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Journal articles on the topic 'Hypercapnic'

Author: Grafiati

Published: 2 June 2025

Last updated: 31 July 2025

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1

Ketabchi, Farzaneh, Bakytbek Egemnazarov, Ralph T. Schermuly, et al. "Effects of hypercapnia with and without acidosis on hypoxic pulmonary vasoconstriction." American Journal of Physiology-Lung Cellular and Molecular Physiology 297, no. 5 (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 hyperc

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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 (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 hy

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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 (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 que

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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 (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 alveo

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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 (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 successiv

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Tregub, Pavel P., Vladimir P. Kulikov, Irada Ibrahimli, et al. "Molecular Mechanisms of Neuroprotection after the Intermittent Exposures of Hypercapnic Hypoxia." International Journal of Molecular Sciences 25, no. 7 (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 predomi

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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 (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 blu

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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 (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+ secreti

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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 (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 e

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Nichol, Alistair D., Donall F. O'Cronin, Finola Naughton, Natalie Hopkins, John Boylan, and Paul McLoughlin. "Hypercapnic Acidosis Reduces Oxidative Reactions in Endotoxin-induced Lung Injury." Anesthesiology 113, no. 1 (2010): 116–25. http://dx.doi.org/10.1097/aln.0b013e3181dfd2fe.

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Background Hypercapnic acidosis frequently occurs when patients with acute lung injury are initially ventilated with low tidal volume "protective" strategies. Hypercapnic acidosis per se, in the absence of any change in tidal volume or airway pressure, is protective when instituted before the onset of injury. However, the mechanisms by which hypercapnic acidosis confers this protection are incompletely understood, in particular, the effects on pulmonary oxidative reactions, which are potent mediators of tissue damage, have not been previously examined in vivo. Methods After anesthesia, tracheo

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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 (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 respo

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Taylor, Barbara E., Michael B. Harris, J. C. Leiter, and Matthew J. Gdovin. "Ontogeny of central CO2 chemoreception: chemosensitivity in the ventral medulla of developing bullfrogs." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 285, no. 6 (2003): R1461—R1472. http://dx.doi.org/10.1152/ajpregu.00256.2003.

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Sites of central CO2 chemosensitivity were investigated in isolated brain stems from Rana catesbeiana tadpoles and frogs. Respiratory neurograms were made from cranial nerve (CN) 7 and spinal nerve 2. Superfusion of the brain stem with hypercapnic artificial cerebrospinal fluid elicited increased fictive lung ventilation. The effect of focal perfusion of hypercapnic artificial cerebrospinal fluid on discrete areas of the ventral medulla was assessed. Sites of chemosensitivity, which are active continuously throughout development, were identified adjacent to CN 5 and CN 10 on the ventral surfac

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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 (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

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Tregub, Pavel P., Yulia K. Komleva, Vladimir P. Kulikov, et al. "Relationship between Hypoxia and Hypercapnia Tolerance and Life Expectancy." International Journal of Molecular Sciences 25, no. 12 (2024): 6512. http://dx.doi.org/10.3390/ijms25126512.

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The review discusses the potential relationship between hypoxia resistance and longevity, the influence of carbon dioxide on the mechanisms of aging of the mammalian organism, and intermittent hypercapnic–hypoxic effects on the signaling pathways of aging mechanisms. In the article, we focused on the potential mechanisms of the gero-protective efficacy of carbon dioxide when combined with hypoxia. The review summarizes the possible influence of intermittent hypoxia and hypercapnia on aging processes in the nervous system. We considered the perspective variants of the application of hypercapnic

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Tiruvoipati, Ravindranath, Sachin Gupta, David Pilcher, and Michael Bailey. "Management of hypercapnia in critically ill mechanically ventilated patients—A narrative review of literature." Journal of the Intensive Care Society 21, no. 4 (2020): 327–33. http://dx.doi.org/10.1177/1751143720915666.

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The use of lower tidal volume ventilation was shown to improve survival in mechanically ventilated patients with acute lung injury. In some patients this strategy may cause hypercapnic acidosis. A significant body of recent clinical data suggest that hypercapnic acidosis is associated with adverse clinical outcomes including increased hospital mortality. We aimed to review the available treatment options that may be used to manage acute hypercapnic acidosis that may be seen with low tidal volume ventilation. The databases of MEDLINE and EMBASE were searched. Studies including animals or tissue

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Zhang, Fangyi, Shane M. Sprague, Farrokh Farrokhi, Matthew N. Henry, Minnette G. Son, and Dennis G. Vollmer. "Reversal of attenuation of cerebrovascular reactivity to hypercapnia by a nitric oxide donor after controlled cortical impact in a rat model of traumatic brain injury." Journal of Neurosurgery 97, no. 4 (2002): 963–69. http://dx.doi.org/10.3171/jns.2002.97.4.0963.

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Object. Traumatic brain injury (TBI) attenuates the cerebral vasodilation to hypercapnia. Cortical spreading depression (CSD) also transiently reduces hypercapnic vasodilation. The authors sought to determine whether the CSD elicited by a controlled cortical impact (CCI) injury masks the true effect of TBI on hypercapnic vasodilation, and whether a nitric oxide (NO) donor can reverse the attenuation of hypercapnic vasodilation following CCI. Methods. Anesthetized rats underwent moderate CCI. Cerebral blood flow was monitored with laser Doppler flowmetry and the response to hypercapnia was dete

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Uchino, H., O. Lindvall, B. K. Siesjö, and Z. Kokaia. "Hyperglycemia and Hypercapnia Suppress BDNF Gene Expression in Vulnerable Regions after Transient Forebrain Ischemia in the Rat." Journal of Cerebral Blood Flow & Metabolism 17, no. 12 (1997): 1303–8. http://dx.doi.org/10.1097/00004647-199712000-00005.

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Preischemic hyperglycemia or superimposed hypercapnia exaggerates brain damage caused by transient forebrain ischemia. Because high regional levels of brain-derived neurotrophic factor (BDNF) protein correlate with resistance to ischemic damage, we studied the expression of BDNF mRNA using in situ hybridization in rats subjected to 10 minutes of forebrain ischemia under normoglycemic, hyperglycemic, or hypercapnic conditions. Compared with normoglycemic animals, the increase of BDNF mRNA in dentate granule cells was attenuated and that in CA3 pyramidal neurons completely prevented in hyperglyc

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Rathburn, Charles K., Natasha J. Sharp, James C. Ryan, et al. "Transcriptomic responses of juvenile Pacific whiteleg shrimp, Litopenaeus vannamei, to hypoxia and hypercapnic hypoxia." Physiological Genomics 45, no. 17 (2013): 794–807. http://dx.doi.org/10.1152/physiolgenomics.00043.2013.

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Estuarine crustaceans are often exposed to low dissolved O2 (hypoxia) accompanied by elevated CO2 (hypercapnia), which lowers water pH. Acclimatory responses to hypoxia have been widely characterized; responses to hypercapnia in combination with hypoxia (hypercapnic hypoxia) are less well known. Here we used oligonucleotide microarrays to characterize changes in global gene expression in the hepatopancreas of Pacific whiteleg shrimp, Litopenaeus vannamei, exposed to hypoxia or hypercapnic hypoxia for 4 or 24 h, compared with time-matched animals held in air-saturated water (normoxia). Unigenes

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Sautegeau, A., J. P. Clozel, C. Saunier, and D. Hartemann. "In vitro effects of hypoxia and (or) hypercapnic acidosis on the myocardial uptake of digoxin." Canadian Journal of Physiology and Pharmacology 63, no. 4 (1985): 344–46. http://dx.doi.org/10.1139/y85-062.

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A recent study has shown in the conscious dog that hypoxia associated with respiratory acidosis could increase the in vivo distribution of digoxin in the myocardium. The aim of the present study was to evaluate in vitro the effects of hypoxia and (or) hypercapnic acidosis on the digoxin uptake. For this purpose, rat myocardium was incubated for 180 min with radiolabelled [3H]digoxin. The uptake of digoxin which was expressed in nanograms of digoxin bound per 100 mg of myocardium was decreased by hypoxia and increased by hypercapnic acidosis. The association of hypoxia and hypercapnic acidosis

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Pisani, Lara, Stefano Nava, Emilia Desiderio, Mario Polverino, Tommaso Tonetti, and V. Marco Ranieri. "Extracorporeal CO2 removal (ECCO2R) in patients with stable COPD with chronic hypercapnia: a proof-of-concept study." Thorax 75, no. 10 (2020): 897–900. http://dx.doi.org/10.1136/thoraxjnl-2020-214744.

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AbstractDomiciliary non-invasive ventilation (NIV) effectively reduces arterial carbon dioxide pressure (PaCO2) in patients with stable hypercapnic chronic obstructive pulmonary disease, but a consistent percentage of them may remain hypercapnic. We hypothesised that extracorporeal CO2 removal (ECCO2R) may lower their PaCO2. Ten patients hypercapnic despite ≥6 months of NIV underwent a 24-hour trial of ECCO2R. Six patients completed the ECCO2R-trial with a PaCO2 drop ranging between 23% and 47%. Time to return to baseline after interruption ranged 48–96 hours. In four patients, mechanical even

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Deckers, Pieter T., Alex A. Bhogal, Mathijs BJ Dijsselhof, et al. "Hemodynamic and metabolic changes during hypercapnia with normoxia and hyperoxia using pCASL and TRUST MRI in healthy adults." Journal of Cerebral Blood Flow & Metabolism 42, no. 5 (2021): 861–75. http://dx.doi.org/10.1177/0271678x211064572.

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Blood oxygenation level-dependent (BOLD) or arterial spin labeling (ASL) MRI with hypercapnic stimuli allow for measuring cerebrovascular reactivity (CVR). Hypercapnic stimuli are also employed in calibrated BOLD functional MRI for quantifying neuronally-evoked changes in cerebral oxygen metabolism (CMRO2). It is often assumed that hypercapnic stimuli (with or without hyperoxia) are iso-metabolic; increasing arterial CO2 or O2 does not affect CMRO2. We evaluated the null hypothesis that two common hypercapnic stimuli, ‘CO2 in air’ and carbogen, are iso-metabolic. TRUST and ASL MRI were used to

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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

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Taylor, Barbara E., Michael B. Harris, E. Lee Coates, Matthew J. Gdovin, and J. C. Leiter. "Central CO2 chemoreception in developing bullfrogs: anomalous response to acetazolamide." Journal of Applied Physiology 94, no. 3 (2003): 1204–12. http://dx.doi.org/10.1152/japplphysiol.00558.2002.

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Central CO2 chemoreception and the role of carbonic anhydrase were assessed in brain stems from Rana catesbeiana tadpoles and frogs. Buccal and lung rhythms were recorded from cranial nerve VII and spinal nerve II during normocapnia and hypercapnia before and after treatment with 25 μM acetazolamide. The lung response to acetazolamide mimicked the hypercapnic response in early-stage and midstage metamorphic tadpoles and frogs. In late-stage tadpoles, acetazolamide actually inhibited hypercapnic responses. Acetazolamide and hypercapnia decreased the buccal frequency but had no effect on the buc

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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 (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 performanc

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White, D. P., K. Gleeson, C. K. Pickett, A. M. Rannels, A. Cymerman, and J. V. Weil. "Altitude acclimatization: influence on periodic breathing and chemoresponsiveness during sleep." Journal of Applied Physiology 63, no. 1 (1987): 401–12. http://dx.doi.org/10.1152/jappl.1987.63.1.401.

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Although the influence of altitude acclimatization on respiration has been carefully studied, the associated changes in hypoxic and hypercapnic ventilatory responses are the subject of controversy with neither response being previously evaluated during sleep at altitude. Therefore, six healthy males were studied at sea level and on nights 1, 4, and 7 after arrival at altitude (14,110 ft). During wakefulness, ventilation and the ventilatory responses to hypoxia and hypercapnia were determined on each occasion. During both non-rapid-eye-movement and rapid-eye-movement sleep, ventilation, ventila

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Jagolino, Amanda L., and William M. Armstead. "PTK, MAPK, and NOC/oFQ impair hypercapnic cerebrovasodilation after hypoxia/ischemia." American Journal of Physiology-Heart and Circulatory Physiology 284, no. 1 (2003): H101—H107. http://dx.doi.org/10.1152/ajpheart.00457.2002.

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This study characterized the contributions of protein tyrosine kinase (PTK) and mitogen-activated protein kinase (MAPK) in nociceptin/orphanin FQ (NOC/oFQ)-induced impairment of hypercapnic pial artery dilation (PAD) after hypoxia/ischemia (H/I) in piglets equipped with a closed cranial window. NOC/oFQ (10−10 M cerebrospinal fluid H/I concentration) impaired hypercapnic PAD (21 ± 2% vs. 13 ± 1%). Coadministration of either of the PTK inhibitors genistein or tyrphostin A23 or the MAPK inhibitors U-0126 or PD-98059 with NOC/oFQ (10−10 M) partially prevented the inhibition of hypercapnic PAD comp

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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 t

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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 (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% C

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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 (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 pa

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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 (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

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Yamaguchi, K., T. Takasugi, H. Fujita, et al. "Endothelial modulation of pH-dependent pressor response in isolated perfused rabbit lungs." American Journal of Physiology-Heart and Circulatory Physiology 270, no. 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 o

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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 (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

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Duelli, Roman, and Wolfgang Kuschinsky. "Changes in Brain Capillary Diameter during Hypocapnia and Hypercapnia." Journal of Cerebral Blood Flow & Metabolism 13, no. 6 (1993): 1025–28. http://dx.doi.org/10.1038/jcbfm.1993.129.

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Since changes in the surface area of capillaries may be relevant to capillary exchange, the distensibility of brain capillaries was investigated. Brain capillary diameters were measured after perfusion fixation of brain tissue at a constant perfusion pressure during hypo- or hypercapnia. Sections were embedded, stained, and analyzed by light microscopy. The results showed significant differences in mean capillary diameter between the hypocapnic and the hypercapnic group. In the eight brain structures analyzed, capillary diameters were always larger in the hypercapnic group. Mean capillary diam

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Barclay, J. K. "Carbonic anhydrase III inhibition in normocapnic and hypercapnic contracting mouse soleus." Canadian Journal of Physiology and Pharmacology 65, no. 1 (1987): 100–104. http://dx.doi.org/10.1139/y87-020.

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The physiological role of carbonic anhydrase III in slow-twitch skeletal muscle was investigated using isolated mouse soleus (N = 30) contracting once every 1.7 min for 75 min in Krebs–Henseleit solution gassed with either 95% oxygen – 5% carbon dioxide (normocapnia) or 90% oxygen – 10% carbon dioxide (hypercapnia). Each contraction was 500 ms in duration at 50 Hz. When muscles contracted in normocapnic solution (pH 7.42), the developed tension decreased an average of 6.1 ± 0.8% over 25 min. For the next 50 min, 15 muscles remained normocapnic, while the remainder contracted in hypercapnic sol

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Gaddis, M. L., C. L. MacAnespie, and C. F. Rothe. "Vascular capacitance responses to hypercapnia of the vascularly isolated head." American Journal of Physiology-Heart and Circulatory Physiology 251, no. 1 (1986): H164—H170. http://dx.doi.org/10.1152/ajpheart.1986.251.1.h164.

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Hypercapnic stimulation of the brain may account for some of the decrease in vascular capacitance (venoconstriction) seen with whole-body hypercapnia. Six mongrel dogs were anesthetized with alpha-chloralose and paralyzed with pancuronium bromide. The vagi were cut and the carotid bodies and sinuses were denervated. The head circulation was isolated and perfused with normoxic [arterial partial pressure of O2 (Pao2) = 112 mmHg], normocapnic (PaCO2 = 40 mmHg) blood, or one of three levels of normoxic, hypercapnic (PaCO2 = 56, 68, or 84 mmHg) blood. A membrane oxygenator was used to change gas te

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Harkema, S. J., and R. A. Meyer. "Effect of acidosis on control of respiration in skeletal muscle." American Journal of Physiology-Cell Physiology 272, no. 2 (1997): C491—C500. http://dx.doi.org/10.1152/ajpcell.1997.272.2.c491.

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The relationships between oxygen consumption (Q(O2)) and calculated cytoplasmic ADP concentration ([ADP]) and the free energy of ATP hydrolysis (deltaG(ATP)) were examined in ex vivo arterially perfused cat soleus muscles during repetitive twitch stimulation under normocapnic (5% CO2) and hypercapnic (70% CO2) conditions. Hypercapnia decreased extra- and intracellular pH by over 0.5 but had no significant effect on Q(O2) or phosphocreatine (PCr)/ATP in muscles at rest. The maximum Q(O2) measured during stimulation and the rate constant for PCr recovery after stimulation both decreased during h

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Peng, Hong-Li, Peter E. Jensen, Holger Nilsson, and Christian Aalkjær. "Effect of acidosis on tension and [Ca2+]iin rat cerebral arteries: is there a role for membrane potential?" American Journal of Physiology-Heart and Circulatory Physiology 274, no. 2 (1998): H655—H662. http://dx.doi.org/10.1152/ajpheart.1998.274.2.h655.

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The cellular mechanism responsible for the reduction of tension in cerebral small arteries to acidosis is not known. In this study the role of smooth muscle intracellular Ca2+ concentration ([Ca2+]i) and membrane potential for the relaxation to acidosis was investigated in isolated rat cerebral small arteries. Isometric force was measured simultaneously with [Ca2+]i(fura 2) or with membrane potential (intracellular microelectrodes), and acidosis was induced by increasing[Formula: see text] or reducing[Formula: see text] of the bathing solution. Both hypercapnic and normocapnic acidosis were as

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Nishio, Kazumi, Yukio Suzuki, Kei Takeshita, et al. "Effects of hypercapnia and hypocapnia on [Ca2+]i mobilization in human pulmonary artery endothelial cells." Journal of Applied Physiology 90, no. 6 (2001): 2094–100. http://dx.doi.org/10.1152/jappl.2001.90.6.2094.

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The hydrogen ion is an important factor in the alteration of vascular tone in pulmonary circulation. Endothelial cells modulate vascular tone by producing vasoactive substances such as prostacyclin (PGI2) through a process depending on intracellular Ca2+ concentration ([Ca2+]i). We studied the influence of CO2-related pH changes on [Ca2+]iand PGI2 production in human pulmonary artery endothelial cells (HPAECs). Hypercapnic acidosis appreciably increased [Ca2+]i from 112 ± 24 to 157 ± 38 nmol/l. Intracellular acidification at a normal extracellular pH increased [Ca2+]i comparable to that observ

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Cohen, Yoram, Lee-Hong Chang, Lawrence Litt, et al. "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 (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 increase

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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 (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 bur

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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 (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 hyperca

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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 (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 hyper

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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 (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 chem

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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 (1993): 296–302. http://dx.doi.org/10.1111/j.1399-6576.1993.tb03718.x.

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WETTERBERG, T., T. SJÖBERG, and S. STEEN. "Effects of buffering in hypercapnia and hypercapnic hypoxemia." Acta Anaesthesiologica Scandinavica 37, no. 4 (1993): 343–49. http://dx.doi.org/10.1111/j.1399-6576.1993.tb03726.x.

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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 (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 nitr

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Montandon, Gaspard, Richard Kinkead, and Aida Bairam. "Disruption of adenosinergic modulation of ventilation at rest and during hypercapnia by neonatal caffeine in young rats: role of adenosine A1 and A2A receptors." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 292, no. 4 (2007): R1621—R1631. http://dx.doi.org/10.1152/ajpregu.00514.2006.

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Caffeine is commonly used to treat respiratory instabilities related to prematurity. However, the role of adenosinergic modulation and the potential long-term effects of neonatal caffeine treatment (NCT) on respiratory control are poorly understood. To address these shortcomings, we tested the following hypotheses: 1) adenosine A1- and A2A-receptor antagonists modulate respiratory activity at rest and during hypercapnia; 2) NCT has long-term consequences on adenosinergic modulation of respiratory control. Rat pups received by gavage either caffeine (15 mg/kg) or water (control) once a day from

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Mukatova, I. Yu, A. S. Serikova, G. S. Nuralieva, and S. N. Avdeev. "The effectiveness of long-term respiratory support in a patient after pneumonectomy." Meditsinskiy sovet = Medical Council, no. 9 (June 6, 2024): 87–91. http://dx.doi.org/10.21518/ms2024-185.

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Respiratory support for chronic respiratory failure in the last stages is widely used, most often in patients with end-stage COPD. It has been proven that the development of chronic hypercapnic respiratory failure is associated with an increasing in exacerbations, increased hospitalization rates, and an acceleration of the time before subsequent decompensation. Also hypercapnia isa determining factor in mortality. Effective treatment method of hypercapnic insufficiency is non-invasive ventilation. Long-term non-invasive ventilation improves daytime hypercapnia, quality of life, increases the p

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Narayanan, Nithya, Charles W. Leffler, and Michael L. Daley. "Influence of hypercapnic vasodilation on cerebrovascular autoregulation and pial arteriolar bed resistance in piglets." Journal of Applied Physiology 105, no. 1 (2008): 152–57. http://dx.doi.org/10.1152/japplphysiol.00988.2007.

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Changes in both pial arteriolar resistance (PAR) and simulated arterial-arteriolar bed resistance (SimR) of a physiologically based biomechanical model of cerebrovascular pressure transmission, the dynamic relationship between arterial blood pressure and intracranial pressure, are used to test the hypothesis that hypercapnia disrupts autoregulatory reactivity. To evaluate pressure reactivity, vasopressin-induced acute hypertension was administered to normocapnic and hypercapnic ( N = 12) piglets equipped with closed cranial windows. Pial arteriolar diameters were used to compute arteriolar res

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Gill, Matthew, Michael J. Natoli, Charles Vacchiano, et al. "Effects of elevated oxygen and carbon dioxide partial pressures on respiratory function and cognitive performance." Journal of Applied Physiology 117, no. 4 (2014): 406–12. http://dx.doi.org/10.1152/japplphysiol.00995.2013.

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Hyperoxia during diving has been suggested to exacerbate hypercapnic narcosis and promote unconsciousness. We tested this hypothesis in male volunteers (12 at rest, 10 at 75 W cycle ergometer exercise) breathing each of four gases in a hyperbaric chamber. Inspired Po2 (PiO2) was 0.21 and 1.3 atmospheres (atm) without or with an individual subject's maximum tolerable inspired CO2 (PiO2 = 0.055–0.085 atm). Measurements included end-tidal CO2 partial pressure (PetCO2), rating of perceived discomfort (RPD), expired minute ventilation (V̇e), and cognitive function assessed by auditory n-back test.

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