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Query: UMLS:C0020440 (hypercapnia)
7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Congenital central hypoventilation syndrome (CCHS) is a rare neurocristopathy characterized by absence of adequate autonomic control of respiration with decreased sensitivity to hypoxia and hypercapnia. Frameshift mutations and polyalanine triplet expansions in the coding region of PHOX2B have been identified in the vast majority of CCHS patients and a correlation between length of the expanded region and severity of CCHS has been reported. In this work, we have undertaken in vitro analyses aimed at identifying the pathogenetic mechanisms which underlie the effects of PHOX2B mutations in CCHS. According to the known role of this gene, a transcription factor expressed during autonomic nervous system development, we have tested the transcriptional activity of WT and mutant PHOX2B expression constructs on the regulatory regions of two target genes, DbetaH and PHOX2A. We observed that the two sets of mutations play different roles in the transcriptional regulation of these genes, showing a correlation between the length of polyalanine expansions and the severity of reduced transcriptional activity. In particular, although reduced transactivation due to polyalanine expansions may be caused by retention of the mutated protein in the cytoplasm or in the nuclear aggregates, frameshift mutations did not impair the PHOX2B nuclear income, suggesting a different mechanism through which they would exert the observed effects on target promoters. Moreover, the frameshift due to deletion of a cytosine residue seems to cause sequestration of the corresponding mutant PHOX2B in the nucleolar compartment.
Hum Mol Genet 2005 Jul 01
PMID:Distinct pathogenetic mechanisms for PHOX2B associated polyalanine expansions and frameshift mutations in congenital central hypoventilation syndrome. 1588 79

The effects of body position on ventilatory responses to chemical stimuli have rarely been studied in experimental animals, despite evidence that position may be a factor in respiratory results. The purpose of this study was to test whether body position could affect acute ventilatory responses to 4-min periods of moderate hypercapnia (5% CO(2) in O(2)) and poikilocapnic hypoxia (15% O(2) in N(2)) in the urethane-anaesthetised mouse. Respiratory measurements were conducted with mice in the prone and supine positions with a whole-body, single-chamber plethysmograph. During hypoxia, the time course of minute ventilation (V (E)) was similar in the two positions, but the breathing pattern was different. After the response peak, V (E) depended on respiratory frequency (f) and tidal volume (V(T)) in the prone position but mainly on V(T) in the supine position. In the supine position, f declined below the baseline values toward the end of hypoxic exposure. During hypercapnia, there were no ventilatory differences between the prone and supine positions. Brief hypoxic exposure elicited f depression in the supine position in the anaesthetised mouse. The depressive effect on f suggests that the supine position may not be optimal for sustaining ventilation, particularly during hypoxia.
Comp Biochem Physiol A Mol Integr Physiol 2005 Jun
PMID:Effect of body position on ventilatory responses in anaesthetised mice. 1594 77

Experiments were conducted to test the hypothesis that branchial gas transfer is enhanced in rainbow trout during hypoxia or hypercarbia by bradycardia and systemic vasoconstriction. Gas transfer was indirectly assessed by continuous monitoring of arterial blood gases, PaO2 and PaCO2. Cardiac frequency was maximally decreased by 34.9+/-4.3 and 8.6+/-3.2 bpm in hypoxic and hypercarbic fish, respectively. Pre-treating fish with atropine (1micromol kg(-1)) attenuated or abolished the bradycardia during hypoxia and hypercarbia, respectively. However, there were no significant differences in the arterial blood gases between the control and atropinized fish. Dorsal aortic blood pressure was increased maximally by 11.3+/-2.8 and 17.7+/-2.0mm Hg in the hypoxic and hypercarbic fish. Pre-treatment of fish with prazosin (2.4micromol kg(-1)) prevented these increases in blood pressure. Blood gases were unaltered by prazosin treatment in the hypercarbic fish. However, in the hypoxic fish, gas transfer appeared to be impaired by prazosin on the basis of lowered PaO2 (by approximately 35 mm Hg compared to control fish) and increased PaCO2 (by approximately 0.3mm Hg). Because the normal hyperventilatory response to hypoxia was prevented by prazosin, it is possible that the impairment of gas transfer was related to inadequate ventilation rather than to any differences in the pressor response. The present results provide no evidence that gas transfer in rainbow trout is enhanced by bradycardia nor do they reveal any obvious benefit associated with the increases in blood pressure that accompany hypoxia and hypercarbia.
Comp Biochem Physiol A Mol Integr Physiol 2006 Jun
PMID:Does bradycardia or hypertension enhance gas transfer in rainbow trout (Oncorhynchus mykiss)? 1657 50

In its natural coastal and estuarine environments, the blue crab, Callinectes sapidus, often encounters hypoxia, accompanied by hypercapnia (increased CO2) and an associated decrease in water pH. Previous studies have shown that exposure to hypercapnic hypoxia (HH) impairs the crab's ability to remove culturable bacteria from its hemolymph. In the present study we demonstrate that the activity of phenoloxidase (PO), an enzyme critical to antibacterial immune defense in crustaceans, is decreased at the low levels of hemolymph O2 and pH that occur in the tissues of blue crabs exposed to HH. Hemocyte PO activity was measured at tissue O2 levels that occur in normoxic (5% and 15% O2, approximate venous and arterial hemolymph, respectively) and hypoxic (1% O2) crabs and compared to PO activity in air-saturated conditions (21% O2). PO activity decreased by 33%, 49% and 70% of activity in air at 15%, 5% and 1% O2, respectively. When O2 was held at 21% and pH lowered within physiological limits, PO activity decreased with pH, showing a 16% reduction at pH 7.0 as compared with a normoxic pH of 7.8. These results suggest that decreased PO activity at low tissue O2 and pH compromises the ability of crustaceans in HH to defend themselves against microbial pathogens.
Comp Biochem Physiol A Mol Integr Physiol 2006 Jun
PMID:The effects of hypoxia and pH on phenoloxidase activity in the Atlantic blue crab, Callinectes sapidus. 1661 37

Many teleostean fish, including rainbow trout, regulate red blood cell (RBC) pH (pH(i)) in the presence of a stress-induced acidosis such as hypoxia, hypercapnia, or exhaustive exercise. This is accomplished through activation of RBC Na+/H+ exchange (beta-NHE), ultimately minimizing impairment to oxygen transport. Presence and characterization of the RBC beta-NHE in fish is best tested in blood from cannulated, resting animals; however, several studies have used blood from stressed animals drawn from the caudal vein and stored prior to use. The effects of sampling procedures and storage on the beta-NHE response is not known and is the focus of this study. Whole blood drawn from cannulated, resting rainbow trout was compared with RBCs obtained from the caudal vein rinsed and stored at 4 degrees C for 0, 6, 24, 48, 96 or 144 h. Isoproterenol (10(-5) M), a beta-adrenergic agonist, was added to hypoxia/hypercapnia incubated RBCs in vitro. In all treatments, isoproterenol induced a large beta-NHE response, and storage duration (< or =96 h) had a minimal affect, indicating that rinsing and storing is an easy and viable means by which to obtain RBCs and investigate function. Storage for 144 h still resulted in a significant RBC beta-NHE response; however, viability of RBCs may be compromised.
Comp Biochem Physiol A Mol Integr Physiol 2006 Jun
PMID:Blood sampling techniques and storage duration: effects on the presence and magnitude of the red blood cell beta-adrenergic response in rainbow trout (Oncorhynchus mykiss). 1671 17

Global climate change is associated with a progressive rise in ocean CO(2) concentrations (hypercapnia) and, consequently, a drop in seawater pH. However, a comprehensive picture of the physiological mechanisms affected by chronic CO(2) stress in marine biota is still lacking. Here we present an analysis of protein biosynthesis rates in isolated muscle of the marine invertebrate Sipunculus nudus, a sediment dwelling worm living at various water depths. We followed the incorporation of (13)C-labelled phenylalanine into muscular protein via high-resolution NMR spectroscopy. Protein synthesis decreased by about 60% at a medium pH of 6.70 and a consequently lowered intracellular pH (pHi). The decrease in protein synthesis rates is much stronger than the concomitant suppression of protein degradation (60% versus 10-15%) possibly posing a threat to the cellular homeostasis of structural as well as functional proteins. Considering the progressive rise in ocean CO(2) concentrations, permanent disturbances of cellular protein turnover might seriously affect growth and reproductive performance in many marine organisms with as yet unexplored impacts on species density and composition in marine ecosystems.
Comp Biochem Physiol A Mol Integr Physiol 2006 Aug
PMID:Effects of environmental hypercapnia on animal physiology: a 13C NMR study of protein synthesis rates in the marine invertebrate Sipunculus nudus. 1675 22

Induction of hypercapnia by breathing high concentrations of carbon dioxide (CO(2)) may have beneficial effects on the pulmonary circulation. We tested the hypothesis that exposure to CO(2) would protect against chronic pulmonary hypertension in newborn rats. Atmospheric CO(2) was maintained at <0.5% (normocapnia), 5.5%, or 10% during exposure from birth for 14 days to normoxia (21% O(2)) or moderate hypoxia (13% O(2)). Pulmonary vascular and hemodynamic abnormalities in animals exposed to chronic hypoxia included increased pulmonary arterial resistance, right ventricular hypertrophy and dysfunction, medial thickening of pulmonary resistance arteries, and distal arterial muscularization. Exposure to 10% CO(2) (but not to 5.5% CO(2)) significantly attenuated pulmonary vascular remodeling and increased pulmonary arterial resistance in hypoxia-exposed animals (P < 0.05), whereas both concentrations of CO(2) normalized right ventricular performance. Exposure to 10% CO(2) attenuated increased oxidant stress induced by hypoxia, as quantified by 8-isoprostane content in the lung, and prevented upregulation of endothelin-1, a critical mediator of pulmonary vascular remodeling. We conclude that hypercapnic acidosis has beneficial effects on pulmonary hypertension and vascular remodeling induced by chronic hypoxia, which we speculate derives from antioxidant properties of CO(2) on the lung and consequent modulating effects on the endothelin pathway.
Am J Physiol Lung Cell Mol Physiol 2006 Nov
PMID:Therapeutic hypercapnia prevents chronic hypoxia-induced pulmonary hypertension in the newborn rat. 1682 30

We have previously observed that the guinea-pig appears to have a relatively poor ventilatory (V (E)) response to hypoxia, compared to other mammals. Therefore, in this study, we questioned the ability of the carotid bodies (primary peripheral chemoreceptors) in the guinea-pig to detect hypoxia. The ventilatory responses to poikilocapnic hypoxia (8% O(2)), poikilooxic hypercapnia (8% CO(2)), hyperoxia (100% O(2)) and cyanide (NaCN - 200 mug/kg, i.v.) were assessed before and after carotid body denervation (CBD) in anaesthetized guinea-pigs. Although CBD attenuated the V (E) responses to hypercapnia and cyanide, it had no effect on normoxic breathing or the V (E) responses to hypoxia or hyperoxia. In a separate group of guinea-pigs, nerve activity was recorded from single or few-fibre preparations of the carotid sinus nerve (CSN). Basal chemoreceptor activity could not be detected from any of the nerve preparations. NaCN and hypercapnia consistently provoked an increase in neural activity. In contrast, hypoxia never clearly increased activity in any of the single or few-fibre preparations isolated from the CSN. In conclusion, although the carotid bodies of the guinea-pig, like those of other mammals, are able to detect hypercapnia and histotoxic hypoxia and elicit a reflex increase in V (E), they are essentially hypoxia-insensitive. The latter may explain, at least in part, the relatively poor V (E) response to hypoxia shown by the guinea-pig.
Comp Biochem Physiol A Mol Integr Physiol 2007 Feb
PMID:Are the carotid bodies of the guinea-pig functional? 1710 20

The neurochemical, serotonin (5-hydroxytryptamine; 5-HT) is involved in the regulation of toadfish pulsatile urea excretion as well as the teleost hypoxia response. Thus, the goal of this study was to determine whether environmental conditions that activate branchial chemoreceptors also trigger pulsatile urea excretion in toadfish, since environmental dissolved oxygen levels in a typical toadfish habitat show significant diel fluctuations, often reaching hypoxic conditions at dawn. Toadfish were fitted with arterial, venous and/or buccal catheters and were exposed to various environmental conditions, and/or injected with the O(2) chemoreceptor agonist NaCN or the 5-HT(2) receptor agonist alpha-methyl-5HT. Arterial PO(2), as well as ammonia and urea excretion were monitored. Natural fluctuations in arterial PO(2) levels in toadfish did not correlate with the occurrence of a urea pulse. Chronic exposure (24 h) of toadfish to hyperoxia was without effect on nitrogen excretion, however, exposure to hypoxia caused a significant reduction in the frequency of urea pulses, and exposure to hypercapnia resulted in a reduction in the percentage of nitrogen waste excreted as urea. Of toadfish exposed acutely to hypoxia, 20% pulsed within 1 h, whereas none pulsed after normoxic or hypercapnic treatments. Furthermore, 20% of fish injected intravenously with NaCN pulsed within 1 h of injection, but no fish pulsed after injection of NaCN into the buccal cavity. To test whether environmental conditions affected 5-HT(2) receptors, toadfish were injected with alpha-methyl-5HT, which elicits urea pulses in toadfish. No significant differences in pulse size occurred among the various environmental treatments. Our findings suggest that neither the environmental conditions of hypoxia, hyperoxia or hypercapnia, nor direct branchial chemoreceptor activation by NaCN play a major role in the regulation of pulsatile urea excretion in toadfish.
Comp Biochem Physiol A Mol Integr Physiol 2007 Mar
PMID:Is urea pulsing in toadfish related to environmental O2 or CO2 levels? 1719 58

Motility of salmonid sperm is inhibited by the presence of carbon dioxide (CO2) in vitro; however, whether this occurs in response to challenges to the adult in vivo is not known. To determine whether CO2 negatively impacts sperm function in vivo, mature males were exposed to exhaustive exercise as well as to acute stress, chronic stress, tricaine anesthesia and environmental hypercapnia and sperm motility and semen CO2 tensions and pH values assessed. Semen CO2 rose and pH decreased significantly only in response to exhaustive exercise and environmental hypercapnia (13 kPa CO2). These changes in semen CO2 and pH were associated with reductions in numbers of sperm becoming motile upon water activation. Chronic and acute stress and tricaine anesthesia were without effect on sperm motility or on semen CO2 or pH. The time course of CO2 inhibition and recovery was evaluated in vitro. At least 50 min was required to note 50% of the inhibitory effect of low CO2 tensions on motility when sperm were exposed to 1.6-3.1 kPa CO2. At higher CO2 levels sperm motility displayed 50% of the inhibitory effect of these tensions within about 30 min. Sperm recovered maximal motility within 1 h of being placed in a nominally CO2-free environment. This study demonstrates sperm vulnerability to not only in vitro CO2 exposure but also in vivo exposure during exhaustive exercise and as result of environmental hypercapnia.
Comp Biochem Physiol A Mol Integr Physiol 2007 May
PMID:Exhaustive exercise, animal stress, and environmental hypercapnia on motility of sperm of steelhead trout (Oncorhynchus mykiss). 1730 60


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