Dissertations / Theses on the topic 'Levosimendan'
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Cavalcanti, Ruben Lundgren. "Efeitos da dobutamina ou levosimendana nas variáveis cardiopulmonares após a dexmedetomidina em pôneis submetidos à hipotensão pelo isoflurano." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2016. http://hdl.handle.net/10183/150240.
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Isoflurano reduz o débito cardíaco e produz vasodilatação periférica resultando em hipotensão sistêmica. Hipotensão pode contribuir para morbidade e mortalidade em equinos. Queda na pressão sanguínea pode ser tratada com inotrópicos e/ou vasopressores. Levosimendana é um inotrópico sensibilizador de cálcio que produz aumento na contratilidade e diminuição na resistência vascular periférica. Dexmedetomidina é um agonista de receptor adrenérgico α2 que aumenta a resistência vascular periférica. Este estudo objetivou avaliar os efeitos cardiopulmonares da dobutamina versus levosimendana após infusão de dexmedetomidina em pôneis com hipotensão induzida pelo isoflurano. Dez pôneis saudáveis (média 13,9 ± DP 2,4 anos) foram anestesiados com detomidina, seguido por quetamina e midazolam e mantidos em um estado hipotensivo induzido por um nível profundo de anestesia com isoflurano (2 CAM). Os animais foram randomizados para receber dexmedetomidina e dobutamina (DD; n=5) ou dexmedetomidina e levosimendana (DL; n=5). Após 45 minutos do estado estável de hipotensão, as variáveis basais foram registradas. Dexmedetomidina foi administrada em 10 minutos (3,5 μg.Kg-1) e as variáveis foram registradas; em seguida, infusão contínua de dexmedetomidina iniciou (1,75 μg.Kg-1.hr-1) e as variáveis foram registradas após 45 minutos. Dobutamina (5 μg.Kg-1.min-1) ou levosimendana (12 μg.Kg-1) foram administradas e as variáveis foram registradas após 10 minutos, seguido por ITC de dobutamina ou de levosimendana (0,2 μg.Kg-1.min-1) com novo registro das variáveis após 45 minutos. Por fim, as infusões foram interrompidas e as variáveis foram registradas após 45 minutos. Isoflurano (2 CAM) reduziu as PAs, o IS e o IC, mas não afetou o IRVS. Em relação ao isoflurano, bolus de dexmedetomidina aumentou as PAs pelo aumento do IRVS e da PVC, mas não afetou o IS e o IC previamente reduzidos pelo isoflurano. Após 45 minutos, dexmedetomidina elevou a PMAP, o VD/VT, o lactato e a creatinina e reduziu as PAs, o IRVS e a FC, mas não afetou o IC. Dexmedetomidina também reduziu o CaO2, a PaO2, a Pv̅O2, a Sv̅O2, o Cv̅O2, a Hb e o ḊO2I em ambos grupos em relação ao tempo basal. Dobutamina e levosimendana aumentaram significativamente o IS e o IC, mas dobutamina aumentou as PAs, o IRVS, o IRVP, a PMAP, a PVC, o CaO2, o Cv̅O2, a Hb, o ḊO2I e reduziu a creatinina e a O2ER, enquanto levosimendana não afetou as PAs, reduziu a PVC e o IRVS e aumentou o VD/VT e o Q̇s/Q̇t. Infusão de dexmedetomidina causa prejuízos cardiopulmonares importantes a despeito de aumentar as PAs após dose em bolus IV durante hipotensão induzida pelo isoflurano em pôneis. Dobutamina é melhor alternativa que levosimendana para restaurar as funções cardiovasculares e manter oxigenação durante infusão de dexmedetomidina associada a dose alta de isoflurano em pôneis.Isoflurane decreases cardiac output and produces peripheral vasodilation resulting in systemic hypotension. Hypotension may contribute to morbidity and mortality in equines. Drop in blood pressure can be treated with inotropic and or vasopressors. Levosimendan is a calcium sensitizer that produces increase in contractility and decrease in systemic vascular resistance. Dexmedetomidine is an α2 adrenergic-receptor agonist that increases systemic vascular resistance. This study aimed to evaluate the cardiopulmonary effects of dobutamine versus levosimendan after infusion of dexmedetomidine on isoflurane-induced hypotension in ponies. Ten healthy ponies (mean 13,9 ± SD 2,4 years) were anesthetized with detomidine followed by ketamine and midazolam and maintained at a steady hypotensive state induced by a deep level of isoflurane anesthesia (2 MAC). Animals were randomized to receive dexmedetomidine and dobutamine (DD; n=5) or dexmedetomidine and levosimendan (DL; n=5). After 45 min of steady state, baseline variables were recorded. Dexmedetomidine was administered over 10 minutes (3,5 μg.Kg-1), and variables were recorded; thereafter, dexmedetomidine CRI started (1,75 μg.Kg-1.hr-1), and variables were recorded after 45 minutes. Dobutamine (5 μg.Kg-1.min-1) or levosimendan (12 μg.Kg-1) were administered over 10 minutes and variables were recorded, followed by dobutamine or levosimendan CRI (0,2 μg.Kg-1.min-1) for 45 minutes, then variables were recorded a sixth time. Lastly, infusions were interrupted and the variables were again recorded after 45 minutes. Isoflurane (2 MAC) decreased arterial blood pressures (ABPs), SI and CI, but not affected SVR. In relation to isoflurane, bolus of dexmedetomidine increased ABPs due to augmentation on RVS and PCV, but not affected SI and CI already reduced by isoflurane. After 45 minutes, dexmedetomidine raised MPAP, VD/VT, lactate and creatinine and reduced ABPs, SVR, and HR, but not affected CI. Dexmedetomidine also reduced CaO2, PaO2, Pv̅O2, Sv̅O2, Cv̅O2, Hb and ḊO2I in both groups compared to baseline. Dobutamine and levosimendan increased SI and CI, but dobutamine increased ABPs, SVRI, PVRI, MPAP, CVP, CaO2, Cv̅O2, Hb, ḊO2I and decreased creatinine and O2ER, while levosimendan not affected ABPs, decreased CVP and SVRI and increased VD/VT and Q̇s/Q̇t. Dexmedetomidine CRI during isoflurane-induced hypotension in ponies causes statistically significant cardiopulmonary effects regardless of increasing the ABPs after bolus administration. Dobutamine is better alternative than levosimendan for restoring cardiovascular function and maintaining oxygenation during CRI dexmedetomidine associated with high-dose isoflurane in ponies. Because the proposed vasoconstriction model produced late opposite physiological effect, further studies with levosimendan in ponies and horses remain to be performed, especially in clinical patients. Likewise, further studies are justified to evaluate the effect of levosimendan on regional tissue perfusion.
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Prem, Susanne [Verfasser], and Robert H. G. [Akademischer Betreuer] Schwinger. "Levosimendan bei Patienten mit akuter Herzinsuffizienz / Susanne Prem. Betreuer: Robert H.G. Schwinger." Regensburg : Universitätsbibliothek Regensburg, 2016. http://d-nb.info/1082128104/34.
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Berg, Blomkvist Sofia, and Linda Eriksson. "Psykosocialt stöd vid kronisk hjärtsvikt och planerade repetitiva behandlingar med levosimendan : -en kvalitativ intervjustudie-." Thesis, Uppsala universitet, Institutionen för folkhälso- och vårdvetenskap, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-255832.
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Taipe, Quispe Neri Nohemi. "Levosimendan y mortalidad en pacientes con síndrome de bajo gasto cardiaco post cirugía cardiaca." Bachelor's thesis, Universidad Nacional Mayor de San Marcos, 2013. https://hdl.handle.net/20.500.12672/12927.
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El documento digital no refiere asesorObjetivo: Determinar que el uso de Levosimendan disminuye la mortalidad hospitalaria en el síndrome de bajo gasto post cirugía cardiaca en pacientes adultos admitidos en el servicio de UCI del HNERM en el periodo 2009-2011. Material y Métodos: La presente investigación es de tipo Descriptivo, Analítico .La población está conformada por 63 pacientes adultos con síndrome de bajo gasto post cirugía cardiaca y que recibieron Levosimendan a una dosis continua de 0.1 mcg/kg/min en una solución glucosada al 5%. Resultados: La investigación concluye que hay una mejora estadísticamente significativa en la fracción de eyección, la media de la Fracción de eyección por ecografía preoperatoria por Simpson aumenta de 28.4% a 38.9% significativamente P<0.05 ,el 50% del total paciente mujeres con síndrome de bajo gasto cardiaco y con uso de Levosimendan tienen edad de 71 a 80 años. Asimismo se aprecia que del total de varones con síndrome de bajo gasto cardiaco y con uso de Levosimendan el 38.2% tiene edad de 61 a 70 años los pacientes en el preoperatorios el 63.5% presentan clase funcional III y el 36.5% presentan clase funcional IV , que del total de pacientes en el postoperatorios el 50.8% presentan clase funcional I y el 44.4% presentan clase funcional II. Se encontró que la media de la estancias hospitalaria es de 2.3 días . Los pacientes síndrome de Bajo Gasto Cardiaco Post Cirugía Cardiaca con el uso de levosimendan el 90.5% permanecen vivos y el 9.5% fallecieron en el posoperatorio temprano. Se encontró un índice cardiaco de 3.8. Conclusiones: Se observó que los pacientes posoperados de cirugía cardiaca que cursaron con sindrome de bajo gasto cardiaco y que recibieron levosimendan, infusión continua de 0.1 mcg/kg/min. presentaron una disminución en la mortalidad postoperatoria, asimismo hay una mejora estadísticamente significativa en la fracción de eyección.
Trabajo académico
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Kohnke, Anja [Verfasser]. "Experimentelle Untersuchungen zur proarrhythmischen Wirkung des Kalzium-Sensitizers Levosimendan sowie möglicher protektiver Therapieoptionen / Anja Kohnke." Hannover : Bibliothek der Tierärztlichen Hochschule Hannover, 2017. http://d-nb.info/1136279342/34.
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Kivikko, Matti. "Hemodynamic effects and pharmacokinetics of levosimendan and its metabolites in patients with severe heart failure." Helsinki : University of Helsinki, 2003. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/kivikko/.
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Kleinebrahm, Maria [Verfasser]. "Einfluss der Gabe von Levosimendan auf die Nierenfunktion bei herzchirurgischen Eingriffen unter Einsatz der extrakorporalen Zirkulation / Maria Kleinebrahm." Lübeck : Zentrale Hochschulbibliothek Lübeck, 2014. http://d-nb.info/1063815916/34.
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de, Winter J. M., B. Joureau, V. Sequeira, N. F. Clarke, der Velden J. van, G. J. Stienen, H. Granzier, A. H. Beggs, and C. A. Ottenheijm. "Effect of levosimendan on the contractility of muscle fibers from nemaline myopathy patients with mutations in the nebulin gene." BioMed Central, 2015. http://hdl.handle.net/10150/610333.
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BACKGROUND: Nemaline myopathy (NM), the most common non-dystrophic congenital myopathy, is characterized by generalized skeletal muscle weakness, often from birth. To date, no therapy exists that enhances the contractile strength of muscles of NM patients. Mutations in NEB, encoding the giant protein nebulin, are the most common cause of NM. The pathophysiology of muscle weakness in NM patients with NEB mutations (NEB-NM) includes a lower calcium-sensitivity of force generation. We propose that the lower calcium-sensitivity of force generation in NEB-NM offers a therapeutic target. Levosimendan is a calcium sensitizer that is approved for use in humans and has been developed to target cardiac muscle fibers. It exerts its effect through binding to slow skeletal/cardiac troponin C. As slow skeletal/cardiac troponin C is also the dominant troponin C isoform in slow-twitch skeletal muscle fibers, we hypothesized that levosimendan improves slow-twitch muscle fiber strength at submaximal levels of activation in patients with NEB-NM. METHODS: To test whether levosimendan affects force production, permeabilized slow-twitch muscle fibers isolated from biopsies of NEB-NM patients and controls were exposed to levosimendan and the force response was measured. RESULTS: No effect of levosimendan on muscle fiber force in NEB-NM and control skeletal muscle fibers was found, both at a submaximal calcium level using incremental levosimendan concentrations, and at incremental calcium concentrations in the presence of levosimendan. In contrast, levosimendan did significantly increase the calcium-sensitivity of force in human single cardiomyocytes. Protein analysis confirmed that the slow skeletal/cardiac troponin C isoform was present in the skeletal muscle fibers tested. CONCLUSIONS: These findings indicate that levosimendan does not improve the contractility in human skeletal muscle fibers, and do not provide rationale for using levosimendan as a therapeutic to restore muscle weakness in NEB-NM patients. We stress the importance of searching for compounds that improve the calcium-sensitivity of force generation of slow-twitch muscle fibers. Such compounds provide an appealing approach to restore muscle force in patients with NEB-NM, and also in patients with other neuromuscular disorders.
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Alomari, Abdul-Hakeem Hussein Electrical Engineering & Telecommunications Faculty of Engineering UNSW. "Spectral analysis of arterial blood prssure and stroke volume variability: the role of Calcium channel blockers and sensitizers." Publisher:University of New South Wales. Electrical Engineering & Telecommunications, 2008. http://handle.unsw.edu.au/1959.4/43923.
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In this thesis, we included results from two studies. The first one considered the effects of the blood volume changes, during blood donation, on the heart rate variability (HRV) measured, non-invasively, form electrocardiographic (ECG) and photoplethysmographic (PPG) signals. Our results showed that, during blood donation, there were no significant changes in the pulsatile area of PPG signal, while heart rate increased. No significant changes were noticed in HRV extracted from both signals. Error analysis between the HRV extracted from ECG and peak interval variability (PIV) suggested that the error during blood donation was increased which means that the use of PIV extracted from PPG signal, used as a replacement diagnostic tool in clinical applications, needs further investigations and should be carefully studied in non-stationary cardiovascular situations such as blood donation. The imbalance between the two branches of the autonomic nervous system, sympathetic and parasympathetic, vagal, may result in a harmful activation of myocardial tissues which cause arrhythmias and sudden cardiac death. Although the study of the sympathovagal balance have been attracting many researchers, further studies are needed to elucidate the effects of many kinds of drugs on the autonomic modulation of the cardiac muscle, specifically, the cells of sinoatrial (SA) node. The aim of the second part of this thesis was to assess the effects of calcium channel blocker (Verapamil), calcium channel sensitizer (Levosimendan), calcium chloride (CaCl2), the combinations of verapamil/ CaCl2, levosimendan/ CaCl2, and noradrenaline infusion on beat-to-beat cardiovascular variability represented, in this research, by systolic blood pressure variability (SBPV), and stroke volume variability (SVV) signals. We used Fat Fourier Transform (FFT) to evaluate the power spectral density of the fluctuations in both signals to evaluate the effects of short-term treatments with those drugs on the sympathovagal balance in normal rats. Then, we compared the spectra obtained from SBPV and SVV to decide which of these fluctuations along with corresponding spectrum was more able to provide a clear feedback about the autonomic nervous system. Our data suggests that there were a significant correlations between low- (LF), mid- (MF), and high-frequency (HF) spectra obtained from SBPV and SVV except between the HF spectra estimated from after the infusion of levosimendan where a poor correlation (r = 0.530, p = 0.281) was noticed. This that both HF components obtained provide different information regarding the autonomic nervous system modulation of the SA node cells, while the results obtained from the rest of experiments showed that both signals provide same information about the modulation of sympathetic and parasympathetic tone due to all stages of different drugs infusion studied in this thesis. Besides that, we found that both spectra may be used to track the fluctuations in the cardiac output as a result of the drugs infusion.
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Axelsson, Birger. "Cardiac effects of non-adrenergic inotropic drugs : clinical and experimental studies." Doctoral thesis, Umeå universitet, Anestesiologi och intensivvård, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-68967.
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Background: Myocardial failure and dysfunction is not uncommon during critical illness and following cardiac surgery. For optimal treatment, a better understanding of the effects of inotropic drugs is needed. In this thesis, two non-adrenergic mediated inotropes, milrinone and levosimendan were studied in different models of myocardial dysfunction. The study aims were to assess the following: the effects of milrinone on blood flow in coronary artery bypass grafts during CABG surgery; the effects of milrinone on left ventricular diastolic function during post-ischaemic myocardial dysfunction; whether milrinone or levosimendan are protective or injurious during acute myocardial ischaemia, and if levosimendan potentiates myocardial function when added to milrinone in an experimental model of post-ischaemic (stunned) myocardium. Material and Methods: In Study I, 44 patients undergoing coronary artery bypass surgery(CABG) were included as subjects. Milrinone or saline was administrated in a single dose during cardio-pulmonary bypass (CPB) and coronary graft flow measurements were recorded after 10 and 30 min following CPB. In Study II; 24 patients undergoing CABG had estimations of peak ventricular filling rates made before and after CPB with administration of milrinone or saline as a single dose during CPB, performed by assessment of the rate of change in diastolic cross-sectional left ventricular area. In Study III, energy-metabolic effects of milrinone and levosimendan were measured in an anaesthetized porcine model during 45 minutes of regional myocardial ischemia. Microdialysis sampling of metabolites of local ischemic metabolism allowed assessment of glycolytic activity and the degree of myocardial calcium overload. In Study IV, in a porcine model of postischaemic myocardial stunning, ventricular pressure-volume relationships were analyzed when milrinone or a combination of milrinone and levosimendan were given together. Results: In Study I, there was a clear increase in non-sequential saphenous vein graft blood flow with milrinone at 10 minutes (64.5 ± 37.4 compared to placebo 43.6 ± 25.7 ml/min (mean ± SD).). A decreasing but still measureable flow increase was seen for milrinone at 30 minutes. In Study II, an increase in early left ventricular filling rate (ventricular cross-sectional area rate of change,dA/dt) was seen in the milrinone treated group. Pre-bypass milrinone group dA/dt 22.0 ± 9.5 changed to post-bypass values dA/dt 27.8 ± 11.5 cm2/sec). Placebo group pre-bypass dA/dt was 21.0 ± 8.7 and post-bypass 17.1 ± 7.1 cm2/sec. A milrinone effect was demonstrated in an adjusted regression model (p = 0.001). In Study III, neither milrinone nor levosimendan led to a change in energy-metabolic activity during ischemia as reflected by interstitial glucose, pyruvate, lactate orglycerol. Neither drug exacerbated the relative myocardial calcium overload during ischemia. In Study IV, milrinone improved active relaxation (tau) in post-ischemic stunned myocardium, but did not markedly improve systolic function by preload recruitable stroke work. Levosimendan added to milrinone showed minimal effect on active relaxation but a positive effect on systolic function in combination with milrinone. Conclusions: We conclude that milrinone treatment leads to an increase in blood flow in newly implanted coronary saphenous vein grafts, and improves ventricular relaxation post-cardiopulmonary bypass. Neither milrinone nor levosimendan, in this porcine model, negatively influence myocardial energy metabolism or calcium overload during acute ischaemia. Addition of levosimendan to milrinone treatment during post-ischaemic ventricular dysfunction may provide additive inotropic effects on systolic function but probably not for active relaxation.
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Leivaditis, Vasileios [Verfasser]. "Titel: The perioperative use of Levosimendan as a means of optimizing the surgical outcome in patients with severe heart insufficiency undergoing cardiac surgery = Die perioperative Anwendung von Levosimendan zur Optimierung des chirurgischen Ergebnisses bei Patienten mit schwerer Herzinsuffizienz, die sich einer Herzoperation unterziehen. / Vasileios Leivaditis." Mainz : Universitätsbibliothek Mainz, 2020. http://d-nb.info/1212960831/34.
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Lipp, Stella Evelyn [Verfasser]. "Einfluss des prophylaktischen Einsatzes des Kalzium-Sensitizers Levosimendan auf die Ergebnisse von Hochrisiko-Patienten bei herzchirurgischen Eingriffen / Stella Evelyn Lipp." Gießen : Universitätsbibliothek, 2016. http://d-nb.info/111828982X/34.
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Lewis, Kristin. "Functional Remodeling Following Myofilament Calcium Sensitization in Rats with Volume Overload Heart Failure." The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1397058520.
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Knors, Henning Hermann Alexander [Verfasser], and Karsten [Akademischer Betreuer] Sydow. "Einfluss von Levosimendan auf die leukozytäre und endotheliale Funktion bei Patienten mit chronischer Herzinsuffizienz / Henning Hermann Alexander Knors. Betreuer: Karsten Sydow." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2015. http://d-nb.info/1073248224/34.
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Lima, Ronald de Albuquerque. "Comparação do uso de noradrenalina, nitroprussiato e levosimendan na terapia do choque hipovolêmico: efeitos sobre a microcirculação e expressão gênica renal." Universidade do Estado do Rio de Janeiro, 2014. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=9141.
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Este trabalho teve como objetivo avaliar os efeitos sistêmicos, microcirculatórios assim como mudanças na expressão gênica renal, causados pela ação da noradrenalina, nitropussiato de sódio e levosimendan no tratamento do choque hemorrágico. Nesse estudo foi utilizado o modelo da câmara dorsal.Os animais foram sujeitos a choque hemorrágico e após, foram aleatoriamente divididos em quatro grupos. Os grupos foram: CTRL, recebeu apenas ringer lactato; NPS recebeu ringer lactato com nitroprussiato de sódio; NA recebeu ringer lactato com noradrenalina e LEV, recebeu ringer lactato com levosimendan. Foram avaliados parâmetros sistêmicos, assim como parâmetros microcirculatórios (comparados como percentual em relação ao momento basal). Além disso, foi avaliada a expressão gênica renal de eNOS, HIF-1α, ICAM e caspase-3. O grupo NPS apresentou uma recuperação sustentada do diâmetro arteriolar ( 89 12 %) e DCF (125 114 %) ao final do tratamento. Houve recuperação da velocidade de hemácias nos grupos CTRL e NPS. Não houve diferença em relação ao número de leucócitos aderidos e/ou rolantes ao final do tratamento. A expressão gênica renal de eNOS e caspase-3 entre os grupos não apontou diferenças, entretanto houve diferença significativa na expressão renal de HIF- 1α no grupo NA (0,65 0,08, UA) em relação ao grupo CTRL (0,44 0,06, UA) e LEV (0,45 0,06, UA). Todos os grupos tiveram uma maior expressão de ICAM (0,65 0,12; 0,7 0,12; 0,069 0,06; 0,65 0,12, UA) em relação ao grupo SHAM (0,50 0,05, UA). Ringer lactato puro ou associado com noradrenalina ou levosimendan não foram suficientes para recuperar e sustentar os parâmetros microvasculares. O tratamento com nitroprussiato de sódio foi o que apresentou os melhores resultados, com recuperação dos diâmetros arteriolar, da DCF e velocidade de hemácias.This work aimed at evaluating the systemic and microcirculatory effects, as well as changes in renal gene expression elicited by noradrenalin, sodium nitroprusside and levosimendan associated to volume resuscitation in the treatment of hemorrhagic shock. The dorsal chamber model was used in this study. Animals were subjected to hemorrhagic shock and after that, were randomly distributed between four groups. Groups were: CTRL, received only lactated ringer's solution; NPS received lactated ringer's solution with sodium nitroprusside; NA received lactated ringer's solution with noradrenaline and LEV received lactated ringer's with levosimendan. Systemic and microcirculatory parameters were evaluated ( as percent change compared to baseline). Furthermore, renal genic expression of eNOS, HIF-1a and caspase-3 were also evaluated. NPS group presented a sustained recovery of arteriolar diameter ( 89 12 %) and FCD (125 114 %) at the end of the treatment. There was a red blood cell velocity recovery in CTRL and NPS groups. There was no difference regarding adhered or rolling leukocytes at the end of the treatment. eNOS and caspase-3 renal genic expression between groups showed no differences, however, there was a significant difference in renal genic expression of HIF-1α in NA group (0,65 0,08, AU) compared to CTRL (0,44 0,06, AU) e LEV (0,45 0,06, AU). All groups had a higher expression of ICAM (0,65 0,12; 0,7 0,12; 0,069 0,06; 0,65 0,12, AU) compared to the SHAM group (0,50 0,05, AU). Ringer's lactate solution associated or not to noradrenaline or levosimendan were not enough to recover and sustain microvascular parameters. Treatment with sodium nitroprusside presented the best results, with sustained arteriolar diameter, FCD and RBCV recoveries.
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Jasulaitis, Dominik [Verfasser]. "Einfluss von Levosimendan auf den intensivmedizinischen Verlauf und das 180-Tage-Überleben bei Patienten mit mechanischen Herzunterstützungsverfahren bei schwerem Postkardiotomieherzversagen / Dominik Jasulaitis." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2013. http://d-nb.info/1032171243/34.
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Thomas, Kai [Verfasser], Lothar A. [Akademischer Betreuer] Schwarte, and Axel [Akademischer Betreuer] Gödecke. "Untersuchungen zur Wirkung von Levosimendan auf die Hämodynamik und den Metabolismus unter akuter Hypoxie bei anästhesierten Hunden / Kai Thomas. Gutachter: Lothar A. Schwarte ; Axel Gödecke." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2013. http://d-nb.info/104358739X/34.
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Immohr, Moritz Benjamin [Verfasser], and Payam [Gutachter] Akhyari. "Einfluss der extrazellulären Superoxiddismutase und des Kalziumsensitizers Levosimendan auf die kardiovaskuläre Ischämie und Reperfusion bei extrakorporaler Zirkulation in einem Rattenmodell / Moritz Benjamin Immohr ; Gutachter: Payam Akhyari." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2019. http://d-nb.info/119198513X/34.
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Kaakinen, H. (Hanna). "Approaches to improving brain protection in cardiac and aortic surgery:an experimental study in a porcine model with hypertonic saline dextran, levosimendan, leukocyte depleting filter and different acid base management strategies." Doctoral thesis, University of Oulu, 2008. http://urn.fi/urn:isbn:9789514289040.
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Abstract
In the repair of complex congenital heart defects or in surgery of the aortic arch, normal circulation may be temporarily halted to ensure a clean, bloodless operation field. The brain is the organ most vulnerable to ischemic injury during this no-flow period, and the mortality and morbidity of these procedures today consists mostly of neurological complications. Hypothermia decreases the need for oxygen and other metabolites, and cooling the patient with an extracorporeal heart-lung machine can provide enough time to perform the necessary surgical procedures during a circulatory standstill. This procedure is referred to as hypothermic circulatory arrest (HCA). Sometimes the cerebral circulation can be maintained even if the rest of the body undergoes circulatory arrest, and this strategy, involving separate catheterization of brain-destined vessels, is referred to as selective cerebral perfusion (SCP).
In this work, four separate brain protection strategies were evaluated. Two studies were performed on a surviving porcine model (I, II) to evaluate neurological recovery as well as cerebral metabolism and histopathology, and two were acute in design (III, IV), employing the modern technology of intravital microscopy to examine cerebral microcirculation.
The first study (I) showed that the administration of hypertonic saline dextran (HSD) led to a decrease in intracranial pressure, improved brain metabolism, better neurological recovery and less histopathological injury of the brain tissue in association with HCA. In the second study (II) a novel pharmacological molecule, levosimendan, reduced the intracranial pressure during the operation, but no improvement in terms of cerebral metabolism, neurological recovery or histopathological brain injury was observed after HCA. In the third study (III), real-time intravital microscopy showed that in association with HCA, a leukocyte depleting filter (LDF) attached to the cardiopulmonary bypass circuit reduces the number of activated leukocytes in cerebral microcirculation. In the fourth study (IV), cerebral metabolism and microcirculation were similar during SCP independent of the acid-base management strategy.
The results of this work suggest that HSD could be assessed in human trials, that levosimendan needs further studies to optimize its potential, that the LDF functions as designed and that the differences between the α- and the pH-stat acid-base management strategies with SCP did not differ in moderate hypothermia.
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Arnold, Andreas Gerhard [Verfasser]. "Der Einfluss prophylaktischer Applikation von Levosimendan verglichen mit prophylaktischer intraaortaler Gegenpulsation auf das Kurz- und Langzeitüberleben von Patienten mit hochgradig eingeschränkter linksventrikulärer Pumpfunktion nach kardiochirurgischem Eingriff unter Einsatz der Herz-Lungen-Maschine / Andreas Gerhard Arnold." Gießen : Universitätsbibliothek, 2020. http://d-nb.info/1219983284/34.
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Arnold, Andreas [Verfasser]. "Der Einfluss prophylaktischer Applikation von Levosimendan verglichen mit prophylaktischer intraaortaler Gegenpulsation auf das Kurz- und Langzeitüberleben von Patienten mit hochgradig eingeschränkter linksventrikulärer Pumpfunktion nach kardiochirurgischem Eingriff unter Einsatz der Herz-Lungen-Maschine / Andreas Gerhard Arnold." Gießen : Universitätsbibliothek, 2020. http://d-nb.info/1219983284/34.
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Despas, Fabien. "Physiopathologie et pharmacologie de l'hyperactivité sympathique de l'insuffisance cardiaque." Toulouse 3, 2010. http://thesesups.ups-tlse.fr/904/.
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L'hyperactivité du système nerveux sympathique (SNS) participe à l'initiation et à la progression de l'insuffisance cardiaque (IC). Nous démontrons pour la 1ère fois que l'insuffisance rénale (IR) contribue à l'augmentation de l'activité du SNS au cours de l'IC. La majoration du tonus sympathique est en partie expliquée par une augmentation de la tonicité de base de l'arc chémoreflexe périphérique. Au cours de l'IC, près de 20% des patients présentent une anémie. Nous démontrons pour la 1ère fois que l'anémie contribue, comme l'IR, à une hyperactivation du SNS. L'histoire naturelle de l'IC se caractérise par la survenue d'épisodes de décompensation, pendant lesquels, le bas débit cardiaque justifie le recours nécessaire aux inotropes positifs dont l'utilisation reste controversée. Le levosimendan est un agent inotrope positif original puisqu'il sensibilise les filaments de troponine C au calcium, sans interagir directement avec la voie ß-adrénergique. Nous avons montré que le levosimendan induisait une diminution de l'activité du SNS accompagnée d'une amélioration attendue des performances cardiaques et d'une vasodilatation. Un des traitements de l'IC est la transplantation cardiaque. Il n'existe pas de recommandations sur le type d'examens pronostiques à réaliser. La scintigraphie myocardique à la métaiodobenzylguanidine (MIBG) permet une évaluation des voies noradrénergiques cardiaques. Nous avons étudié la valeur pronostique de cet examen et comparé cette dernière à celles d'autres marqueurs : dosage du Brain Natriuretic Peptide (BNP) et évaluation de la VO2max. La MIBG n'est pas plus informative que des examens moins onéreux et plus aisément disponiblesSympathetic activation is a hallmark of chronic heart failure (CHF) involved in both initiation and progression of this syndrome. The aim of our work was to evaluate sympathetic nervous system by microneurography. We show for the first time that chronic renal failure (CRF) increases sympathetic activity in CHF patients through tonic chemoreflex activation, and that this effect is correlated with renal failure severity. Consequently we also showed that another comorbidity, namely anemia, also increases sympathetic activity in patients with CHF. Episode of acute decompensated heart failure remains the main causes of hospitalization in patients with HF. Patients are generally treated with inotropic therapy, however there is no evidence that these agents improve outcome. Levosimendan an original mechanism of action since inotropism is mediated through sensitizing of myofilaments to calcium. We show for the 1st time that levosimendan decrease sympathetic nerve activity. Finally we focused on the prognostic value of sympathetic markers in patients with end stage heart failure. Among these cardiac sympathetic neuronal activity can be non-invasively assessed by the use of I123 radiolabeled metaiodobenzylguanidine (MIBG). We sought to ascertain the prognostic value of MIBG in patients with advanced heart failure and developed comparisons with other prognostic indices such as brain natriuretic peptide (BNP) and peak VO2. Our results suggest that altered adrenergic nerve function assessed by MIBG has a prognostic value in AHF patient awaiting heart transplant, which is however less than that of peak VO2 and BNP
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Genis, Amanda. "Possible mechanisms for levosimendaninduced cardioprotection." Thesis, Stellenbosch : Stellenbosch University, 2008. http://hdl.handle.net/10019.1/1575.
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Thesis (MScMedSc (Biomedical Sciences. Medical Physiology))--Stellenbosch University, 2008.Background and purpose. To limit ischaemic injury, rapid restoration of coronary blood flow is required, which will in turn reduce infarct size. However, reperfusion itself causes myocyte death – a phenomenon termed lethal reperfusion-induced injury, which limits protection of the ischaemic myocardium. Thus the reperfusion of irreversibly damaged myocytes may accelerate the process of cell necrosis. Additive protection of the ischaemic myocardium in the form of adjunct therapy remains a topic of intensive research. Levosimendan, a calcium sensitizing agent with positive inotropic effects has in several studies been found to alleviate the damaging effects of reperfusion injury. Levosimendan has been shown to be a KATP channel opener. These channels have been implicated to play an important role in ischaemic preconditioning (IPC). With this knowledge, the aim of this study was to determine whether levosimendan and IPC have certain cardioprotective mechanisms in common and whether protection with pharmacological preconditioning could be elicited with levosimendan. In this study, we investigated whether: 1) the isolated guinea pig heart could be protected by ischaemic preconditioning (IPC) and postconditioning (IPostC), 2) the heart could be pharmacologically pre- and postconditioned, using levosimendan (LPC & LPostC), 3) a combination of IPC & LPC had an additive protective effect on the heart, 4) the KATP (both mitochondrial and sarcolemmal) channels are involved in this protection and 5) the pro-survival kinases of the RISK (reperfusion injury salvage kinase) pathway are involved. Experimental approach. Isolated perfused guinea pig hearts were subjected to three different IPC protocols (1x5, 2x5 and 3x5 minutes of ischaemia) or levosimendan (0.1μM) preconditioning, before coronary artery occlusion (CAO – 40min@36.5ºC), followed by 30 minutes of reperfusion. Hearts were also subjected to a combination of IPC & LPC, to establish whether they had additive protective effects. In addition, hearts were pre-treated with levosimendan directly before induction of sustained ischaemia (without washout of the drug – levosimendan pre-treatment (LPT)) for 10min. With the postconditioning protocol, iii the hearts were subjected to 3x30second cycles of ischaemia/reperfusion or levosimendan/vehicle. In a separate series of experiments, hearts were treated with KATP channel blockers (for both sarcolemmal & mitochondrial), before LPC, LPT and LPostC. The endpoints that were measured were: cardiac reperfusion function, myocardial infarct size and RISK pathway expression and phosphorylation (PKB/Akt and extracellular signal-regulated kinase – ERK42/44). Results. IPC, IPostC, LPC & LPostC decreased myocardial infarct size significantly compared with their controls (21.9±2.2%, 21.4±2.2%, 20.6±3.1% and 20.6±1.8% respectively vs. 46.4±1.8% for controls, p<0.05). The combination of IPC & LPC had no additive protective effect. Pre-treating the hearts with levosimendan (without washout), before index ischaemia, proved to be the most effective method of cardioprotection (infarct size: 5.8±0.9% vs. 46.4±1.8% for controls, p<0.001). With LPT a significant increase (p < 0.05 vs. control) in phosphorylation of ER42/44 was also observed. An increase in the activity of one of the RISK pathway kinases, ERK42/44 seems to be one of the reasons for LPT’s efficacy. Treating the hearts with KATP channel blockers before subjecting them to LPC, LPT & LPostC abolished the protective effects induced by levosimendan, suggesting a role for the sarcolemmal and mitochondrial KATP channels in levosimendan-induced cardioprotection. Conclusions and implications. 1) Isolated guinea pig hearts could be pre- and postconditioned within the setting of ischaemia, 2) Hearts could be pharmacologically pre- and postconditioned with levosimendan, 3) levosimendan pre-treatment is the most effective way to reduce infarct size, possibly acting by increasing the phosphorylation of ERK42/44, 4) Myocardial protection was not increased by combining IPC & LPC (suggesting similar mechanisms of protection), 5) LPC, LPT and LPostC were abolished by both sarcolemmal and mitochondrial KATP channel blockers. .LPC and especially LPT, could be useful before elective cardiac surgery while LPostC may be considered after acute coronary artery events.
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Li, Ping-Chun, and 李秉純. "Studies on Protective Actions of Levosimendan in Human Progenitor Cell-Derived Cardiomyocytes after Anoxia- Reoxygenation." Thesis, 2014. http://ndltd.ncl.edu.tw/handle/38601382796273490892.
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博士東海大學
生命科學系
102
Ischemic heart disease is the leading cause of death worldwide as a single disease entity. To salvage cardiomyocytes suffering acute ischemic insult, it is mandatory to restore blood supply as early as possible. Paradoxically reperfusion per se inflicts additional damages on the cells. Rapid death of ischemic but still viable cardiomyocytes may ensue following successful reestablishment of blood flow. This lethal reperfusion injury diminishes the benefit of early reperfusion and is an important subject of investigation. Ca2+ overload, a prominent feature of cells subject to ischemia-reperfusion(I/R) that originates from a preceding intracellular Na+ accumulation and the action of reverse mode Na+-Ca2+ exchanger(NCX) on the plasma membrane, could lead to necrosis or apoptosis. NCX plays an important role in controlling Ca2+ homeostasis, both under physiological conditions and during I/R. The mitochondrion, when containing excessive Ca2+, triggers necrosis or apoptosis. Because there are attachments and Ca2+ communications between endoplasmic reticulum (ER) and mitochondria, interactions of these 2 organelles might affect mitochondrial Ca2+ content, which, when excessive, could to cell death during I/ R. Preserving cardiomyocyte viability has also become an paradigm in treatment of heart failure, while the use of conventional inotropes, which enhances cardiac contractility by increasing intracellular Ca2+ concentration, could decrease patient survival. Levosimendan, a known calcium sensitizer with positive inotropic and vasodilating properties, might also be cardioprotective during I/R. Its effects on calcium homeostasis and apoptosis in I/R injury remain unclear. A human cardiomyocyte culture model was established to avoid inconsistencies arising from species difference if animal cells were used for experiments. We probed effects and underlying mechanisms of levosimendan on apoptosis and NCX activity in cultured human cardiac progenitor cells(hCPC)-derived cardiomyocytes undergoing anoxia-reoxygenation (A/R), simulating I/R in vivo. Administration of levosimendan decreased apoptosis of hCPC-derived cardiomyocytes induced by A/R. The increase in reverse-mode NCX activity after A/R was curtailed by levosimendan, and NCX1 was translocated away from the cell membrane. Concomitantly, ER stress response induced by A/R was attenuated in hCPC-derived cardiomycytes treated with NCX-targeted siRNA or levosimendan with no synergistic effect. Results indicated levosimendan inhibited reverse-mode NCX activity to protect hCPC- derived cardiomyocytes from A/R-induced ER stress and cell death, and also suggested that during A/R heightened NCX reverse mode action-induced intracellular Ca2+ increase plays an decisive role in apoptosis induced by ER stress response and mitochondrial Ca2+ overload resulting from ER- mitochondrial communication. Confirmation of results awaits further studies.
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LI, Kai-Yi, and 李凱益. "Therapeutic Effects of Levosimendan on Peritonitis-Induced Septic Shock with Multiple Organ Dysfunction Syndrome in Rats." Thesis, 2010. http://ndltd.ncl.edu.tw/handle/34075137309031189172.
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碩士國防醫學院
藥理學研究所
98
Sepsis/septic shock and its sequelae, multiple organ dysfunction syndrome (MODS), are major contributors of mortality in critically ill patients. In sepsis, bacterial products and toxins activate cells of innate immune system (macrophages and neutrophils) to release amount of inflammatory mediator and the formation of free radicals results in producing large quantity of nitric oxide (NO), leading to circulatory failure and an imbalance between systemic oxygen delivery and demand, and finally causing MODS. Although the use of vasopressors is recommended, but there is still no significant improvement in survival rate of patients with septic shock. Enhanced lymphocyte apoptosis has been identified as a cornerstone in sepsis pathophysiology, thus creating a state of immunosuppression and preventing lymphocyte apoptosis during the course of sepsis may represent a way of effectively treating this disorder. Levosimendan (LS) is not a vasopressor, but a fairly new calcium sensitizer with positive inotropic properties without increasing myocardial oxygen consumption or inducing ventricular arrhythmias. Therefore, we evaluated the effects of LS in Wistar rats with MODS induced by cecal ligation and puncture (CLP). Rats were divided into six groups: (1) sham-operation (SOP), (2) SOP + vehicle (infusion dose (5％ glucose): 30 μl/kg/min for 6 h, loading dose: 120 μl/kg for 10 min i.v. at 3 hr after SOP), (3) SOP + LS (infusion dose: 0.3 μg/kg/min for 6 hr, loading dose 12 μg/kg for 10 min i.v. at 3 hr after SOP) (4) CLP, (5) CLP + vehicle (infusion dose (5％ glucose): 30 μl/kg/min for 6 h, loading dose: 120 μl/kg for 10 min i.v. at 3 hr after CLP) and (6) CLP + LS (infusion dose: 0.3 μg/kg/min for 6 hr, loading dose 12 μg/kg for 10 min i.v. at 3 hr after CLP). The changes of hemodynamics, blood glucose, blood gas, rectal temperature, cell damage, hepatic function and renal function, plasma NO, interleukin (IL)-1 level and survival rate were monitored over 18 h. After sacrifice, most organs were excised for histological examination studies, inducible NO synthase expression (iNOS) (lung), Caspase-3 protein expression (spleen) and superoxide anion measurement. Our results showed that LS (1) improved hypotension, hypoglycemia, and vascular hyporeactivity caused by CLP, (2) reduced GPT, GOT, CRE, BUN and LDH in plasma, (3) reduced plasma NO and IL-1 level, superoxide anion levels and lung iNOS expression, (4) decreased lung, liver, kidney, intestine polymorphonuclear neutrophils (PMN) infiltration, (5) attenuated apoptosis of spleen, (6) improved metabolic acidosis, (7) improved the survival rate compared to the CLP + vehicle group. Thus, the beneficial effect of LS may contribute to reducing the plasma concentration of NO and IL-1 as well as organ superoxide anion levels and decreasing lung, liver, intestine PMN infiltration and spleen apoptosis, thereby decreasing the mortality rate in peritonitis-induced septic animals.
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Geilfus, Diana. "Direkte kardiale Effekte positiv inotroper Pharmaka bei Sepsis-induzierter kardialer Dysfunktion am isoliert perfundierten Rattenherzen." Doctoral thesis, 2010. http://hdl.handle.net/11858/00-1735-0000-0006-AF7F-4.
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