Relevant bibliographies by topics / Hypercapnia

Academic literature on the topic 'Hypercapnia'

Author: Grafiati
Published: 4 June 2021
Last updated: 31 July 2024

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Journal articles on the topic "Hypercapnia"

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Ketabchi, Farzaneh, Bakytbek Egemnazarov, Ralph T. Schermuly, Hossein A. Ghofrani, Werner Seeger, Friedrich Grimminger, Mostafa Shid-Moosavi, Gholam A. Dehghani, Norbert Weissmann, and Natascha Sommer. "Effects of hypercapnia with and without acidosis on hypoxic pulmonary vasoconstriction." American Journal of Physiology-Lung Cellular and Molecular Physiology 297, no. 5 (November 2009): L977—L983. http://dx.doi.org/10.1152/ajplung.00074.2009.

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Acute respiratory disorders and permissive hypercapnic strategy may lead to alveolar hypoxia and hypercapnic acidosis. However, the effects of hypercapnia with or without acidosis on hypoxic pulmonary vasoconstriction (HPV) and oxygen diffusion capacity of the lung are controversial. We investigated the effects of hypercapnic acidosis and hypercapnia with normal pH (pH corrected with sodium bicarbonate) on HPV, capillary permeability, gas exchange, and ventilation-perfusion matching in the isolated ventilated-perfused rabbit lung. No alteration in vascular tone was noted during normoxic hypercapnia with or without acidosis compared with normoxic normocapnia. Hypercapnia with normal pH resulted in a transient increase in HPV during the course of consecutive ventilation maneuvers, whereas hypercapnic acidosis increased HPV over time. Hypercapnic acidosis decreased exhaled NO during hypoxia more than hypercapnia with normal pH and normocapnia, whereas intravascular NO release was unchanged. However, inhibition of NO synthesis by nitro-l-arginine (l-NNA) resulted in a loss of the increased HPV caused by hypercapnic acidosis but not that caused by hypercapnia with normal pH. Furthermore, capillary permeability increased during hypoxic hypercapnia with normal pH but not hypoxic hypercapnic acidosis. This effect was NO-dependent because it disappeared during l-NNA administration. Ventilation-perfusion matching and arterial Po2 were improved according to the strength of HPV in hypercapnia compared with normocapnia during Tween nebulization-induced lung injury. In conclusion, the increased HPV during hypercapnic acidosis is beneficial to lung gas exchange by improving ventilation-perfusion matching and preserving the capillary barrier function. These effects seem to be linked to NO-mediated pathways.
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Higgins, Brendan D., Joseph Costello, Maya Contreras, Patrick Hassett, Daniel O' Toole, and John G. Laffey. "Differential Effects of Buffered Hypercapnia versus Hypercapnic Acidosis on Shock and Lung Injury Induced by Systemic Sepsis." Anesthesiology 111, no. 6 (December 1, 2009): 1317–26. http://dx.doi.org/10.1097/aln.0b013e3181ba3c11.

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Background Acute hypercapnic acidosis protects against lung injury caused by nonseptic insults and after both pulmonary and systemic sepsis. The authors wished to dissect the contribution of the acidosis versus hypercapnia per se to the effects of hypercapnic acidosis on the hemodynamic profile and severity of lung injury induced by systemic sepsis. Methods In the hypercapnic acidosis series, adult male Sprague-Dawley rats were randomized to normocapnia or hypercapnic acidosis-produced by adding 5% carbon dioxide to the inspired gas-and cecal ligation and puncture performed. In the buffered hypercapnia series, animals were first randomized to housing under conditions of environmental normocapnia or hypercapnia-produced by exposure to 8% carbon dioxide-to allow renal buffering. After 96 h, cecal ligation and puncture was performed. In both series, the animals were ventilated for 6 h, and the severity of the lung injury and hemodynamic deterioration were assessed. Results Both hypercapnic acidosis and buffered hypercapnia attenuated the development and severity of hypotension and reduced lactate accumulation compared to normocapnia. Hypercapnic acidosis reduced lung injury and inflammation, decreased mean (+ or - SD) bronchoalveolar lavage protein concentration (232 + or - 50 versus 279 + or - 27 microg x ml(-1)) and median neutrophil counts (3,370 versus 9,120 cells x ml(-1)), and reduced histologic lung injury. In contrast, buffered hypercapnia did not reduce the severity of systemic sepsis induced lung injury. Conclusions Both hypercapnic acidosis and buffered hypercapnia attenuate the hemodynamic consequences of systemic sepsis. In contrast, hypercapnic acidosis, but not buffered hypercapnia, reduced the severity of sepsis-induced lung injury.
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Raff, H., C. W. Kane, and C. E. Wood. "Arginine vasopressin responses to hypoxia and hypercapnia in late-gestation fetal sheep." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 260, no. 6 (June 1, 1991): R1077—R1081. http://dx.doi.org/10.1152/ajpregu.1991.260.6.r1077.

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The purpose of this study was to determine the interaction of hypoxia and hypercapnia in the control of arginine vasopressin (AVP) secretion in fetal sheep and to determine the role of the peripheral arterial chemoreceptors in that response. We measured the plasma AVP response to hypercapnia and/or hypoxia in catheterized intact or sinoaortic-denervated fetal sheep between 123 and 144 days of gestation. Ewes were exposed to the following inspired gases: two successive 30-min periods of normocapnic normoxia, 30 min of normocapnic normoxia followed by 30 min of normocapnic hypoxia, two successive 30-min periods of hypercapnic normoxia, or 30 min of hypercapnic normoxia followed by 30 min of hypercapnic hypoxia (i.e., asphyxia). Hypercapnia per se had no significant effect on fetal plasma AVP. Normocapnic hypoxia per se resulted in a significant increase in fetal plasma AVP. Although hypercapnia resulted in a significant acidemia, the decrease in arterial pH was more marked under hypoxic conditions. Hypercapnia/acidemia augmented the AVP response to hypoxia. Fetal sinoaortic denervation did not significantly attenuate any of the AVP responses. We conclude that hypercapnia augments the fetal AVP response to hypoxia and that the AVP response to neither normocapnic nor hypercapnic hypoxia is dependent on afferent information carried in the carotid sinus or aortic nerves.
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Talor, Z., W. C. Yang, J. Shuffield, E. Sack, and J. A. Arruda. "Chronic hypercapnia enhances Vmax of Na-H antiporter of renal brush-border membranes." American Journal of Physiology-Renal Physiology 253, no. 3 (September 1, 1987): F394—F400. http://dx.doi.org/10.1152/ajprenal.1987.253.3.f394.

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Chronic hypercapnia is associated with increased proximal HCO3 reabsorption that is thought to be mediated by a Na-H antiporter. We hypothesized that chronic hypercapnia would be associated either with increased Vmax or with decreased Km of the Na-H antiporter. To test this hypothesis we made rabbits hypercapnic for 48 h by exposure to 10% CO2. In both control and hypercapnic animals, cortical luminal membranes were enriched over the homogenate 16-fold in alkaline phosphatase and 10-fold in maltase activity. The kinetic activity of the Na-H antiporter was measured by the dissipation of the quenching of acridine orange by addition of different Na concentrations. Chronic hypercapnic rabbits had significantly higher Vmax of the Na-H antiporter of luminal membranes than controls (593 +/- 81 vs. 252 +/- 40 arbitrary fluorescence units X min-1 X 300 micrograms protein-1, P less than 0.01). The Km, however, was not different between control and hypercapnic rabbits. 22Na uptake in presence of an outwardly directed pH gradient was significantly higher in vesicles from hypercapnic rabbits than controls. Amiloride inhibited the Na-H antiporter (as assessed by acridine orange quenching or 22Na uptake) to the same degree in membranes from both control and hypercapnic rabbits, suggesting that the increase in Vmax is mediated by the electroneutral component of the Na-H antiporter. In addition, under voltage clamp conditions by K and valinomycin the Vmax was still increased in membranes from hypercapnic animals, again suggesting that the increase in Vmax is mediated by the electroneutral component of the Na-H antiporter. The uptake of D-[3H]glucose by luminal membranes was not different between control and hypercapnic rabbits, indicating a specific enhancement of the Na-H antiporter. Acute hypercapnia (4 h) failed to increase the Vmax of the Na-H antiporter despite comparable increase in PCO2. Thus chronic hypercapnia, but not acute hypercapnia, induces a selective and specific increase in the Vmax of Na-H antiporter, and this may mediate the adaptation to chronic hypercapnia.(ABSTRACT TRUNCATED AT 250 WORDS)
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Williams, J. L., S. C. Jones, R. B. Page, and R. M. Bryan. "Vascular responses of choroid plexus during hypercapnia in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 260, no. 6 (June 1, 1991): R1066—R1070. http://dx.doi.org/10.1152/ajpregu.1991.260.6.r1066.

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The response of blood flow to choroid plexus (CPBF) during hypercapnia is controversial. The goal of this study was to determine the effect of hypercapnia on CPBF in unanesthetized rats. Rats breathed air or a mixture of 5-8% CO2 in air, and CPBF was measured with [14C]isopropyliodoamphetamine and quantitative autoradiography. In hypercapnic rats [arterial PCO2 61.6 +/- 1.6 (SE) mmHg; n = 7] CPBF was similar to that of normocapnic control rats (525 +/- 39 ml.min-1.100 g-1; arterial PCO2 42.7 +/- 0.6 mmHg; n = 5). In contrast, blood flow to cerebral cortex increased 67% during hypercapnia. CPBF in normocapnic rats that were treated with phentolamine was similar to untreated normocapnic and hypercapnic rat CPBF. However, during hypercapnia, CPBF in phentolamine-treated rats increased 29%. Responses were similar in blood flow to choroid plexus of lateral, third, and fourth ventricles. Our findings indicate that hypercapnia has no effect on CPBF when alpha-adrenergic receptors are intact. In contrast, after blockade of alpha-adrenergic receptors, hypercapnia increases CPBF. These findings suggest that, during hypercapnia, levels of sympathetic activity or blood-borne catecholamines are increased that prevent increases in CPBF.
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Yamaguchi, K., T. Takasugi, H. Fujita, M. Mori, Y. Oyamada, K. Suzuki, A. Miyata, T. Aoki, and Y. Suzuki. "Endothelial modulation of pH-dependent pressor response in isolated perfused rabbit lungs." American Journal of Physiology-Heart and Circulatory Physiology 270, no. 1 (January 1, 1996): H252—H258. http://dx.doi.org/10.1152/ajpheart.1996.270.1.h252.

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With the use of isolated perfused rabbit lungs (n = 152), roles of endothelium-derived relaxing factor (EDRF) in pulmonary vascular responses to hypocapnia and hypercapnia were studied. Lungs were ventilated with a gas mixture containing 1, 5, or 10% CO2 and 21% O2, adjusting the perfusate pH to 7.8, 7.4, or 7.1, respectively. Methemoglobin (MetHb), hemoglobin (Hb), methylene blue (MB), and L-argininosuccinic acid (L-ASA) were used as modulators of EDRF. To eliminate augmented shear stress, we used papaverine during hypercapnia. As a measure of EDRF, we spectrophotometrically examined nitric oxide (NO) metabolites in the perfusate. Hypocapnia and hypercapnia evoked, respectively, unsustainable vasodilatation and vasoconstriction. Hb, MB, and L-ASA, but not MetHb, produced an increase in baseline pulmonary arterial pressure (Ppa). These agents also exacerbated vasoconstriction during hypercapnia. Hypercapnia and hypocapnia caused an increase and decrease, respectively, in EDRF production. L-ASA suppressed EDRF production in hypercapnic lungs. Papaverine did not suppress EDRF production under hypercapnia. In conclusion, 1) the effects of pH on pulmonary circulation are transient, 2) the increase in Ppa caused by hypercapnia is modulated by EDRF, and 3) the pulmonary EDRF genesis is activated by hypercapnic acidosis but suppressed by hypocapnic alkalosis.
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Clayson, Maxwell S., Maiah E. M. Devereaux, and Matthew E. Pamenter. "Neurokinin-1 receptor activation is sufficient to restore the hypercapnic ventilatory response in the Substance P-deficient naked mole-rat." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 318, no. 4 (April 1, 2020): R712—R721. http://dx.doi.org/10.1152/ajpregu.00251.2019.

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Naked mole-rats (NMRs) live in large colonies within densely populated underground burrows. Their collective respiration generates significant metabolic carbon dioxide (CO2) that diffuses slowly out of the burrow network, creating a hypercapnic environment. Currently, the physiological mechanisms that underlie the ability of NMRs to tolerate environmental hypercapnia are largely unknown. To address this, we used whole-body plethysmography and respirometry to elucidate the hypercapnic ventilatory and metabolic responses of awake, freely behaving NMRs to 0%–10% CO2. We found that NMRs have a blunted hypercapnic ventilatory response (HCVR): ventilation increased only in 10% CO2. Conversely, metabolism was unaffected by hypercapnia. NMRs are insensitive to cutaneous acid-based pain caused by modified substance P (SP)-mediated peripheral neurotransmission, and SP is also an important neuromodulator of ventilation. Therefore, we re-evaluated physiological responses to hypercapnia in NMRs after an intraperitoneal injection of exogenous substance P (2 mg/kg) or a long-lived isoform of substance P {[pGlu5-MePhe8-MeGly9]SP(5-11), DiMe-C7; 40–400 μg/kg}. We found that both drugs restored hypercapnia sensitivity and unmasked an HCVR in animals breathing 2%–10% CO2. Taken together, our findings indicate that NMRs are remarkably tolerant of hypercapnic environments and have a blunted HCVR; however, the signaling network architecture required for a “normal” HCVR is retained but endogenously inactive. This muting of chemosensitivity likely suits the ecophysiology of this species, which presumably experiences hypercapnia regularly in their underground niche.
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Takenaka, Motoyasu, Hiroki Iida, Mami Iida, and Shuji Dohi. "Intrathecal Dexmedetomidine Attenuates Hypercapnic but Not Hypoxic Cerebral Vasodilation in Anesthetized Rabbits." Anesthesiology 92, no. 5 (May 1, 2000): 1376–84. http://dx.doi.org/10.1097/00000542-200005000-00028.

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Background Systemic dexmedetomidine (DXM) attenuates the cerebral vasodilation induced by hypercapnia and decreases the cerebral blood flow response to hypoxia. We determined whether lumbar intrathecal DXM affected the cerebrovascular reactivity to hypercapnia and hypoxia. Methods Rabbits (n = 55) anesthetized with pentobarbital were prepared for measurement of pial vessel diameters using a closed cranial window preparation. The first study evaluated the response to hypercapnia after intrathecal administration of DXM (2 microg/kg; n = 7) or normal saline (n = 8). The second evaluated the response to hypercapnia after intrathecal DXM in the presence of yohimbine (20 microg/kg followed by DXM 2 microg/kg; n = 7). The third evaluated the response to mild or moderate hypoxia after intrathecal DXM (2 microg/kg; n = 7) or normal saline (n = 7). The hypercapnic responses were also examined in the presence of systemic DXM (2, 10 microg/kg; n = 6), topical DXM (10-8 m, 10-6 m; n = 6) and of intrathecal clonidine (2 microg/kg; n = 7). Results The pial arteriolar dilator response to hypercapnia was significantly attenuated after intrathecal administration of DXM. Pretreatment with yohimbine completely blocked the decreased reactivity to hypercapnia. Intrathecal clonidine, although less than DXM, also attenuate the hypercapnic response. Intrathecal DXM did not affect the vasodilation of pial arterioles induced by mild or moderate hypoxia. The systemic DXM 10 microg/kg and topical DXM 10-6 m, but not systemic 2 microg/kg and topical 10-8 m, attenuated hypercapnic vasodilation of pial arterioles. Conclusions The presence of alpha2-adrenoceptor agonist administered intrathecally into the lumbar spinal region attenuates hypercapnic but not hypoxic cerebral vasodilation, probably via a stimulation of central alpha2-adrenergic receptors of the central nervous system.
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Tregub, Pavel P., Vladimir P. Kulikov, Irada Ibrahimli, Oksana F. Tregub, Artem V. Volodkin, Michael A. Ignatyuk, Andrey A. Kostin, and Dmitrii A. Atiakshin. "Molecular Mechanisms of Neuroprotection after the Intermittent Exposures of Hypercapnic Hypoxia." International Journal of Molecular Sciences 25, no. 7 (March 25, 2024): 3665. http://dx.doi.org/10.3390/ijms25073665.

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The review introduces the stages of formation and experimental confirmation of the hypothesis regarding the mutual potentiation of neuroprotective effects of hypoxia and hypercapnia during their combined influence (hypercapnic hypoxia). The main focus is on the mechanisms and signaling pathways involved in the formation of ischemic tolerance in the brain during intermittent hypercapnic hypoxia. Importantly, the combined effect of hypoxia and hypercapnia exerts a more pronounced neuroprotective effect compared to their separate application. Some signaling systems are associated with the predominance of the hypoxic stimulus (HIF-1α, A1 receptors), while others (NF-κB, antioxidant activity, inhibition of apoptosis, maintenance of selective blood–brain barrier permeability) are mainly modulated by hypercapnia. Most of the molecular and cellular mechanisms involved in the formation of brain tolerance to ischemia are due to the contribution of both excess carbon dioxide and oxygen deficiency (ATP-dependent potassium channels, chaperones, endoplasmic reticulum stress, mitochondrial metabolism reprogramming). Overall, experimental studies indicate the dominance of hypercapnia in the neuroprotective effect of its combined action with hypoxia. Recent clinical studies have demonstrated the effectiveness of hypercapnic–hypoxic training in the treatment of childhood cerebral palsy and diabetic polyneuropathy in children. Combining hypercapnic hypoxia with pharmacological modulators of neuro/cardio/cytoprotection signaling pathways is likely to be promising for translating experimental research into clinical medicine.
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Dave, Chirag, Simon Wharton, Rahul Mukherjee, Bandar M. Faqihi, Robert A. Stockley, and Alice M. Turner. "Development and Relevance of Hypercapnia in COPD." Canadian Respiratory Journal 2021 (February 22, 2021): 1–8. http://dx.doi.org/10.1155/2021/6623093.

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Background. Identification of patients who may become hypercapnic, or develop acidotic hypercapnic respiratory failure (AHRF), is important in chronic obstructive pulmonary disease (COPD) to avoid hospital admission and select patients for use of home NIV. This study aimed to identify factors associated with presence and development of hypercapnia. Methods. 1224 patients, 637 with COPD and 587 with alpha 1 antitrypsin deficiency (AATD), from 4 previously established patient cohorts, were included in cross-sectional analyses of hypercapnia (PaCO2 ≥ 6.5 kPa or 48.8 mmHg), focusing on phenotypic features of COPD and mortality. Longitudinal associations of rising PaCO2 were also assessed. A second cohort of 160 COPD patients underwent sleep studies and 1-year follow-up, analysing in a similar way, incorporating additional information from their sleep studies if appropriate. Results. Hypercapnia was 15 times more common in usual COPD than AATD ( p < 0.01 ) after adjustment for baseline differences by regression. Independent predictors of hypercapnia in COPD included FEV1 and current use of oxygen; these variables, together with lack of emphysema, explained 11% of variance in CO2. Increasing PaCO2 also associated with higher risk of death ( p = 0.03 ). 44/160 patients exhibited sleep disordered breathing. The sleep study cohort also showed an association of low FEV1 with hypercapnia. Prior hospital admission for AHRF was also clinically significant, being a feature of almost double the number of hypercapnic patients in both test and sleep study COPD cohorts. Conclusion. Lower FEV1 and prior AHRF are the main associations of hypercapnia in COPD, which carries a poor prognosis, particularly worsening over time.
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Dissertations / Theses on the topic "Hypercapnia"

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Jeton, Florine. "Etude du rôle de l’Erythropoïétine et des systèmes de neurotransmission dans la mise en place des réponses ventilatoires à l’hypoxie et à l’hypercapnie." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCD078/document.

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Lors de variations de PO2 et PCO2, différents mécanismes se mettent en place afin demaintenir l’oxygénation des tissus, notamment au niveau du métabolisme et de la ventilation. En casde stimulation hypoxique ou hypercapnique, on observe alors une réponse ventilatoire, caractériséepar une augmentation progressive de la ventilation. Parmi les facteurs qui influencent la réponse àl’hypoxie, on trouve l’érythropoïétine (Epo) qui, en plus de son rôle dans l’érythropoïèse, possèded’autres rôles, notamment au sein du système nerveux central. Cette thèse présente l’étude del’implication de l’Epo et de différents systèmes de neurotransmission dans les réponses ventilatoiresà l’hypoxie (RVH) et à l’hypercapnie (RVHc).Nous avons alors pu mettre en évidence l’implication du NO, du glutamate et de la sérotonine dansla RVH et dans l’acclimatation ventilatoire à une hypoxie prolongée (VAH) chez un modèle de sourisanémique déficient en Epo (Epo-TAgh) et un animal adapté à la vie en altitude, la plateau Pika. Nousavons ensuite étudié l’impact de la déficience en Epo sur la RVHc, et nous avons confirmé que l’Epon’était pas nécessaire à l’obtention de la RVHc, tout en mettant en évidence un rôle de l’Epo sur lepatron ventilatoire et sur l’implication de certaines structures du système nerveux central dans lamise en place de cette réponse. Une étude en parallèle sur les femelles a permis de mettre enévidence que le cycle oestral n’était pas impliqué dans les réponses ventilatoires mais qu’il semble yavoir une interaction entre l’Epo et les hormones sexuelles femelles dans la RVH et la RVHc. Enfin,différentes expériences réalisées lors de collaborations (Chili, Canada) ont permis d’étudier les effetsde l’Epo sur les chémorécepteurs centraux et périphériques dans la mise en place des réponsesventilatoires.In fine, ces différentes expériences ont permis de préciser les différents facteurs impliqués dans lamise en place des réponses ventilatoires à l’hypoxie et à l’hypercapnie, ce qui pourrait aider par lasuite à mieux comprendre les modifications respiratoires induites par des pathologiques liées àl’anémie ou l’exposition prolongée à l’altitude
When PO2 and PCO2 are modified, various mechanisms are being established to maintaintissue oxygenation, such as ventilation and metabolism adaptations. In case of hypoxia orhypercapnia stimulation, we observed a ventilatory response, characterized by an increase in minuteventilation. Among the factors involved in the hypoxic response, Epo plays a key role. In addition toits role in erythropoiesis, Epo has other functions, especially in the central nervous system. Thisthesis presents the study of Epo involvement in the ventilatory responses to hypoxia (HVR) andhypercapnia (HcVR).We demonstrate the involvement of NO, glutamate and serotonin in the HVR and in acclimatizationto sustained hypoxia (VAH) in Epo deficient mice (Epo-TAgh) and in an animal adapted to highaltitude, the plateau Pika. Then we studied the impact of Epo-deficiency on HcVR and confirmed thatEpo is not mandatory to obtained HcVR but we demonstrate that Epo can modulate the ventilatorypattern and central nervous system structures involvement in this response. During this study, wealso demonstrate that in female mice, estrous cycle is not involved in HVR or HcVR but it seems thatthere is an interaction between Epo and female sexual hormones in these responses. Finally, someexperiments in collaboration with different countries (Chile, Canada) allowed us to study the effectsof Epo on peripheral and central chemoreceptors during HVR and HcVR.In fine, these experiments allows us to specify the factors involved in ventilatory responses tohypoxia and hypercapnia, which could be helpful to better understand respiratory pathologies suchas anemia or pathologies associated with high altitude
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Wang, Zhen. "Adjunctive therapies in a clinical revelant ovine model of septic shock." Doctoral thesis, Universite Libre de Bruxelles, 2009. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210196.

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Sepsis has been defined as a systemic response to an infection. With an incidence of 3 per 1000 population per year or about 750 000 cases a year, this syndrome ranks as the 10th leading cause of death in the United States (1). Increasing severity of sepsis correlates with increasing mortality, which rises from 30-40% for severe sepsis up to 40-60% for septic shock. This thesis examines the effectiveness of adjunctive therapies, including activated protein C, hypercapnia and acidosis, and sodium selenite, in a clinically relevant ovine model of septic shock. The results from these studies can provide valuable information for future clinical trials on sepsis.

This thesis is divided into four sections: 1) sepsis overview; 2) an autologous fecal peritonitis model in sheep and its evaluation; 3) the series of studies on adjunctive therapeutics; and 4) ongoing studies and future perspective.

In the first section, a broad overview gives a rough introduction to delineate many aspects of sepsis syndrome such as terminology, etiology, epidemiology, pathophysiology and current guidelines for management. Hemodynamics in sepsis are especially elaborated since these are major observations throughout the studies presented later.

In the second section, the general characteristics of the sepsis models used in this thesis are elucidated. Data on hemodynamics, lung mechanics, gas exchange, etc. are presented to feature the ovine peritonitis model. The results of laboratory examinations for hematology, coagulation, bacteriology, biochemistry and hormonology are also presented. And then, I review currently used sepsis models with regards to their advantages and disadvantages.

The third section discusses three studies with their objectives, the methods used, the major findings, and the potential clinical implications.

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1) Beneficial effects of recombinant human activated protein C in experimental septic shock. Activated protein C has a multitude of beneficial effects in severe sepsis and septic shock, including anti-inflammation, anti-coagulation, profibrinolysis, anti-apoptosis and endothelial protection. A clinical Phase III trial demonstrated that the administration of recombinant human activated protein C improved survival in patients with severe sepsis. However, doubts on the protective effects of activated protein C have persisted and been refueled by the recently published negative trials in less severely ill patients and in children. In the light of these ambiguities and uncertainties, we reinvestigated the effects of activated protein C in experimental septic shock.

2) Acute hypercapnia improves indices of tissue oxygenation more than dobutamine in septic shock. Hepercapnia has been found to possess beneficial effects in diverse acute inflammatory states independent of protective lung mechanics. To prove the hypothesis that acute hypercapnia has similar or superior hemodynamic effects to those of a dobutamine infusion, which may be particularly relevant in the presence of hemodynamic instability associated with respiratory failure, we investigated the effects of hypercapnia, which induced by inspiring extrinsic carbon dioxide in experimental septic shock.

3) High bolus dose of sodium selenite prolongs survival in an ovine model of septic shock. Selenite has both pro- and anti-oxidant effects. The administration of high dose sodium selenite may improve survival in septic shock patients. The benefit may be greater with the administration of a bolus (to achieve higher concentrations) rather than a continuous infusion. To test this hypothesis, we examined the effects of a high dose bolus administration of sodium selenite in experimental septic shock.

The fourth and final section talks about currently ongoing studies and offers some perspective on future direction.
Doctorat en Sciences médicales
info:eu-repo/semantics/nonPublished

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Bailey, Elizabeth Fiona. "Breathing behavior during speech production in hypercapnia." Diss., The University of Arizona, 1998. http://hdl.handle.net/10150/282812.

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This investigation was designed to examine speech production, the motion of the chest wall, and breathing-related perceptions under a condition of heightened respiratory drive. Ten healthy young men were studied during spontaneous breathing and during speaking in three gas conditions: room air, air delivered from a pressurized tank, and a gas mixture high in carbon dioxide (7% CO₂) delivered from a pressurized tank. Magnetometers that transduced diameter changes of the rib cage and abdomen were used to study chest wall motion. Subjects also reported their breathing-related perceptions. Results indicate that chest wall behavior during spontaneous breathing and speaking did not differ between room-air and tank-air conditions, but differed substantially in the high-CO₂ condition. In the high-CO₂ condition, spontaneous breathing and speaking usually were characterized by larger lung volumes, larger rib cage volumes, higher breathing rates, longer expiratory times, and higher expiratory flows than in the two air conditions. Further, speaking in high-CO₂ was characterized by shorter speech duration, fewer syllables per breath group, and greater average lung volume expenditure per syllable compared to speaking in air. In high-CO₂, subjects reported a range of breathing-related percepts including "breathlessness," "effortful breathing," and "gasping for air." Without exception, speaking in high-CO₂ was judged by the subjects to be more difficult than breathing in high-CO₂.
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Tansley, John Guion. "Human ventilatory responses to prolonged hypoxia and hypercapnia." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.363954.

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Binks, Andrew Paul. "Breathlessness and the pattern of breathing." Thesis, University of Newcastle Upon Tyne, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.263019.

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Taylor, John Andrew 1960. "RESPIRATORY CHEMOSENSITIVITY IN SYNCHRONIZED SWIMMERS AND SWIM-TRAINED WOMEN." Thesis, The University of Arizona, 1987. http://hdl.handle.net/10150/276444.

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Jarsky, Tim M. "The effects of hypoxia and hypercapnia on hamster activity rhythms." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0009/MQ29356.pdf.

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Miller, Scott. "Cardiac Responses to Carbon Dioxide in Developing Zebrafish (Danio rerio)." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/24210.

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The ontogeny of carbon dioxide (CO2) sensing in zebrafish (Danio rerio) has not been studied. In this thesis, CO2-mediated increases in heart rate were used to gauge the capacity of zebrafish larvae to sense CO2. CO2 is thought to be sensed through neuroepithelial cells (NECs), which are homologous to mammalian carotid body glomus cells. Owing to its role in facilitating intracellular acidification during exposure to hypercapnia, it was hypothesized that carbonic anhydrase (CA) is involved in CO2 sensing, and that inhibition of CA would blunt the downstream responses. The cardiac response to hypercapnia (0.75% CO2) was reduced in fish exposed to acetazolamide, a CA inhibitor, and in fish experiencing CA knockdown. Based on pharmacological evidence using β-adrenergic receptor (ß-AR) antagonists, and confirmed by β1AR gene knockdown, the efferent limb of the reflex tachycardia accompanying hypercapnia is probably mediated by sympathetic adrenergic neurons interacting with cardiac β1 receptors.
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Nanagas, Vivian C. "Clamping of Intracellular pH in Neurons from Neonatal Rat Brainstem during Hypercapnia." Wright State University / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=wright1246393988.

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Martin, James. "The Responses of Blue Crabs (Callinectes sapidus) to Hypoxia/Hypercapnia in Freshwater." VCU Scholars Compass, 2009. http://scholarscompass.vcu.edu/etd/1847.

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The present research examined respiratory responses of blue crabs to long term (4, 13, and 21 days) hypercapnic hypoxia in freshwater at 23 C. Hypoxic conditions (50-60 & 75-85 mmHg O2) were induced by allowing the crabs to consume their oxygen supply, resulting in a hypercapnic induced decrease in pH that remained through the exposure. Postbranchial hemolymph responses to hypoxia/hypercapnia in freshwater demonstrate decreases in PO2, increases in PCO2, and decreases in pH. Lactate levels decreased over time, but hemocyanin concentration was highly variable with no trends. PH, lactate, and hemocyanin observations also demonstrated high variability and a variety of different responses in individual crabs. There was no evidence of improving oxygen transport abilities. Despite varying responses high mortality rates were observed. The high mortality rate suggests blue crabs are not able to survive the multiple stress of hypoxia/hypercapnia along with the stress of living in freshwater. The mortality rates observed are much greater than previous blue crab hypoxic studies in saltwater. Elevated mortality may result from a failure of oxygen transport, acid-base balance or ion regulation.
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Books on the topic "Hypercapnia"

1

Al-Abdulmunem, M. A. Effects of hypoxia and hypercapnia associated withcontactlenswearon corneal epithelium. Manchester: UMIST, 1994.

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Jarsky, Tim M. The effects of hypoxia and hypercapnia on hamster activity rhythms. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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Peever, John H. Day-night differences in ventilation, metabolism, and body temperature during normoxia, hypoxia and hypercapnia in the awake adult rat. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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Piracha, Kashif. Hypercapnic Respiratory Failure. Cham: Springer Nature Switzerland, 2023. http://dx.doi.org/10.1007/978-3-031-36128-9.

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U, Sliwka, and United States. National Aeronautics and Space Administration., eds. Effects of sustained low-level elevations of carbon dioxide on cerebral blood flow and autoregulation of the intracerebral arteries in humans. [Washington, DC: National Aeronautics and Space Administration, 1996.

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United States. National Aeronautics and Space Administration., ed. "CO₂-O₂ interactions in extension of tolerance to acute hypoxia": Final report. [Washington, DC]: National Aeronautics and Space Administration, 1995.

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United States. National Aeronautics and Space Administration., ed. "CO₂-O₂ interactions in extension of tolerance to acute hypoxia": Final report. [Washington, DC]: National Aeronautics and Space Administration, 1995.

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Laffey, John G., and Brian P. Kavanagh. Hypercapnia in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0086.

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Hypercapnia is a central component of current ‘protective’ ventilator management. Hypercapnia, and the associated acidosis, has potentially important biologic effects on immune responses, injury and repair. Arterial carbon dioxide tension PaCO2 is tightly governed under physiological conditions and small elevations rapidly increase spontaneous minute ventilation. In the mechanically-ventilated patient, elevated PaCO2 usually reflects reduced elimination. This can be because tidal volume or respiratory rate delivered by the ventilator are reduced, or because of the diseased lung per se. Hypercapnia has many effects that are clinically obvious, but research over the last decade reveals important consequences on inflammatory and cellular mechanisms that are not apparent at the bedside.
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Claudette Marie.* St. Croix. The effect of aging and aerobic fitness level on the ventilatory response to hypercapnia. 1991.

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Kreit, John W. Respiratory Failure and the Indications for Mechanical Ventilation. Edited by John W. Kreit. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190670085.003.0007.

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Respiratory failure occurs when a disease process significantly interferes with the respiratory system’s vital functions and causes arterial hypoxemia, hypercapnia, or both. Typically, respiratory failure is divided into three categories based on the underlying pathophysiology: ventilation failure, oxygenation failure, and oxygenation-ventilation failure. With severe disturbances in gas exchange, mechanical ventilation is often needed to assist the respiratory system and restore the PaCO2, PaO2, or both, to normal. Respiratory Failure and the Indications for Mechanical Ventilation defines and describes the three types of respiratory failure and reviews the four indications for intubation and mechanical ventilation—acute or acute-on-chronic hypercapnia, refractory hypoxemia, inability to protect the lower airway, and upper airway obstruction.
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Book chapters on the topic "Hypercapnia"

1

Metze, Dieter, Vanessa F. Cury, Ricardo S. Gomez, Luiz Marco, Dror Robinson, Eitan Melamed, Alexander K. C. Leung, et al. "Hypercapnia." In Encyclopedia of Molecular Mechanisms of Disease, 887. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_8098.

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Hassett, Patrick, John G. Laffey, and Brian P. Kavanagh. "Permissive Hypercapnia." In Pediatric and Neonatal Mechanical Ventilation, 727–42. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-01219-8_26.

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Amato, M. B. "Permissive Hypercapnia." In Update in Intensive Care and Emergency Medicine, 258–75. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-60733-2_16.

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Kastrup, A., T. Q. Li, and M. E. Moseley. "Functional MRI and Hypercapnia." In Functional MRI, 433–39. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-58716-0_35.

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Contreras, Maya, John G. Laffey, and Brian P. Kavanagh. "Mechanical Ventilation, Permissive Hypercapnia." In Encyclopedia of Trauma Care, 928–33. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-29613-0_253.

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Johnson, Rebecca A. "Troubleshooting Hypercapnia and Hypocapnia." In Questions and Answers in Small Animal Anesthesia, 139–46. Hoboken, NJ, USA: John Wiley & Sons, Inc, 2015. http://dx.doi.org/10.1002/9781118912997.ch19.

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Manca, T., L. C. Welch, and J. I. Sznajder. "The Cardiopulmonary Effects of Hypercapnia." In Yearbook of Intensive Care and Emergency Medicine, 282–89. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-77290-3_26.

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Servillo, G., L. D’amato, and R. Tufano. "How Permissive Should Hypercapnia Be?" In Anaesthesia, Pain, Intensive Care and Emergency Medicine — A.P.I.C.E., 287–98. Milano: Springer Milan, 2002. http://dx.doi.org/10.1007/978-88-470-2099-3_27.

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Tao, Li, and Wei Zhou. "Hypercapnia and Hypocapnia in Neonates." In Applied Technologies in Pulmonary Medicine, 210–16. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000322779.

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Somers, Virend K., Allyn L. Mark, and François M. Abboud. "Circulatory Regulation during Hypoxia and Hypercapnia." In Hypoxia, Metabolic Acidosis, and the Circulation, 3–20. New York, NY: Springer New York, 1992. http://dx.doi.org/10.1007/978-1-4614-7542-2_1.

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Conference papers on the topic "Hypercapnia"

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Bräunlich, Jens, Kristin Turba, and Hubert Wirtz. "Predictors of persistent hypercapnia after an hypercapnic AECOPD." In ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.pa1777.

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Bräunlich, J., K. Turba, and H. Wirtz. "Predictors of persistent hypercapnia after a hypercapnic COPD exacerbation." In 61. Kongress der Deutschen Gesellschaft für Pneumologie und Beatmungsmedizin e.V. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1723341.

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Sun, B., and T. Simoneau. "A Cardiac Cause of Hypercapnia." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a6203.

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Welch, Lynn C., Galina Gusarova, Laura A. Dada, and Jacob I. Sznajder. "Hypercapnia Leads To Muscle Dysfunction Via Ubiquitination." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3025.

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Angulo, Martin, Adriana Cassina, Carlos Batthyany, Juan Soto, Javier Hurtado, and Arturo Briva. "Hypercapnia Impairs Diaphragmatic Contractility By Mitochondrial Dysfunction." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5047.

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Corbellini, Camilo, Saverio Tavella, Elisa Gugliotta, Stefano Zampese, Eleuterio A. Sanchez Romero, and Jorge Villafane. "HYPERCAPNIA AND FUNCTIONAL IMPROVEMENTS DURING PULMONARY REHABILITATION." In ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.pa1827.

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Roy, P., M. Ghose, and E. Silverman. "Permissive Hypercapnia: Protecting the Lung With Permission." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a5560.

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Dawson, W. M. "Hypercapnia Due to Limb-Girdle Muscular Dystrophy." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a4583.

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Ryu, J., GP Heldt, M. Nguyen, O. Gavrialov, and GG Haddad. "Chronic Hypercapnia Induces Collagen Degradation in Mice Pups." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4122.

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Saure, EW, TM Eagan, PS Bakke, and JA Hardie. "Predictors of Hypoxia and Hypercapnia in COPD Patients." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4326.

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Reports on the topic "Hypercapnia"

1

Selkirk, Alaleh, Barbara Shykoff, and James Briggs. Cognitive Effects of Hypercapnia on Immersed Working Divers. Fort Belvoir, VA: Defense Technical Information Center, October 2010. http://dx.doi.org/10.21236/ada561029.

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Zhuo, Guifeng, Hengwang Yu, Ran Liao, Xuexia Zheng, Dongmin Liu, Libing Mei, and Guiling Wu. Auricular point pressing therapy for obstructive sleep apnea hypoventilation syndrome: A protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0015.

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Review question / Objective: Patients with obstructive sleep apnea hypoventilation syndrome (OSAHS) suffer from repeated hypoxemia, hypercapnia, and sleep structure disorders at night, leading to daytime lethargy and complications of heart, brain, lung, and blood vessel damage, which seriously affect their quality of life and life span. Clinical studies have shown that auricular point pressing therapy has an excellent therapeutic effect on OSAHS, and has the potential to be a complementary and alternative therapy for patients with OSAHS. Currently, systematic reviews and meta-analyses evaluating the efficacy and safety of electroacupuncture for the treatment of OSAHS are lacking. This study aimed to address this deficiency. Information sources: RCTs of auricular point pressing therapy in the treatment of OSAHS were searched in the Web of Science, PubMed, Cochrane Library, Embase, Allied and Complementary Medicine Database (AMED), China Science and Technology Journal Database (VIP), China National Knowledge Infrastructure (CNKI), and Wan-Fang Database. The retrieval time is from database construction to the present.
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Czerwaty, Katarzyna, Karolina Dżaman, Krystyna Maria Sobczyk, and Katarzyna Irmina Sikrorska. The Overlap Syndrome of Obstructive Sleep Apnea and Chronic Obstructive Pulmonary Disease: A Systematic Review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2022. http://dx.doi.org/10.37766/inplasy2022.11.0077.

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Review question / Objective: To provide the essential findings in the field of overlap syndrome of chronic obstructive pulmonary disease and obstructive sleep apnea, including prevalence, possible predictors, association with clinical outcomes, and severity compared to both chronic obstructive pulmonary disease and obstructive sleep apnea patients. Condition being studied: OSA is characterized by complete cessation (apnea) or significant decrease (hy-popnea) in airflow during sleep and recurrent episodes of upper airway collapse cause it during sleep leading to nocturnal oxyhemoglobin desaturations and arousals from rest. The recurrent arousals which occur in OSA lead to neurocognitive consequences, daytime sleepiness, and reduced quality of life. Because of apneas and hypopneas, patients are experiencing hypoxemia and hypercapnia, which result in increasing levels of catecholamine, oxidative stress, and low-grade inflammation that lead to the appearance of cardio-metabolic consequences of OSA. COPD is a chronic inflammatory lung disease defined by persistent, usually pro-gressive AFL (airflow limitation). Changes in lung mechanics lead to the main clini-cal manifestations of dyspnea, cough, and chronic expectoration. Furthermore, patients with COPD often suffer from anxiety and depression also, the risk of OSA and insomnia is higher than those hospitalized for other reasons. Although COPD is twice as rare as asthma but is the cause of death eight times more often.
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Hariswar, Pari Thenmozhi, Ramanathan Venkateswaran, George Melvin, kshirsagar Shivani, and M. Rajeswari. Acetazolamide in weaning from mechanical ventilation in hypercapnic respiratory failure. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2023. http://dx.doi.org/10.37766/inplasy2023.7.0108.

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