Journal articles on the topic 'Hypercapnia'
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1
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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Tolstun, Denis, and Viktor Kholin. "Neuroprotective effect of hypoxic-hypercapnic training. Review." Issue 4 2023, no. 4 2023 (December 29, 2023): 129–36. http://dx.doi.org/10.47855/jal9020-2023-4-5.
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The neuroprotective effects of hypercapnia, especially with hypoxia combined, interested in the context of nerve cells forming protective mechanisms. Hypercapnia not only acts as a potent neuroprotector but also increases tissue tolerance to ischemia and reperfusion. Hypercapnic effects are based on many different mechanisms including energy metabolism modulation, adaptive signaling pathways activation, histological damage reduction, pro-inflammatory factors, angiogenesis activation, and activation of synthetic processes in neurons. The summarized data indicate prospects for further research to better understand the molecular and physiological aspects of neuroprotection during hypercapnia and hypoxia, as well as to determine the conditions under which the best neuroprotective effect is achieved with a subsequent reduction in neurological deficits. __________________________________________________________________________________________ Keywords: hypercapnia, hypoxia, neuroprotection, permissive hypercapnia, ischemia, stroke
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Willis, A. P., and C. W. Leffler. "NO and prostanoids: age dependence of hypercapniaand histamine-induced dilations of pig pial arterioles." American Journal of Physiology-Heart and Circulatory Physiology 277, no. 1 (July 1, 1999): H299—H307. http://dx.doi.org/10.1152/ajpheart.1999.277.1.h299.
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Responses to hypercapnia and acetylcholine by newborn piglet pial arterioles are prostanoid dependent but appear to require both prostanoids and nitric oxide in juvenile pigs. We hypothesized that cerebrovascular dilatory responses become less prostanoid dependent and more NO dependent with development. Pial arteriolar responses to hypercapnia and histamine were recorded from α-chloralose-anesthetized newborn and juvenile pigs with closed cranial windows. Responses were recorded during control, after indomethacin or N ω-nitro-l-arginine (l-NNA), and after inhibitor plus iloprost or sodium nitroprusside. Indomethacin blocked newborn hypercapnic responses and markedly attenuated histamine dilations, but only reduced the dilations to about half in juveniles. Iloprost at subdilator concentrations restored newborn responses to hypercapnia and histamine but did not alter either response in indomethacin-treated juveniles. l-NNA attenuated juvenile, but not newborn, hypercapnia-induced dilations. Sodium nitroprusside did not restore the response.l-NNA did not alter responses to histamine in either age group. Cerebrovascular dilations to hypercapnia and histamine are prostanoid dependent and nitric oxide independent in the newborn pig, whereas nitric oxide assumes an increasing role in hypercapnic, but not histamine, responses with development.
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Tajima, Yosuke, Hiroyuki Takuwa, Daisuke Kokuryo, Hiroshi Kawaguchi, Chie Seki, Kazuto Masamoto, Yoko Ikoma, et al. "Changes in Cortical Microvasculature during Misery Perfusion Measured by Two-Photon Laser Scanning Microscopy." Journal of Cerebral Blood Flow & Metabolism 34, no. 8 (May 21, 2014): 1363–72. http://dx.doi.org/10.1038/jcbfm.2014.91.
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This study aimed to examine the cortical microvessel diameter response to hypercapnia in misery perfusion using two-photon laser scanning microscopy (TPLSM). We evaluated whether the vascular response to hypercapnia could represent the cerebrovascular reserve. Cerebral blood flow (CBF) during normocapnia and hypercapnia was measured by laser-Doppler flowmetry through cranial windows in awake C57/BL6 mice before and at 1,7, 14, and 28 days after unilateral common carotid artery occlusion (UCCAO). Diameters of the cortical microvessels during normocapnia and hypercapnia were also measured by TPLSM. Cerebral blood flow and the vascular response to hypercapnia were decreased after UCCAO. Before UCCAO, vasodilation during hypercapnia was found primarily in arterioles (22.9% ± 3.5%). At 14 days after UCCAO, arterioles, capillaries, and venules were autoregulatorily dilated by 79.5% ± 19.7%, 57.2% ±32.3%, and 32.0% ± 10.8%, respectively. At the same time, the diameter response to hypercapnia in arterioles was significantly decreased to 1.9% ± 1.5%. A significant negative correlation was observed between autoregulatory vasodilation and the diameter response to hypercapnia in arterioles. Our findings indicate that arterioles play main roles in both autoregulatory vasodilation and hypercapnic vasodilation, and that the vascular response to hypercapnia can be used to estimate the cerebrovascular reserve.
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Ritucci, Nick A., Jay B. Dean, and Robert W. Putnam. "Somatic vs. dendritic responses to hypercapnia in chemosensitive locus coeruleus neurons from neonatal rats." American Journal of Physiology-Cell Physiology 289, no. 5 (November 2005): C1094—C1104. http://dx.doi.org/10.1152/ajpcell.00329.2004.
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Cardiorespiratory control is mediated in part by central chemosensitive neurons that respond to increased CO2 (hypercapnia). Activation of these neurons is thought to involve hypercapnia-induced decreases in intracellular pH (pHi). All previous measurements of hypercapnia-induced pHi changes in chemosensitive neurons have been obtained from the soma, but chemosensitive signaling could be initiated in the dendrites of these neurons. In this study, membrane potential ( Vm) and pHi were measured simultaneously in chemosensitive locus coeruleus (LC) neurons from neonatal rat brain stem slices using whole cell pipettes and the pH-sensitive fluorescent dye pyranine. We measured pHi from the soma as well as from primary dendrites to a distance 160 μm from the edge of the soma. Hypercapnia [15% CO2, external pH (pHo) 7.00; control, 5% CO2, pHo 7.45] resulted in an acidification of similar magnitude in dendrites and soma (∼0.26 pH unit), but acidification was faster in the more distal regions of the dendrites. Neither the dendrites nor the soma exhibited pHi recovery during hypercapnia-induced acidification; but both regions contained pH-regulating transporters, because they exhibited pHi recovery from an NH4Cl prepulse-induced acidification (at constant pHo 7.45). Exposure of a portion of the dendrites to hypercapnic solution did not increase the firing rate, but exposing the soma to hypercapnic solution resulted in a near-maximal increase in firing rate. These data show that while the pHi response to hypercapnia is similar in the dendrites and soma, somatic exposure to hypercapnia plays a major role in the activation of chemosensitive LC neurons from neonatal rats.
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Perry, S. F., S. Malone, and D. Ewing. "Hypercapnic acidosis in the rainbow trout (Salmo gairdneri). II. Renal ionic fluxes." Canadian Journal of Zoology 65, no. 4 (April 1, 1987): 896–902. http://dx.doi.org/10.1139/z87-143.
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The involvement of the rainbow trout kidney in acid–base regulation was assessed before, during, and after 72 h of exposure to external hypercapnia (1% CO2). Hypercapnia caused a significant elevation of renal acid excretion throughout most of the hypercapnic period, which could account for 16% of the overall compensatory increase in plasma bicarbonate concentration. The two predominant urine buffers, phosphate and ammonia, both increased markedly during hypercapnia, thereby preventing reductions in urine pH during the period of enhanced urinary acidification. Stimulation of tubular H+ secretion was the mechanism responsible for the elevation of acid excretion and, more importantly, ensured tubular reabsorption of the additional [Formula: see text] that must have appeared in the glomerular filtrate. Such a mechanism is considered essential for the ultimate compensation of hypercapnic acidosis. The results are discussed with respect to the possible involvement of increased plasma epinephrine levels in mediating the various renal responses of hypercapnic acidosis.
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Stipica Safic, Ivona, Renata Pecotic, Ivana Pavlinac Dodig, Zoran Dogas, Zoran Valic, and Maja Valic. "Phrenic long-term depression evoked by intermittent hypercapnia is modulated by serotonergic and adrenergic receptors in raphe nuclei." Journal of Neurophysiology 120, no. 1 (July 1, 2018): 321–29. http://dx.doi.org/10.1152/jn.00776.2017.
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Intermittent hypercapnia evokes prolonged depression of phrenic nerve activity (phrenic long-term depression, pLTD). This study was undertaken to investigate the role of 5-HT and α2-adrenergic receptors in the initiation of pLTD. Adult male urethane-anesthetized, vagotomized, paralyzed, and mechanically ventilated Sprague-Dawley rats were exposed to a protocol of acute intermittent hypercapnia (AIHc; 5 episodes of 15% CO2in air, each episode lasting 3 min). The experimental group received microinjection of the selective 5-HT1Areceptor agonist 8-hydroxy-2-(dipropylamino)tetralin hydrobromide (8-OH-DPAT), the broad-spectrum 5-HT antagonist methysergide, or the α2-adrenergic antagonist yohimbine, whereas the control group received microinjection of 0.9% saline into the caudal raphe region. Peak phrenic nerve activity (pPNA) and burst frequency ( f) were analyzed during baseline (T0), during 5 hypercapnic episodes (THc1–THc5), and at 15, 30, and 60 min after the end of the last hypercapnic episode. In the control group, pPNA decreased 60 min after the end of the last hypercapnic episode compared with baseline values, i.e., pLTD developed ( P = 0.023). In the 8-OH-DPAT group, pPNA significantly decreased at T15, T30, and T60 compared with baseline values, i.e., pLTD developed ( P = 0.01). In the methysergide and yohimbine groups, AIHc did not evoke significant changes of the pPNA at T15, T30, and T60 compared with baseline values. In conclusion, activation of 5-HT1Areceptors accentuated induction of pLTD, whereas blockade of α2-adrenergic receptors prevented development of pLTD following AIHc in anesthetized rats. These results suggest that chemical modulation of 5-HT and α2-adrenergic receptors in raphe nuclei affects hypercapnia-induced pLTD, offering important insights in understanding the mechanisms involved in development of respiratory plasticity.NEW & NOTEWORTHY Hypercapnia is a concomitant feature of many breathing disorders, including obstructive sleep apnea. In this study, acute intermittent hypercapnia evoked development of phrenic long-term depression (pLTD) 60 min after the last hypercapnic episode that was preserved if the selective 5-HT1Areceptor agonist 8-hydroxy-2-(dipropylamino)tetralin hydrobromide was microinjected in the caudal raphe region before the hypercapnic stimulus. This study highlights that both 5-HT and adrenergic receptor activation is needed for induction of pLTD in urethane-anesthetized rats following intermittent hypercapnia exposure.
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LeMaster, William, Dale Jun, Sharon De Cruz, Michelle Zeidler, and Rajan Saggar. "1262 Case Series on the Use of Volume Assured Pressure Support (VAPS) in Patients with Interstitial Lung Disease and Progressive Hypercapnia." Sleep 43, Supplement_1 (April 2020): A480. http://dx.doi.org/10.1093/sleep/zsaa056.1256.
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Abstract Introduction Many patients with interstitial lung disease (ILD) experience progressive respiratory failure. While various therapies are implemented for acute hypercapnic respiratory failure during inpatient ILD flares, there is little data regarding the management of chronic hypercapnia in ILD with nocturnal Volume Assured Pressure Support (VAPS). We present three patients who were prescribed nocturnal VAPS for their progressive hypercapnia as a bridge to lung transplantation. Report of Case Patient 1 is a 45-year-old woman with rheumatoid arthritis related ILD and progressive hypercapnia. Despite optimal therapy, her ILD resulted in an admission for hypercapnic and hypoxemic respiratory failure requiring treatment with BPAP, then transition to nocturnal VAPS on discharge. Dyspnea and pCO2 improved as an outpatient (Fig. 1). Patient 2 is a 70-year-old female with history of scleroderma associated ILD with severe PH and hypercapnia. Initiation of VAPS improved her pCO2 levels although she was readmitted after a few months of treatment for an ILD flare. Patient 3 is a 60-year-old patient with connective tissue disease related ILD who was admitted for respiratory failure due to pneumonia and was transitioned to BPAP for hypercapnic respiratory failure. Due to insurance issues she has been unable to obtain a home VAPS and her pCO2 remains elevated. A plot of each patient’s pCO2 over time is in Figure 1. Conclusion In patients with severe lung disease, the normal decrease in tidal volumes that occurs with sleep can result in CO2 retention. Non-invasive ventilation (NIV) is well-studied in both stable obstructive lung disease and exacerbations but there is little data examining the utility of NIV to treat the chronic hypercapnia of ILD. In this case series, nocturnal VAPS stabilized or reduced PCO2 in patients with ILD and hypercapnia. Additional studies are needed to assess long term effects of VAPS in these patients.
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Tsuji, Takao, Kazutetsu Aoshiba, Masayuki Itoh, Hiroyuki Nakamura, and Kazuhiro Yamaguchi. "Hypercapnia Accelerates Wound Healing in Endothelial Cell Monolayers Exposed to Hypoxia." Open Respiratory Medicine Journal 7, no. 1 (February 22, 2013): 6–12. http://dx.doi.org/10.2174/1874306401307010006.
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Introduction: While tissue hypoxia is known to play a critical role in the process of vascular injury and repair, the effect of hypercapnia on this process remains uncertain. We investigated whether hypercapnia might influence endothelial cell wound healing under the influence of hypoxia. Materials and Methodology: Monolayers of human umbilical venous endothelial cells (HUVECs) were scratch-wounded and incubated under different levels of O2, CO2, and pH in the environment. Results: Inhibition of wound healing was observed in the HUVEC monolayers under the hypoxic condition as compared to the normoxic condition. Both hypercapnic acidosis and buffered hypercapnia, but not normocapnic acidosis improved the rate of wound healing under the influence of hypoxia. The beneficial effect of hypercapnia was associated with stimulation of cell proliferation, without effects on cell adhesion, migration or apoptosis. On the other hand, the stimulatory effect of hypercapnia on wound healing and cell proliferation was not noted under normoxic conditions. Conclusion: These results suggest that hypercapnia, rather than acidosis per se, accelerated the wound healing in HUVEC monolayers cultured under hypoxic conditions. The effect of hypercapnia on wound healing was due, at least in part, to the stimulation of cell proliferation by hypercapnia.
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Zhang, Sarah Y., and Matthew E. Pamenter. "Fossorial Damaraland mole rats do not exhibit a blunted hypercapnic ventilatory response." Biology Letters 15, no. 3 (March 2019): 20190006. http://dx.doi.org/10.1098/rsbl.2019.0006.
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Damaraland mole rats (DMRs, Fukomys damarensis ) are a eusocial fossorial species that spend the majority of their life in densely populated underground burrows, in which they likely experience intermittent periods of elevated CO 2 (i.e. hypercapnia). The primary physiological response to hypercapnia in most mammals is to increase depth and rate of breathing (i.e. hyperpnoea), but this response is often blunted in species that inhabit hypercapnic environments. In their natural habitat, DMRs putatively experience a gaseous environment ranging from normocapnic (0.1% CO 2 ) to hypercapnic (6.0% CO 2 ) conditions (Roper et al. 2001 J. Zool. 254 , 101–107). As such, we hypothesized that DMRs would exhibit blunted hypercapnic ventilatory and metabolic responses, relative to those of non-fossorial rodent species. To test this hypothesis, we exposed awake, freely behaving DMRs to normoxic normocapnia (21% O 2 , 0% CO 2 , balance N 2 ) or graded normoxic hypercapnia (21% O 2 , 0, 2, 5, 7 and 10% CO 2 , balance N 2 ), and measured ventilation and metabolism using whole-body plethysmography and indirect calorimetry, respectively. We found that ventilation and metabolism were unchanged during prolonged normocapnia, whereas during graded hypercapnia, ventilation was elevated at 2% CO 2 and above. As a result, O 2 extraction efficiency at the lungs decreased with increasing hyperpnoea. Conversely, metabolic rate did not increase until 10% CO 2 , presumably due to the metabolic cost of hyperpnoea. Taken together, our results suggest that despite their fossorial lifestyle, DMRs do not exhibit adaptations in their ventilatory or metabolic responses to environmental hypercapnia.
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McNally, E., M. Fitzpatrick, S. Bourke, R. Costello, and WT McNicholas. "Reversible hypercapnia in acute exacerbations of chronic obstructive pulmonary disease (COPD)." European Respiratory Journal 6, no. 9 (October 1, 1993): 1353–56. http://dx.doi.org/10.1183/09031936.93.06091353.
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We prospectively studied emergency hospitalizations due to acute exacerbations of chronic obstructive pulmonary disease (COPD) among 74 hypercapnic patients, in order to determine factors which predict reversal to normocapnia as a result of therapy. Clinical, arterial blood gas and pulmonary function data on presentation were compared to predischarge values among those 58 patients who survived the admission. Patients were divided into those who reverted to normocapnia (reversible, 40% of surviving patients), and those who remained hypercapnic (chronic, 60% of surviving patients). Reversible patients had higher admission arterial oxygen tension (PaO2) levels than those with chronic hypercapnia (6.4 +/- 1.3 kPa (mean +/- SD), as compared to 5.7 +/- 1.1 kPa) better pulmonary function (forced expiratory volume in one second (FEV1) 35 +/- 16% predicted, as compared to 26 +/- 7.9), and a lower prevalence of cor pulmonale (30% as compared to 63% of patients). No admission variable(s) distinguished individual patients as reversible or chronic hypercapnic, and, in particular, admission arterial carbon dioxide tension (PaCO2) and pH levels were similar in both groups. Furthermore, there were no differences between survivors and those 16 patients who died during the admission, apart from a higher urea level among those who died. These findings suggest that reversible patients have milder underlying disease than those with chronic hypercapnia. Our data establish the high prevalence of reversible hypercapnia among patients hospitalized with exacerbations of COPD, and, furthermore, indicate that patients who are normocapnic in the stable state can develop similar levels of hypercapnia during exacerbations as those with chronic hypercapnia.
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Baumbach, G. L., W. G. Mayhan, and D. D. Heistad. "Protection of the blood-brain barrier by hypercapnia during acute hypertension." American Journal of Physiology-Heart and Circulatory Physiology 251, no. 2 (August 1, 1986): H282—H287. http://dx.doi.org/10.1152/ajpheart.1986.251.2.h282.
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The purpose of this study was to examine effects of hypercapnia on susceptibility of the blood-brain barrier to disruption during acute hypertension. Two methods were used to test the hypothesis that cerebral vasodilatation during hypercapnia increases disruption of the blood-brain barrier. First, permeability of the blood-brain barrier was measured in anesthetized cats with 125I-labeled serum albumin. Severe hypertension markedly increased permeability of the blood-brain barrier during normocapnia, but not during hypercapnia. The protective effect of hypercapnia was not dependent on sympathetic nerves. Second, in anesthetized rats, permeability of the barrier was quantitated by clearance of fluorescent dextran. Disruption of the blood-brain barrier during hypertension was decreased by hypercapnia. Because disruption of the blood-brain barrier occurred primarily in pial venules, we also measured pial venular diameter and pressure (with a servo-null method). Acute hypertension increased pial venular pressure and diameter in normocapnic rats. Hypercapnia alone increased pial venular pressure and pial venular diameter, and acute hypertension during hypercapnia further increased venular pressure. The magnitude of increase in pial venular pressure during acute hypertension was significantly less in hypercapnic than in normocapnic rats. We conclude that hypercapnia protects the blood-brain barrier. Possible mechanisms of this effect include attenuation of the incremental increase in pial venular pressure by hypercapnia or a direct effect on the blood-brain barrier not related to venous pressure.
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Shigemura, Masahiko, Emilia Lecuona, Martín Angulo, Tetsuya Homma, Diego A. Rodríguez, Francisco J. Gonzalez-Gonzalez, Lynn C. Welch, et al. "Hypercapnia increases airway smooth muscle contractility via caspase-7–mediated miR-133a–RhoA signaling." Science Translational Medicine 10, no. 457 (September 5, 2018): eaat1662. http://dx.doi.org/10.1126/scitranslmed.aat1662.
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The elevation of carbon dioxide (CO2) in tissues and the bloodstream (hypercapnia) occurs in patients with severe lung diseases, including chronic obstructive pulmonary disease (COPD). Whereas hypercapnia has been recognized as a marker of COPD severity, a role for hypercapnia in disease pathogenesis remains unclear. We provide evidence that CO2acts as a signaling molecule in mouse and human airway smooth muscle cells. High CO2activated calcium-calpain signaling and consequent smooth muscle cell contraction in mouse airway smooth muscle cells. The signaling was mediated by caspase-7–induced down-regulation of the microRNA-133a (miR-133a) and consequent up-regulation of Ras homolog family member A and myosin light-chain phosphorylation. Exposure of wild-type, but not caspase-7–null, mice to hypercapnia increased airway contraction and resistance. Deletion of theCaspase-7gene prevented hypercapnia-induced airway contractility, which was restored by lentiviral transfection of a miR-133a antagonist. In a cohort of patients with severe COPD, hypercapnic patients had higher airway resistance, which improved after correction of hypercapnia. Our data suggest a specific molecular mechanism by which the development of hypercapnia may drive COPD pathogenesis and progression.
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Leffler, C. W., R. Mirro, L. J. Pharris, and M. Shibata. "Permissive role of prostacyclin in cerebral vasodilation to hypercapnia in newborn pigs." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 1 (July 1, 1994): H285—H291. http://dx.doi.org/10.1152/ajpheart.1994.267.1.h285.
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Hypercapnic cerebral vasodilation in piglets is accompanied by increased cerebral prostanoid synthesis. Interventions that prevent the increased prostanoids also interfere with the vasodilation. However, the increased prostanoids may not produce vasodilation directly; instead, they may allow or enhance function of another mechanism. The present experiments examined the hypothesis that prostacyclin can allow, but may not directly produce, cerebral vasodilation to hypercapnia. Chloralose-anesthetized piglets were equipped with closed cranial windows for measurements of pial arteriolar diameters. Hypercapnia (arterial CO2 partial pressure approximately 70 mmHg) was administered before and after indomethacin (5 mg/kg iv) in all animals. Then artificial cerebrospinal fluid (aCSF) under the cranial window was replaced for the remainder of the experiment with aCSF containing vehicle, carbaprostacyclin (60 pM), iloprost (1 pM), prostaglandin E2 (PGE2; 1.7 and 3.3 nM), isoproterenol (10 and 100 nM), or sodium nitroprusside (1 microM), and hypercapnia was repeated. The two prostacyclin receptor agonists restored cerebral vasodilation to hypercapnia that had been blocked by indomethacin (to 92 +/- 31% and 76 +/- 11% of the before-indomethacin dilation for carbaprostacyclin and iloprost, respectively.) The highest dose of PGE2 partially restored the dilation (43 +/- 7% of the pre-indomethacin response). In contrast, neither isoproterenol nor sodium nitroprusside permitted significant dilation to hypercapnia following indomethacin treatment. These data indicate that prostacyclin can allow hypercapnic vasodilation to occur, but increasing levels do not appear to be necessary to cause the dilation directly. The short half-life of prostacyclin may explain why active prostanoid synthesis appears to be necessary for hypercapnia-induced cerebral vasodilation in newborn pigs.
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Nakahata, Katsutoshi, Hiroyuki Kinoshita, Yusei Hirano, Yoshiki Kimoto, Hiroshi Iranami, and Yoshio Hatano. "Mild Hypercapnia Induces Vasodilation via Adenosine Triphosphate-sensitive K+Channels in Parenchymal Microvessels of the Rat Cerebral Cortex." Anesthesiology 99, no. 6 (December 1, 2003): 1333–39. http://dx.doi.org/10.1097/00000542-200312000-00014.
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Background Carbon dioxide is an important vasodilator of cerebral blood vessels. Cerebral vasodilation mediated by adenosine triphosphate (ATP)-sensitive K+ channels has not been demonstrated in precapillary microvessel levels. Therefore, the current study was designed to examine whether ATP-sensitive K+ channels play a role in vasodilation induced by mild hypercapnia in precapillary arterioles of the rat cerebral cortex. Methods Brain slices from rat cerebral cortex were prepared and superfused with artificial cerebrospinal fluid, including normal (Pco2 = 40 mmHg; pH = 7.4), hypercapnic (Pco2 = 50 mmHg; pH = 7.3), and hypercapnic normal pH (Pco2 = 50 mmHg; pH = 7.4) solutions. The ID of a cerebral parenchymal arteriole (5-9.5 microm) was monitored using computerized videomicroscopy. Results During contraction to prostaglandin F2alpha (5 x 10(-7) m), hypercapnia, but not hypercapnia under normal pH, induced marked vasodilation, which was completely abolished by the selective ATP-sensitive K+ channel antagonist glibenclamide (5 x 10(-6) m). However, the selective Ca2+-dependent K+ channel antagonist iberiotoxin (10(-7) m) as well as the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (10(-4) m) did not alter vasodilation. A selective ATP-sensitive K+ channel opener, levcromakalim (3 x 10(-8) to 3 x 10(-7) m), induced vasodilation, whereas this vasodilation was abolished by glibenclamide. Conclusion These results suggest that in parenchymal microvessels of the rat cerebral cortex, decreased pH corresponding with hypercapnia, but not hypercapnia itself, contributes to cerebral vasodilation produced by carbon dioxide and that ATP-sensitive K+ channels play a major role in vasodilator responses produced by mild hypercapnia.
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Cohen, Yoram, Lee-Hong Chang, Lawrence Litt, Francis Kim, John W. Severinghaus, Philip R. Weinstein, Richard L. Davis, Isabelle Germano, and Thomas L. James. "Stability of Brain Intracellular Lactate and 3P-Metabolite Levels at Reduced Intracellular pH during Prolonged Hypercapnia in Rats." Journal of Cerebral Blood Flow & Metabolism 10, no. 2 (March 1990): 277–84. http://dx.doi.org/10.1038/jcbfm.1990.45.
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The tolerance of low intracellular pH (pHi) was examined in vivo in rats by imposing severe, prolonged respiratory acidosis. Rats were intubated and ventilated for 10 min with 20% CO2, for 75 min with 50% CO2, and for 10 min with 20% CO2. The maximum Paco2 was 320 mm Hg. Cerebral intracellular lactate, pHi, and high-energy phosphate metabolites were monitored in vivo with 31P and 1H nuclear magnetic resonance (NMR) spectroscopy, using a 4.7-T horizontal instrument. Within 6 min after the administration of 50% CO2, pHi fell by 0.57 ± 0.03 unit, phosphocreatine decreased by ∼20%, and Pi increased by ∼100%. These values were stable throughout the remainder of the hypercapnic period. Cerebral intracellular lactate, visible with 1H NMR spectroscopy in the hyperoxic state, decreased during hypercapnia, suggesting either a favorable change in oxygen availability (decreased lactate production) or an increase in lactate clearance or both. All hypercapnic animals awakened and behaved normally after CO2 was discontinued. Histological examination of cortical and hippocampal areas, prepared using a hematoxylin and eosin stain, showed no areas of necrosis and no glial infiltrates. However, isolated, scattered, dark-staining, shrunken neurons were detected both in control animals (no exposure to hypercapnia) and in animals that had been hypercapnic. This subtle histological change could represent an artifact resulting from imperfect perfusion-fixation, or it could represent subtle neurologic injury during the hypercapnia protocol. In summary, extreme hypercapnia and low pHi (∼6.5) are well tolerated in rats for periods up to 75 min if adequate oxygenation is maintained. The prolonged stability of metabolite concentrations during hypercapnia makes its use convenient for in vivo animal studies of the relevance of pHi to brain injury.
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Grissom, Colin K., Martin I. Radwin, Mary Beth Scholand, Chris H. Harmston, Mark C. Muetterties, and Tim J. Bywater. "Hypercapnia increases core temperature cooling rate during snow burial." Journal of Applied Physiology 96, no. 4 (April 2004): 1365–70. http://dx.doi.org/10.1152/japplphysiol.00531.2003.
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Previous retrospective studies report a core body temperature cooling rate of 3°C/h during avalanche burial. Hypercapnia occurs during avalanche burial secondary to rebreathing expired air, and the effect of hypercapnia on hypothermia during avalanche burial is unknown. The objective of this study was to determine the core temperature cooling rate during snow burial under normocapnic and hypercapnic conditions. We measured rectal core body temperature (Tre) in 12 subjects buried in compacted snow dressed in a lightweight clothing insulation system during two different study burials. In one burial, subjects breathed with a device (AvaLung 2, Black Diamond Equipment) that resulted in hypercapnia over 30-60 min. In a control burial, subjects were buried under identical conditions with a modified breathing device that maintained normocapnia. Mean snow temperature was -2.5 ± 2.0°C. Burial time was 49 ± 14 min in the hypercapnic study and 60 min in the normocapnic study ( P = 0.02). Rate of decrease in Tre was greater with hypercapnia (1.2°C/h by multiple regression analysis, 95% confidence limits of 1.1-1.3°C/h) than with normocapnia (0.7°C/h, 95% confidence limit of 0.6-0.8°C/h). In the hypercapnic study, the fraction of inspired carbon dioxide increased from 1.4 ± 1.0 to 7.0 ± 1.4%, minute ventilation increased from 15 ± 7 to 40 ± 12 l/min, and oxygen saturation decreased from 97 ± 1 to 90 ± 6% ( P < 0.01). During the normocapnic study, these parameters remained unchanged. In this study, Tre cooling rate during snow burial was less than previously reported and was increased by hypercapnia. This may have important implications for prehospital treatment of avalanche burial victims.
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Reid, J. M., A. G. Davies, F. M. Ashcroft, and D. J. Paterson. "Effect of L-NMMA, cromakalim, and glibenclamide on cerebral blood flow in hypercapnia and hypoxia." American Journal of Physiology-Heart and Circulatory Physiology 269, no. 3 (September 1, 1995): H916—H922. http://dx.doi.org/10.1152/ajpheart.1995.269.3.h916.
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Sulfonylureas reduce cerebral blood flow (CBF) during hypoxia but not during hypercapnia, whereas blockers of nitric oxide (NO) synthesis reduce hypercapnic CBF. However, the effect of NO blockers on hypoxic CBF is uncertain. CBF was measured in the cortex of 51 enflurane-anesthetized rats by the hydrogen clearance technique during eucapnia, hypercapnia (arterial PCO2 65 Torr), and hypoxia (arterial PO2 40 Torr). CBF increased twofold in both hypercapnia and hypoxia from eucapnia. Intracortical (ic) NG-monomethyl-L-arginine (L-NMMA, 100 microM-5 mM) attenuated both the hypercapnic and hypoxic dilations by 60-70%, and L-arginine (300 mg/kg iv) partially reversed these effects. Glibenclamide (10 microM ic) and L-NMMA gave no further attenuation of the hypoxic dilation than L-NMMA alone. Cromakalim (10 microM, ic) increased CBF in eucapnia, but this was not seen in the presence of glibenclamide. The adenosine antagonist 8-phenyl-theophylline did not attenuate the hypoxic dilation. This suggests that NO synthesis plays a major role in the regulation of CBF in hypercapnia and hypoxia. But the combined effects of glibenclamide and L-NMMA do not further attenuate CBF in hypoxia.
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Busija, D. W., and C. W. Leffler. "Hypothermia reduces cerebral metabolic rate and cerebral blood flow in newborn pigs." American Journal of Physiology-Heart and Circulatory Physiology 253, no. 4 (October 1, 1987): H869—H873. http://dx.doi.org/10.1152/ajpheart.1987.253.4.h869.
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We examined effects of hypothermia on cerebral metabolic rate and cerebral blood flow in anesthetized, newborn pigs (1-4 days old). Cerebral blood flow (CBF) was determined with 15-micronS radioactive microspheres. Regional CBF ranged from 44 to 66 ml . min-1.100 g-1, and cerebral metabolic rate was 1.94 +/- 0.23 ml O2.100 g-1 . min-1 during normothermia (39 degrees C). Reduction of rectal temperature to 34-35 degrees C decreased CBF and cerebral metabolic rate 40-50%. In another group of piglets, we examined responsiveness of the cerebral circulation to arterial hypercapnia during hypothermia. Although absolute values for normocapnic and hypercapnic CBF were reduced by hypothermia and absolute values for normocapnic and hypercapnic cerebrovascular resistance were increased, the percentage changes from control in these variables during hypercapnia were similar during normothermia and hypothermia. In another group of animals that were maintained normothermic and exposed to two episodes of hypercapnia, there was no attenuation of cerebrovascular dilatation during the second episode. We conclude that hypothermia reduces CBF secondarily to a decrease in cerebral metabolic rate and that percent dilator responsiveness to arterial hypercapnia is unaltered when body temperature is reduced.
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Horvath, Ildiko, Norbert T. Sandor, Zoltan Ruttner, and Alan C. McLaughlin. "Role of Nitric Oxide in Regulating Cerebrocortical Oxygen Consumption and Blood Flow during Hypercapnia." Journal of Cerebral Blood Flow & Metabolism 14, no. 3 (May 1994): 503–9. http://dx.doi.org/10.1038/jcbfm.1994.62.
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The effect of the nitric oxide (NO) synthase inhibitor Nω-nitro-l-arginine methyl ester (l-NAME) on the response of cerebrocortical oxygen consumption (CMRO2) and blood flow (CBF) to two levels of hypercapnia (Paco2 ∼ 60 mm Hg and Paco2 ∼ 90 mm Hg) was investigated in ketamine-anesthetized rats. CBF was calculated using the Kety–Schmidt approach and CMRO2 was calculated from the product of CBF and the arteriovenous (superior sagittal sinus) difference for oxygen. l-NAME treatment did not have a significant effect on either CMRO2 or CBE under normocapnic conditions but inhibited the hypercapnic increase of CMRO2 and the hypercapnic increase in CBF. These results suggest that NO plays a role in the response of CMRO2 and CBF during hypercapnia and are consistent with the suggestion that at least part of the increase in CBF observed during hypercapnia is coupled to an increase in CMRO2.
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Davis, James T., Lindsey M. Boulet, Alyssa M. Hardin, Alex J. Chang, Andrew T. Lovering, and Glen E. Foster. "Ventilatory responses to acute hypoxia and hypercapnia in humans with a patent foramen ovale." Journal of Applied Physiology 126, no. 3 (March 1, 2019): 730–38. http://dx.doi.org/10.1152/japplphysiol.00741.2018.
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Subjects with a patent foramen ovale (PFO) have blunted ventilatory acclimatization to high altitude compared with subjects without PFO. The blunted response observed could be because of differences in central and/or peripheral respiratory chemoreflexes. We hypothesized that compared with subjects without a PFO (PFO−), subjects with a PFO (PFO+) would have blunted ventilatory responses to acute hypoxia and hypercapnia. Sixteen PFO+ subjects (9 female) and 15 PFO− subjects (8 female) completed four 20-min trials on the same day: 1) normoxic hypercapnia (NH), 2) hyperoxic hypercapnia (HH), 3) isocapnic hypoxia (IH), and 4) poikilocapnic hypoxia (PH). Hypercapnic trials were completed before the hypoxic trials, the order of the hypercapnic (NH & HH) and hypoxic (IH & PH) trials were randomized, and trials were separated by ≥40 min. During the NH trials but not the HH trials subjects who were PFO+ had a blunted hypercapnic ventilatory response compared with subjects who were PFO− (1.41 ± 0.46 l·min−1·mmHg−1 vs. 1.98 ± 0.71 l·min−1·mmHg−1, P = 0.02). There were no differences between the PFO+ and PFO− subjects with respect to the acute hypoxic ventilatory response during IH and PH trials. Hypoxic ventilatory depression was similar between subjects who were PFO+ and PFO− during IH. These data suggest that compared with subjects who were PFO−, subjects who were PFO+ have normal ventilatory chemosensitivity to acute hypoxia but blunted ventilatory chemosensitivity to carbon dioxide, possibly because of reduced carbon dioxide sensitivity of either the central and/or the peripheral chemoreceptors. NEW & NOTEWORTHY Patent foramen ovale (PFO) is found in ~25%–40% of the population. The presence of a PFO appears to be associated with blunted ventilatory responses during acute exposure to normoxic hypercapnia. The reason for this blunted ventilatory response during acute exposure to normoxic hypercapnia is unknown but may suggest differences in either central and/or peripheral chemoreflex contribution to hypercapnia.
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Peng, Shin-Lei, Harshan Ravi, Min Sheng, Binu P. Thomas, and Hanzhang Lu. "Searching for a truly “iso-metabolic” gas challenge in physiological MRI." Journal of Cerebral Blood Flow & Metabolism 37, no. 2 (July 20, 2016): 715–25. http://dx.doi.org/10.1177/0271678x16638103.
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Hypercapnia challenge (e.g. inhalation of CO2) has been used in calibrated fMRI as well as in the mapping of vascular reactivity in cerebrovascular diseases. An important assumption underlying these measurements is that CO2 is a pure vascular challenge but does not alter neural activity. However, recent reports have suggested that CO2 inhalation may suppress neural activity and brain metabolic rate. Therefore, the goal of this study is to propose and test a gas challenge that is truly “iso-metabolic,” by adding a hypoxic component to the hypercapnic challenge, since hypoxia has been shown to enhance cerebral metabolic rate of oxygen (CMRO2). Measurement of global CMRO2 under various gas challenge conditions revealed that, while hypercapnia (P = 0.002) and hypoxia (P = 0.002) individually altered CMRO2 (by −7.6 ± 1.7% and 16.7 ± 4.1%, respectively), inhalation of hypercapnic-hypoxia gas (5% CO2/13% O2) did not change brain metabolism (CMRO2 change: 1.5 ± 3.9%, P = 0.92). Moreover, cerebral blood flow response to the hypercapnic-hypoxia challenge (in terms of % change per mmHg CO2 change) was even greater than that to hypercapnia alone (P = 0.007). Findings in this study suggest that hypercapnic-hypoxia gas challenge may be a useful maneuver in physiological MRI as it preserves vasodilatory response yet does not alter brain metabolism.
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Allam, M., C. Saunier, A. Sautegeau, and D. Hartemann. "The inotropic effect of digoxin on an isolated rat heart in hypercapnia and (or) hypoxia." Canadian Journal of Physiology and Pharmacology 68, no. 3 (March 1, 1990): 455–61. http://dx.doi.org/10.1139/y90-064.
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The explanation for the increased frequency of troubles with digoxin therapy in patients with chronic pulmonary diseases is debated. The reported effects of hypoxia in vivo on myocardial levels of digoxin are contradictory, and there have been few studies on the effects of hypercapnia. In the past, it has been shown in rat myocardial tissue at rest in vitro that hypoxia decreased and hypercapnia acidosis increased the digoxin uptake. We performed a new study in vitro in an isolated beating rat heart perfused at constant flow (37 °C) and stimulated at a constant frequency (6 Hz). The performances were recorded with an intraventricular balloon equipped with a tip-manometer catheter. The action of digoxin was studied by recording systolic pressure (PS) and diastolic pressure (PD), the left ventricular developed pressure (LVDP = PS − PD), the (dP/dt)max, and the ratio (dP/dt)max/PS. First, the heart was perfused for 30 min with a modified Tyrode's solution perfusate aerated with carbogen (pH = 7.40; [Formula: see text]; [Formula: see text]) (1 mmHg = 133.32 Pa). Various parameters of contractions were recorded (initial control values). Then the heart was perfused for 15 min with Tyrode's solution aerated either with a hypoxic gas mixture (pH = 7.41; [Formula: see text]; [Formula: see text]), a hypercapnic gas mixture (pH = 7.08; [Formula: see text]; [Formula: see text]), or a hypoxic–hypercapnic gas mixture (pH = 7.09; [Formula: see text]; [Formula: see text]). Control hearts were continuously perfused with Tyrode's solution aerated with carbogen. During heart perfusion with hypercapnic, hypoxic, or hypoxic–hypercapnic Tyrode's solution, a decrease in LVDP and (dP/dt)max was observed. Finally, the heart was perfused with the same Tyrode's solution plus 1.75 × 10−5 M digoxin. The increase in myocardial contractility produced by digoxin was enhanced by hypercapnia and abolished by hypoxia. The addition of hypercapnia to hypoxia in Tyrode's solution seems to enhance the depressor action of the hypoxia.Key words: isolated heart, digoxin, hypoxia, hypercapnia, myocardial contractility.
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Caples, Sean M., Deborah L. Rasmussen, Won Y. Lee, Marla Z. Wolfert, and Rolf D. Hubmayr. "Impact of buffering hypercapnic acidosis on cell wounding in ventilator-injured rat lungs." American Journal of Physiology-Lung Cellular and Molecular Physiology 296, no. 1 (January 2009): L140—L144. http://dx.doi.org/10.1152/ajplung.90339.2008.
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We measured the effects of raising perfusate pH on ventilator-induced cell wounding and repair in ex vivo mechanically ventilated hypercapnic rat lungs. Lungs were randomized to one of three perfusate groups: 1) unbuffered hypercapnic acidosis, 2) bicarbonate-buffered hypercapnia, or 3) tris-hydroxymethyl aminomethane (THAM)-buffered hypercapnia. The membrane-impermeant label propidium iodide was added to the perfusate either during or after injurious ventilation providing a means to subsequently identify transiently wounded and permanently wounded cells in optical sections of subpleural alveoli. Normalizing perfusate pH in hypercapnic preparations attenuated ventilator-induced cell injury, particularly in THAM-buffered preparations. This was observed despite greater amounts of edema and impaired lung mechanics compared with other treatment groups. Protective effects of buffering of hypercapnic acidosis on injury and repair were subsequently confirmed in a cell scratch model. We conclude that buffering of hypercapnic acidosis attenuates plasma cell injury induced by mechanical hyperinflation.
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Voulgaris, Athanasios, Kostas Archontogeorgis, Konstantina Chadia, Dimitra Siopi, Evangelia Nena, and Paschalis Steiropoulos. "Differences in Anthropometric, Sleep and Respiratory Characteristics between Hypercapnic and Normocapnic Patients with COPD-OSA Overlap Syndrome." Journal of Personalized Medicine 14, no. 6 (June 4, 2024): 600. http://dx.doi.org/10.3390/jpm14060600.
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Background: Overlap syndrome (OS), the coexistence of chronic obstructive pulmonary disease and obstructive sleep apnea, is frequently characterized by the presence of daytime hypercapnia (pCO2 ≥ 45 mmHg). The aim of this study was to investigate potential differences in anthropometric, sleep and respiratory characteristics between hypercapnic and normocapnic patients with OS. Methods: Consecutive patients who underwent polysomnography, pulmonary function testing and arterial blood gases and had been diagnosed with OS were enrolled in the study. Results: According to pCO2 levels in wakefulness, the patients were divided into group A, consisting of OS patients without hypercapnia (n = 108) or group B, consisting of OS patients with hypercapnia (n = 55). The majority of included patients in both groups were males (n = 92 in group A vs. n = 50 in group B). Group B had increased BMI (p = 0.001), neck (p = 0.017) and waist circumference (p = 0.013), higher scores in Epworth sleepiness scale (ESS) (p = 0.008), increased sleep efficiency (p = 0.033), oxygen desaturation index (p = 0.004) and time with oxyhemoglobin saturation <90% (p = 0.006) than group A. Also, Group B had decreased average and minimum oxyhemoglobin saturation during sleep (p < 0.001). Hypercapnic patients had lower FEV1% (p = 0.003), FVC% (p = 0.004), pO2 and pCO2 (p < 0.001 for both) values compared with normocapnic patients. In binary regression analysis, which assessed various predictors on the likelihood of having hypercapnia, it was found that BMI (OR: 1.313, 95% CI: 1.048–1.646, p = 0.018) and FVC (OR: 0.913, 95% CI: 0.845–0.986, p = 0.020) were the major determinants of hypercapnia in OS patients. Conclusions: Hypercapnic OS patients were more obese and sleepy and presented worse respiratory function in wakefulness and sleep hypoxia characteristics compared with normocapnic OS patients.
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Raff, H., and T. P. Roarty. "Renin, ACTH, and aldosterone during acute hypercapnia and hypoxia in conscious rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 254, no. 3 (March 1, 1988): R431—R435. http://dx.doi.org/10.1152/ajpregu.1988.254.3.r431.
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The control of aldosterone secretion may be altered during acute changes in arterial blood gases. We studied the blood gas, plasma electrolyte, renin (PRA), adrenocorticotropic hormone (ACTH), and aldosterone (ALDO) responses to acute hypercapnia (4 and 8% CO2), acute hypocapnic hypoxia (10% O2), acute severe normocapnic hypoxia (7% O2-4% CO2), and acute hypercapnic hypoxia (7% O2-8% CO2) in conscious, cannulated Long-Evans rats. Normoxia resulted in normal levels of PRA (6.9 +/- 2.0 ng.ml-1.h-1), ACTH (96 +/- 32 pg/ml), and ALDO (10 +/- 3 ng/dl). Hypercapnia had no effect on PRA but did lead to an increase in ACTH (to 298 +/- 69 pg/ml) and ALDO (to 33 +/- 7 ng/dl) during 8% CO2 exposure. Normocapnic hypoxia resulted in a significant increase in ACTH (to 196 +/- 14 pg/ml) and ALDO (to 30 +/- 3 ng/dl). Hypercapnic hypoxia resulted in the greatest increases in PRA (to 30 +/- 2 ng.ml-1.h-1), ACTH (to 397 +/- 114 pg/ml), and ALDO (to 41 +/- 5 ng/dl). We conclude that in conscious rats 1) hypercapnia (less than 80 Torr) had no significant effect on PRA, 2) isocapnic, severe hypoxia (Po2 approximately 34 Torr) increased ACTH, and 3) the combination of hypercapnia and hypoxia was a very potent stimulus to PRA, ACTH, and ALDO. The ALDO responses to increases in endogenous ACTH and angiotensin II appear to be normal in conscious rats during acute hypoxia and/or hypercapnia.
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Gidday, Jeffrey M., and T. S. Park. "Effect of 2-Chloroadenosine on Cerebrovascular Reactivity to Hypercapnia in Newborn Pig." Journal of Cerebral Blood Flow & Metabolism 12, no. 4 (July 1992): 656–63. http://dx.doi.org/10.1038/jcbfm.1992.90.
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The effect of local administration of vasodilative concentrations of the adenosine receptor agonist 2-chloroadenosine (2-CADO) on the hyperemic responses of the pial and parenchymal microcirculations to graded hypercapnia was determined. The cranial window and brain microdialysis–hydrogen clearance techniques were utilized in two groups of isoflurane-anesthetized newborn pigs to measure changes in pial diameters and local CBF, respectively, in response to graded hypercapnia in the absence and presence of 2-CADO. Progressive size-dependent dilations of pial arterioles [small = 41 ± 7 μm (mean ± SD), intermediate = 78 ± 13 μm, and large = 176 ± 57 μm in diameter] occurred in response to graded hypercapnia alone (Paco2 = 58 and 98 mm Hg) and to superfusions of 2-CADO (10−5 M) during normocapnia; the magnitude of the dilative response to each of these stimuli was inversely proportional to vessel size. When hypercapnia was induced concomitantly with 2-CADO superfusion, the dilative effects of each stimulus were directly additive. Similarly, local microdialysis infusion of 10−5 M 2-CADO, which doubled CBF during normocapnia, did not affect the hyperemic response of the parenchymal circulation to graded hypercapnia (Paco2 = 69 and 101 mm Hg). Our findings are consistent with the participation of adenosine in the mediation of cerebral hypercapnic hyperemia. If, however, adenosine is not involved in this dilative response, our results indicate that concomitant vascular and neuromodulatory actions induced by adenosine receptor stimulation do not affect the mechanism responsible for the hypercapnic hyperemic response.
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Helenius, Iiro Taneli, Aisha Nair, Humberto E. Trejo Bittar, Jacob I. Sznajder, Peter H. S. Sporn, and Greg J. Beitel. "Focused Screening Identifies Evoxine as a Small Molecule That Counteracts CO2-Induced Immune Suppression." Journal of Biomolecular Screening 21, no. 4 (December 23, 2015): 363–71. http://dx.doi.org/10.1177/1087057115624091.
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Patients with severe lung disease may develop hypercapnia, elevation of the levels of CO2 in the lungs and blood, which is associated with increased risk of death, often from infection. To identify compounds that ameliorate the adverse effects of hypercapnia, we performed a focused screen of 8832 compounds using a CO2-responsive luciferase reporter in Drosophila S2* cells. We found that evoxine, a plant alkaloid, counteracts the CO2-induced transcriptional suppression of antimicrobial peptides in S2* cells. Strikingly, evoxine also inhibits hypercapnic suppression of interleukin-6 and the chemokine CCL2 expression in human THP-1 macrophages. Evoxine’s effects are selective, since it does not prevent hypercapnic inhibition of phagocytosis by THP-1 cells or CO2-induced activation of AMPK in rat ATII pulmonary epithelial cells. The results suggest that hypercapnia suppresses innate immune gene expression by definable pathways that are evolutionarily conserved and demonstrate for the first time that specific CO2 effects can be targeted pharmacologically.
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Casalino-Matsuda, S. Marina, Sergejs Berdnikovs, Naizhen Wang, Aisha Nair, Khalilah L. Gates, Greg J. Beitel, and Peter H. S. Sporn. "Hypercapnia selectively modulates LPS-induced changes in innate immune and DNA replication-related gene transcription in the macrophage." Interface Focus 11, no. 2 (February 12, 2021): 20200039. http://dx.doi.org/10.1098/rsfs.2020.0039.
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Hypercapnia, the elevation of CO 2 in blood and tissues, commonly occurs in severe acute and chronic respiratory diseases and is associated with increased risk of death. Recent studies have shown that hypercapnia inhibits expression of select innate immune genes and suppresses host defence against bacterial and viral pneumonia in mice. In the current study, we evaluated the effect of culture under conditions of hypercapnia (20% CO 2 ) versus normocapnia (5% CO 2 ), both with normoxia, on global gene transcription in human THP-1 and mouse RAW 264.7 macrophages stimulated with lipopolysaccharide (LPS). We found that hypercapnia selectively downregulated transcription of LPS-induced genes associated with innate immunity, antiviral response, type I interferon signalling, cytokine signalling and other inflammatory pathways in both human and mouse macrophages. Simultaneously, hypercapnia increased expression of LPS-downregulated genes associated with mitosis, DNA replication and DNA repair. These CO 2 -induced changes in macrophage gene expression help explain hypercapnic suppression of antibacterial and antiviral host defence in mice and reveal a mechanism that may underlie, at least in part, the high mortality of patients with severe lung disease and hypercapnia.
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Perry, S. F., S. Malone, and D. Ewing. "Hypercapnic acidosis in the rainbow trout (Salmo gairdneri). I. Branchial ionic fluxes and blood acid–base status." Canadian Journal of Zoology 65, no. 4 (April 1, 1987): 888–95. http://dx.doi.org/10.1139/z87-142.
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Branchial solute fluxes as well as blood respiratory, ionic, and acid–base variables were monitored before, during, and after 72 h of exposure to external hypercapnia (1% CO2; [Formula: see text]). Hypercapnia induced an immediate extracellular respiratory acidosis that was gradually regulated over the 72-h period by an elevation of the plasma bicarbonate [Formula: see text] level. Red blood cell pH changed in a manner similar to whole blood pH but the reduction of red blood cell pH during hypercapnia was significantly less than that predicted from in vitro experiments. We argue that elevated plasma levels of epinephrine in the first 12 h of hypercapnia may serve to stabilize red blood cell pH during the severe reduction of whole blood pH, thereby preventing excessive depressions of arterial oxygen content. Elevated external CO2 tension caused changes in the branchial net flux (JnetCl−) such that the arithmetic difference between sodium net flux (JnetNa+) and JnetCl− (JnetNa+ – JnetCl−) increased during hypercapnia and then decreased post-hypercapnia. These results are consistent with enhanced branchial acid excretion and are discussed with reference to the involvement of the gill in the regulation of hypercapnic acidosis.
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Massik, J., M. D. Jones, M. Miyabe, Y. L. Tang, M. L. Hudak, R. C. Koehler, and R. J. Traystman. "Hypercapnia and response of cerebral blood flow to hypoxia in newborn lambs." Journal of Applied Physiology 66, no. 3 (March 1, 1989): 1065–70. http://dx.doi.org/10.1152/jappl.1989.66.3.1065.
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Individual effects of hypoxic hypoxia and hypercapnia on the cerebral circulation are well described, but data on their combined effects are conflicting. We measured the effect of hypoxic hypoxia on cerebral blood flow (CBF) and cerebral O2 consumption during normocapnia (arterial PCO2 = 33 +/- 2 Torr) and during hypercapnia (60 +/- 2 Torr) in seven pentobarbital-anesthetized lambs. Analysis of variance showed that neither the magnitude of the hypoxic CBF response nor cerebral O2 consumption was significantly related to the level of arterial PCO2. To determine whether hypoxic cerebral vasodilation during hypercapnia was restricted by reflex sympathetic stimulation we studied an additional six hypercapnic anesthetized lambs before and after bilateral removal of the superior cervical ganglion. Sympathectomy had no effect on base-line CBF during hypercapnia or on the CBF response to hypoxic hypoxia. We conclude that the effects of hypoxic hypoxia on CBF and cerebral O2 consumption are not significantly altered by moderate hypercapnia in the anesthetized lamb. Furthermore, we found no evidence that hypercapnia results in a reflex increase in sympathetic tone that interferes with the ability of cerebral vessels to dilate during hypoxic hypoxia.
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Xie, Ailiang, James B. Skatrud, Dominic S. Puleo, and Barbara J. Morgan. "Exposure to hypoxia produces long-lasting sympathetic activation in humans." Journal of Applied Physiology 91, no. 4 (October 1, 2001): 1555–62. http://dx.doi.org/10.1152/jappl.2001.91.4.1555.
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The relative contributions of hypoxia and hypercapnia in causing persistent sympathoexcitation after exposure to the combined stimuli were assessed in nine healthy human subjects during wakefulness. Subjects were exposed to 20 min of isocapnic hypoxia (arterial O2 saturation, 77–87%) and 20 min of normoxic hypercapnia (end-tidal Pco 2, +5.3–8.6 Torr above eupnea) in random order on 2 separate days. The intensities of the chemical stimuli were manipulated in such a way that the two exposures increased sympathetic burst frequency by the same amount (hypoxia: 167 ± 29% of baseline; hypercapnia: 171 ± 23% of baseline). Minute ventilation increased to the same extent during the first 5 min of the exposures (hypoxia: +4.4 ± 1.5 l/min; hypercapnia: +5.8 ± 1.7 l/min) but declined with continued exposure to hypoxia and increased progressively during exposure to hypercapnia. Sympathetic activity returned to baseline soon after cessation of the hypercapnic stimulus. In contrast, sympathetic activity remained above baseline after withdrawal of the hypoxic stimulus, even though blood gases had normalized and ventilation returned to baseline levels. Consequently, during the recovery period, sympathetic burst frequency was higher in the hypoxia vs. the hypercapnia trial (166 ± 21 vs. 104 ± 15% of baseline in the last 5 min of a 20-min recovery period). We conclude that both hypoxia and hypercapnia cause substantial increases in sympathetic outflow to skeletal muscle. Hypercapnia-evoked sympathetic activation is short-lived, whereas hypoxia-induced sympathetic activation outlasts the chemical stimulus.
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Bryan, R. M., C. L. Myers, and R. B. Page. "Regional neurohypophysial and hypothalamic blood flow in rats during hypercapnia." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 255, no. 2 (August 1, 1988): R295—R302. http://dx.doi.org/10.1152/ajpregu.1988.255.2.r295.
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Regional cerebral blood flow (rCBF) was measured in the neurohypophysis and hypothalamus in normocapnic and hypercapnic rats using [14C]isopropyliodoamphetamine. Rats were surgically prepared using nitrous oxide and halothane and placed in plaster restraining casts. Hypercapnia was produced by increasing the fractional concentration of inspired CO2 (FICO2). rCBF in normocapnic rats was higher in the paraventricular nucleus, supraoptic nucleus, median eminence, and neural lobe than rates previously measured by use of diffusible tracers. During hypercapnia blood flow increased linearly with arterial PCO2 (PACO2) in all regions except the median eminence and neural lobe, which were not affected by hypercapnia. When rats were pretreated with phentolamine (1 mg/kg) to block the alpha-adrenergic receptors, blood flow in the median eminence and neural lobe increased significantly during hypercapnia. We conclude that blood flow in the cell bodies of the paraventricular nucleus and supraoptic nucleus is regulated differently during hypercapnia than blood flow in the nerve terminals in the median eminence and neural lobe. Furthermore, vasodilation produced by increased CO2 is offset by alpha-receptor stimulation in the median eminence and neural lobe.
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MILSOM, W. K., and P. CHAN. "The Relationship between Lung Volume, Respiratory Drive and Breathing Pattern in the Turtle, Chrysemys Picta." Journal of Experimental Biology 120, no. 1 (January 1, 1986): 233–47. http://dx.doi.org/10.1242/jeb.120.1.233.
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Induced changes in resting lung volume (VLR) in the turtle Chrysemys picta (Schneider) had no effect on resting levels of minute ventilation in animals breathing room air but did change their breathing pattern. Increasing VLR caused an increase in the number of breaths in each episode (burst) of breathing but a reduction in the incidence of such breathing bursts and thus an increase in the length of periods of breath-holding. The data indicate that these effects were largely the consequence of changes in lung volume per se rather than changes in lung gas stores. Although both hypoxia and hypercapnia stimulated ventilation via increases in tidal volume and breathing frequency, they produced distinct changes in breathing pattern. While hypoxia (3% O2) caused an increase in the number of bursts of breathing (B/min) and reduced the number of breaths (b) in each burst (b/B), hypercapnia (5% CO2) increased both B/min and b/B. These data suggest that the size and incidence of bursts of breathing must be under separate control. One consequence of the different effects of hypoxia and hypercapnia on breaths per burst (b/B) was that hypoxic-hypercapnic gas mixtures (3% O2+5% CO2) failed to stimulate ventilation as much as hypercapnia alone. Administration of hypoxic, hypercapnic and hypoxic-hypercapnic gas mixtures to elevate respiratory drive eliminated the effects of changes in VLR on breathing pattern. Thus, although changes in VLR are important in the control of breathholding in animals breathing air, their effect decreases as respiratory drive increases.
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Campen, Matthew J., Yugo Tagaito, Todd P. Jenkins, Alex Balbir, and Christopher P. O’Donnell. "Heart rate variability responses to hypoxic and hypercapnic exposures in different mouse strains." Journal of Applied Physiology 99, no. 3 (September 2005): 807–13. http://dx.doi.org/10.1152/japplphysiol.00039.2005.
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Heart rate variability (HRV) is a well-characterized, noninvasive means of assessing cardiac autonomic nervous system activity. This study examines the basic cardiac responses to hypoxic and hypercapnic challenges in seven strains of commonly used inbred mice (A/J, BALB/cJ, C3H/HeJ, C57BL/6J, CBA/J, DBA/2J, and FVB/J). Adult male mice, 8–12 wk of age, were chronically instrumented to a femoral artery catheter for the continuous measurement of systemic arterial blood pressure and heart rate. Mice were exposed to multiple 4-min periods of hypoxia (10% O2), hypercapnia (5% CO2), and combined hypoxia/hypercapnia (10% O2 + 5% CO2). HRV was derived from pulse intervals of the blood pressure tracings. Hypoxia induced increases in high-frequency HRV power and decreased low-frequency (LF) HRV power in most strains. Hypercapnia led to decreased high-frequency HRV power and increased LF HRV power in most strains. Strain differences were most notable in regard to the concomitant exposures of hypoxia and hypercapnia, with FVB/J mice mirroring their own response to hypercapnia alone, whereas CBA/J mice mirrored their own responses to hypoxia. As blood pressure is most likely the driving factor for heart rate changes via the baroreflex pathway, it is interesting that LF, considered to reflect cardiac sympathetic activity, was negatively correlated with heart rate, suggesting that LF changes are driven by baroreflex oscillation and not necessarily by absolute sympathetic or parasympathetic activity to the heart. These findings suggest that genetic background can influence the centrally mediated cardiovascular responses to basic hypoxic and hypercapnic challenges.
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Colby, C., D. L. Kilgore, and S. Howe. "Effects of hypoxia and hypercapnia on VT, f, and VI of nestling and adult bank swallows." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 253, no. 6 (December 1, 1987): R854—R860. http://dx.doi.org/10.1152/ajpregu.1987.253.6.r854.
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The effects of hypoxia, hypercapnia, and hypoxic hypercapnia on ventilation, and breathing pattern in adult and nestling bank swallows (Riparia riparia) were assessed. The CO2 threshold above which inhaled minute volume (VI) increased significantly in adults and nestlings was 0.045. At each level of fractional concentration of inspired CO2 (FICO2), ventilation in nestlings was lower than that in adults. At a FICO2 of 0.09, VI of adults increased by 284%, whereas VI in nestlings changed 238%. Adult bank swallows also showed a blunted ventilatory response to hypoxia, and the nestling's response was similar to other birds. Adults exhibited greater changes in VI at all levels of hypoxic hypercapnia compared with nestlings. Combined hypoxic and hypercapnic stimuli had an additive effect on ventilation in both groups. Chronic exposure of nestlings to the hypercapnia and hypoxia within burrows seems to significantly alter their ventilatory response to these respiratory stimuli.
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Almanza-Hurtado, Amilkar, Camilo Polanco Guerra, María Cristina Martínez-Ávila, Diana Borré-Naranjo, Tomás Rodríguez-Yanez, and Carmelo Dueñas-Castell. "Hypercapnia from Physiology to Practice." International Journal of Clinical Practice 2022 (September 23, 2022): 1–10. http://dx.doi.org/10.1155/2022/2635616.
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Acute hypercapnic ventilatory failure is becoming more frequent in critically ill patients. Hypercapnia is the elevation in the partial pressure of carbon dioxide (PaCO2) above 45 mmHg in the bloodstream. The pathophysiological mechanisms of hypercapnia include the decrease in minute volume, an increase in dead space, or an increase in carbon dioxide (CO2) production per sec. They generate a compromise at the cardiovascular, cerebral, metabolic, and respiratory levels with a high burden of morbidity and mortality. It is essential to know the triggers to provide therapy directed at the primary cause and avoid possible complications.
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Asadi, Amran K., Rui Carlos Sá, Tatsuya J. Arai, Rebecca J. Theilmann, Susan R. Hopkins, Richard B. Buxton, and G. Kim Prisk. "Regional pulmonary perfusion patterns in humans are not significantly altered by inspiratory hypercapnia." Journal of Applied Physiology 127, no. 2 (August 1, 2019): 365–75. http://dx.doi.org/10.1152/japplphysiol.00254.2018.
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Pulmonary vascular tone is known to be sensitive to both local alveolar Po2 and Pco2. Although the effects of hypoxia are well studied, the hypercapnic response is relatively less understood. We assessed changes in regional pulmonary blood flow in humans in response to hypercapnia using previously developed MRI techniques. Dynamic measures of blood flow were made in a single slice of the right lung of seven healthy volunteers following a block-stimulus paradigm (baseline, challenge, recovery), with CO2 added to inspired gas during the challenge block to effect a 7-Torr increase in end-tidal CO2. Effects of hypercapnia on blood flow were evaluated based on changes in spatiotemporal variability (fluctuation dispersion, FD) and in regional perfusion patterns in comparison to hypoxic effects previously studied. Hypercapnia increased FD 2.5% from baseline (relative to control), which was not statistically significant ( P = 0.07). Regional perfusion patterns were not significantly changed as a result of increased [Formula: see text] ( P = 0.90). Reanalysis of previously collected data using a similar protocol but with the physiological challenge replaced by decreased [Formula: see text] ([Formula: see text] = 0.125) showed marked flow redistribution ( P = 0.01) with the suggestion of a gravitational pattern, demonstrating hypoxia has the ability to affect regional change with a global stimulus. Taken together, these data indicate that hypercapnia of this magnitude does not lead to appreciable changes in the distribution of pulmonary perfusion, and that this may represent an interesting distinction between the hypoxic and hypercapnic regulatory response. NEW & NOTEWORTHY Although it is well known that the pulmonary circulation responds to local alveolar hypoxia, and that this mechanism may facilitate ventilation-perfusion matching, the relative role of CO2 is not well appreciated. This study demonstrates that an inspiratory hypercapnic stimulus is significantly less effective at inducing changes in pulmonary perfusion patterns than inspiratory hypoxia, suggesting that in these circumstances hypercapnia is not sufficient to induce substantial integrated feedback control of ventilation-perfusion mismatch across the lung.
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Balnis, Joseph, Tanner C. Korponay, and Ariel Jaitovich. "AMP-Activated Protein Kinase (AMPK) at the Crossroads Between CO2 Retention and Skeletal Muscle Dysfunction in Chronic Obstructive Pulmonary Disease (COPD)." International Journal of Molecular Sciences 21, no. 3 (January 31, 2020): 955. http://dx.doi.org/10.3390/ijms21030955.
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Skeletal muscle dysfunction is a major comorbidity in chronic obstructive pulmonary disease (COPD) and other pulmonary conditions. Chronic CO2 retention, or hypercapnia, also occur in some of these patients. Both muscle dysfunction and hypercapnia associate with higher mortality in these populations. Over the last years, we have established a mechanistic link between hypercapnia and skeletal muscle dysfunction, which is regulated by AMPK and causes depressed anabolism via reduced ribosomal biogenesis and accelerated catabolism via proteasomal degradation. In this review, we discuss the main findings linking AMPK with hypercapnic pulmonary disease both in the lungs and skeletal muscles, and also outline potential avenues for future research in the area based on knowledge gaps and opportunities to expand mechanistic research with translational implications.
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Uno, Tomoki, Tetsuya Homma, Masahiko Shigemura, Yosuke Fukuda, Tomoyuki Kimura, Chihiro Onitsuka, Tomoko Kawahara, et al. "Correlation of Arterial CO2 and Respiratory Impedance Values among Subjects with COPD." Journal of Clinical Medicine 9, no. 9 (August 31, 2020): 2819. http://dx.doi.org/10.3390/jcm9092819.
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Chronic obstructive pulmonary disease (COPD) is a respiratory illness characterized by airflow limitation and chronic respiratory symptoms with a global prevalence estimated to be more than 10% in 2010 and still on the rise. Furthermore, hypercapnic subject COPD leads to an increased risk of mortality, morbidity, and poor QoL (quality of life) than normocapnic subjects. Series of studies showed the usefulness of the forced oscillation technique (FOT) to measure small airway closure. Traditional findings suggested that hypercapnia may not be the main treating targets, but recent findings suggested that blood stream CO2 may lead to a worse outcome. This study aimed to seek the relationship between CO2 and small airway closure by using FOT. Subjects with COPD (n = 124; hypercapnia 22 and normocapnia 102) were analyzed for all pulmonary function values, FOT values, and arterial blood gas analysis. Student’s t-test, Spearman rank correlation, and multi linear regression analysis were used to analyze the data. COPD subjects with hypercapnia showed a significant increase in R5, R20, Fres, and ALX values, and a greater decrease in X5 value than normocapnic patients. Also, multiple linear regression analysis showed R5 was associated with hypercapnia. Hypercapnia may account for airway closure among subjects with COPD and this result suggests treating hypercapnia may lead to better outcomes for such a subject group.
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Wetterberg, T., T. Sjöberg, and S. Steen. "Effects of hypothermia in hypercapnia and hypercapnic hypoxemia." Acta Anaesthesiologica Scandinavica 37, no. 3 (April 1993): 296–302. http://dx.doi.org/10.1111/j.1399-6576.1993.tb03718.x.
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