specificity towards isoforms would come from the kinetics of the channels and state dependencies of ligands rather than identified interactions. Finally, the binding of the ligands to the closed conformation of the HCN1 channel suggests that there would be a closed-bound conformation that is not known since no ligand has been able to access the pore.

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Lajiness, Jacquelyn D. "Shp2 deletion in post-migratory neural crest cells results in impaired cardiac sympathetic innervation". Thesis, 2014. http://hdl.handle.net/1805/5495.

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Indiana University-Purdue University Indianapolis (IUPUI)
Autonomic innervation of the heart begins in utero and continues during the neonatal phase of life. A balance between the sympathetic and parasympathetic arms of the autonomic nervous system is required to regulate heart rate as well as the force of each contraction. Our lab studies the development of sympathetic innervation of the early postnatal heart in a conditional knockout (cKO) of Src homology protein tyrosine phosphatase 2 (Shp2). Shp2 is a ubiquitously expressed non-receptor phosphatase involved in a variety of cellular functions including survival, proliferation, and differentiation. We targeted Shp2 in post-migratory neural crest (NC) lineages using our novel Periostin-Cre. This resulted in a fully penetrant mouse model of diminished cardiac sympathetic innervation and concomitant bradycardia that progressively worsen. Shp2 is thought to mediate its basic cellular functions through a plethora of signaling cascades including extracellular signal-regulated kinases (ERK) 1 and 2. We hypothesize that abrogation of downstream ERK1/2 signaling in NC lineages is primarily responsible for the failed sympathetic innervation phenotype observed in our mouse model. Shp2 cKOs are indistinguishable from control littermates at birth and exhibit no gross structural cardiac anomalies; however, in vivo electrocardiogram (ECG) characterization revealed sinus bradycardia that develops as the Shp2 cKO ages. Significantly, 100% of Shp2 cKOs die within 3 weeks after birth. Characterization of the expression pattern of the sympathetic nerve marker tyrosine hydroxylase (TH) revealed a loss of functional sympathetic ganglionic neurons and reduction of cardiac sympathetic axon density in Shp2 cKOs. Shp2 cKOs exhibit lineage-specific suppression of activated pERK1/2 signaling, but not of other downstream targets of Shp2 such as pAKT (phosphorylated-Protein kinase B). Interestingly, restoration of pERK signaling via lineage-specific expression of constitutively active MEK1 (Mitogen-activated protein kinase kinase1) rescued TH-positive cardiac innervation as well as heart rate. These data suggest that the diminished sympathetic cardiac innervation and the resulting ECG abnormalities are a result of decreased pERK signaling in post-migratory NC lineages.

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Duverger, James Elber. "Stimulateur cardiaque biologique : effets de la répartition spatiale des cardiomyocytes avec activité spontanée et de l'étirement uniaxial". Thèse, 2017. http://hdl.handle.net/1866/20268.

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FANG, TONG-JING, i 房同經. "Central actions of vasopressin, angiotensin and catecholamines on the barore flex bradycardic response". Thesis, 1985. http://ndltd.ncl.edu.tw/handle/11456554448325013826.

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Kočková, Radka. "Vliv positivně inotropních a antiarytmických farmak na kardiovaskulární systém". Doctoral thesis, 2015. http://www.nusl.cz/ntk/nusl-333581.

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Heart rate changes mediate the embryotoxic effect of antiarrhythmic drugs in the chick embryo A significant increase in cardiovascular medication use during pregnancy has occurred in recent years but only limited evidence on its safety profile is available. We hypothesized that drug-induced bradycardia is the leading mechanism of developmental toxicity. We tested metoprolol, carvedilol, or ivabradine for embryotoxicity and their acute effect on chick embryonic model. We used video microscopy and ultrasound biomicroscopy. Significant dose-dependent mortality was achieved in embryos injected with carvedilol and ivabradine. In ED4 embryos, metoprolol, carvedilol and ivabradine reduced the heart rate by 33%, 27%, and 55%, respectively, compared to controls (6%). In ED8 embryos this effect was more pronounced with a heart rate reduction by 71%, 54%, 53%, respectively (controls 36%). Cardiac output decreased in all tested groups but only proved significant in the metoprolol group in ED8 embryos. The number of -adrenergic receptors showed a downward tendency during embryonic development but a negative chronotropic effect of tested drugs was increasingly pronounced with embryonic maturity. This effect was associated with reduced cardiac output in chick embryos, probably leading to premature death....

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(9178664), Maria I. Muzquiz, i Ivette M. Muzquiz (9178658). "Reversible Nerve Conduction Block Using Low Frequency Alternating Currents". Thesis, 2020.

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This thesis describes a novel method to reversibly and safely block nerve conduction using a low frequency alternating current (LFAC) waveform at 1 Hz applied through a bipolar extrafascicular electrode. This work follows up on observations made on excised mammalian peripheral nerves and earthworm nerve cords. An in-situ electrophysiology setup was used to assess the LFAC
waveform on propagating action potentials (APs) within the cervical vagus nerve in anaesthetized Sprague-Dawley rats (n = 12). Two sets of bipolar cuff or hook electrodes were applied unilaterally to the cervical vagus nerve, which was crushed rostral to the electrodes to exclude reflex effects
on the animal. Pulse stimulation was applied to the rostral electrode, while the LFAC conditioning waveform was applied to the caudal electrode. The efferent volley, if unblocked, elicits acute bradycardia and hypotension. The degree of block of the vagal stimulation induced bradycardia
was used as a biomarker. Block was assessed by the ability to reduce the bradycardic drive by monitoring the heart rate (HR) and blood pressure (BP) during LFAC alone, LFAC with vagal stimulation, and vagal stimulation alone. LFAC applied via a hook electrode (n = 7) achieved 86.6 +/- 11% block at current levels 95 +/- 38 uAp (current to peak). When applied via a cuff electrode (n = 5) 85.3 +/- 4.60% block was achieved using current levels of 110 +/- 65 uAp. Furthermore, LFAC was explored on larger vagal afferent fibers in larger human sized nerve bundles projecting to effects mediated by a reflex. The effectiveness of LFAC was assessed in an in-situ electrophysiological setup on the left cervical vagus in anaesthetized domestic swine (n = 5). Two bipolar cuff electrodes were applied unilaterally to the cervical vagus nerve, which was crushed caudal to the electrodes to eliminate cardiac effects. A tripolar extrafascicular cuff electrode was placed most rostral on the nerve for recording of propagating APs induced by
electrical stimulation and blocked via the LFAC waveform.
Standard pulse stimulation was applied to the left cervical vagus to induce the Hering-Breuer reflex. If unblocked, the activation of the Hering-Breuer reflex would cause breathing to slow down and potentially cease. Block was quantified by the ability to reduce the effect of the Hering-Breuer
reflex by monitoring the breathing rate during LFAC alone, LFAC and vagal stimulation, and vagal stimulation alone. LFAC achieved 87.2 +/- 8.8% (n = 5) block at current levels of 0.8 +/- 0.3 mAp. Compound nerve action potentials (CNAP) were monitored directly. They show changes
in nerve activity during LFAC, which manifests itself as the slowing and amplitude reduction of components of the CNAPs. Since the waveform is balanced, all forward reactions are reversed, leading to a blocking method that is similar in nature to DC block without the potential issues of
toxic byproduct production. These results suggest that LFAC can achieve a high degree of nerve block in both small and large nerve bundles, resulting in the change in behavior of a biomarker, in-vivo in the mammalian nervous system at low amplitudes of electrical stimulation that are within the water window of the electrode.

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