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

DBcAMP or crystalline glucagon was utilized to elevate the intracellular cyclic AMP concentration in isolated rat hearts. Butyric acid, a metabolite of DBcAMP, was also investigated. Their effect on the intracellular pH (pHi) as determined by the distribution of [14C]DMO was investigated. Rat hearts, perfused with a recirculated modified Krebs-Henseleit solution maintained at 30 degrees C, were exposed to respiratory acidosis by bubbling the perfusate with 20% CO2. alpha- and beta-receptor antagonists were used to block the effects of endogenous catecholamines. Hypercapnia decreased the pHi from 7.09 to 6.82. A similar degree of hypercapnia decreased the pHi to only 6.95 in the presence of DBcAMP and to only 6.96 in the presence of glucagon. The effective buffer values (delta[HCO-3]i/deltapHi) were: control, 19; butyric acid, 16; DBcAMP, 139; glucagon, 148. These data suggest that cAMP mediates the effect of norepinephrine, which has been shown to diminish the change in pHi accompanying respiratory acidosis.
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PMID:The effect of dibutyryl cyclic AMP and glucagon on the myocardial cell pH1. 2 69

Using a 14C-labeled DMO, 36Cl and 3H method, we have determined the in vivo buffering capacity of lung, kidney, heart, skeletal muscle, and extracellular fluid (ECF) of guinea pigs during hypercapnia (FICO2 = 0.15). After 1 days' exposureto 15% CO2, both the relative CO2 buffer values (delta HCO3/deltapH) and the "%pH regulation" were lung greater than kidney greater than heart greater than ECF greater than skeletal muscle. For lung tissue the intracellular pH was significantly decreased only during acute (8 h) hypercapnia and had completely returned to control values after 7 days with arterial PCO2 congruent to 122 Torr. Kidney and cardiac muscle also showed ca. 100% regulation of pH at 7 days, whereas skeletal muscle and ECF showed only 80 and 70% pH regulation, respectively. The results are discussed with respect to the important (and pH-dependent) metabolic functions of the lung and kidney.
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PMID:Regulation of intracellular pH in lungs and other tissues during hypercapnia. 2 85

During various time periods lasting 3--28 days rats were continuously exposed to FICO2 = 0.08 or 0.16 in normoxic conditions, pHi was measured by the 3H-inulin and 14C-DMO method in the erythrocyte, the gastrocnemius and in the whole body. The erythrocyte acid base disturbances were linked to the extracellular acidosis. The muscle and the mean body pHi developments were the same during 9 or 14 days depending on the FICO2. They diverged after 28 days at FICO2 = 0.08 (Tables and Fig. 2). This could be explained as an acid base reaction of the "non-muscular" part of the whole body intracellular compartment which may be different from the acid base development of the muscular mass. A short term (1 h) acute hypercapnia (FICO2 - 0.20--0.22) was superimposed on the sustained hypercapnia (FICO2 = 0.16). Acid base disturbance was greater when the acute hypercapnia was added at the beginning (3rd day) of the CO2 exposure (Fig.1).
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PMID:Intracellular pH changes during experimental sustained hypercapnia. 3 89

Exposure of rainbow trout to environmental hyperoxia (PIO2 approximately 530 Torr) resulted in an extracellular respiratory acidosis which was fully compensated by 72 h; return to normoxia (PIO2 approximately 145 Torr) at this time induced a metabolic alkalosis which was corrected by 24 h. Intracellular pHi ([14C]DMO method), fluid volumes [3H]PEG-4000 method), and electrolytes were monitored. Environmental hypercapnia (PICO2 approximately 6.5 Torr) was employed to confirm that intracellular responses were specific to respiratory acidosis. Gill pHi did not change during respiratory acidosis despite a very low non-HCO3- buffer capacity, but gill ICFV decreased markedly. A large loss of gill intracellular [Cl-]i in excess of [Na+]i, combined with a substantial gain in [K+]i, contributed to gill pHi regulation by raising branchial [SID]i. In weakly buffered brain tissue, active adjustment of pHi started within 3 h, but two well buffered tissues, RBC and white muscle, exhibited compounding metabolic acidoses during the first 12-24 h. The muscle response was associated with small increases in ICFV and [Cl-]i, and a large decrease in [K+]i which reduced muscle [SID]i. We hypothesize that this initial export of K+ and basic equivalents served to regulate pH in more critical compartments (e.g. gills, brain) at the expense of muscle acidosis. By 48 h, pHi restoration in all tissues was complete, in advance of pHe regulation (72 h). Return to normoxia at 72 h elevated muscle, brain, and gill pHi, but there was no evidence of a comparable 'altruistic' role of muscle during this metabolic alkalosis. Regulation of pHi was complete by 24 h recovery, accompanied by partial or complete restoration of intracellular ions and fluid volumes.
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PMID:Intracellular acid-base responses to environmental hyperoxia and normoxic recovery in rainbow trout. 175 56

This study examined the possible role(s) of central acid-base stimuli in the increase in ventilation induced by hypercapnia in the skate, a response that is not due to an O2 signal (Graham et al., Respir. Physiol., 1990, 80: 251-270). Skate were sampled for cerebrospinal fluid (CSF) acid-base status, intracellular pH of the brain (14C-DMO method), and pHi in other tissues throughout 24 h of exposure to PICO2 = 7.5 Torr. CSF PCO2 rapidly equilibrated with the elevated PaCO2. Despite the much lower non-HCO3- buffer capacity in the CSF, CSF pH was not depressed to the same extent as blood pHa. CSF pH was also regulated rapidly, returning to control levels by 8-10 h, whereas pHa remained significantly depressed at 24 h. Similarly, the pHis of the weakly buffered brain and heart ventricle were initially compensated more rapidly than those of more strongly buffered white muscle and red blood cells. However, brain pHi adjustment slowed markedly after 4 h and stabilized at only 70% compensation by 20-24 h, suggesting that brain intracellular acidosis may play a role in the long-term increase in ventilation. CSF and brain were the only compartments which did not exhibit an apparent compounding metabolic acidosis during the initial stages of hypercapnic exposure. While these results illustrate the primacy of central acid-base regulation, they do not support a role for CSF pH in the long-term elevation of ventilation in response to hypercapnia. Depressions in pHa and brain pHi appear the two most likely candidates for proximate stimuli.
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PMID:Control of ventilation in the hypercapnic skate Raja ocellata: II. Cerebrospinal fluid and intracellular pH in the brain and other tissues. 212 Jul 54

The effects of hypercapnia (1% CO2), and the independent effects of changes in extracellular pH (pHe), PCO2 and [HCO3-] on intracellular pH (measured by the DMO method) and lactate metabolism (measured by utilization of 14C-labelled lactate), were examined in rainbow trout hepatocytes in vitro. Simulated uncompensated hypercapnia (high PCO2, low pHe, moderately increased [HCO3-] led to a substantial depression in the production of CO2 (44%) and glucose (51%) from lactate. In simulated compensated hypercapnia (high PCO2, normal pHe, high [HCO3-], metabolism was still significantly inhibited (18-33%). Subsequent multifactorial design experiments determined that variations in PCO2, pH and [HCO3-] independently affected metabolism; increased PCO2 and decreased pH inhibited metabolism, but increased [HCO3-] stimulated metabolism. These results are interpreted in terms of the effects of acid-base variables on enzymatic and transport pathways, and the possible causes of decreased hepatic glycogen stores during in vivo hypercapnia are discussed.
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PMID:Effects of acid-base variables on in vitro hepatic metabolism in rainbow trout. 313 77

Intracellular pH was determined (DMO method) in European hamsters, in the spontaneously-occurring respiratory acidosis of hibernation, in hypercapnia due to breathing 12% CO2 in air in euthermy in spring, and in euthermicnormocapnic controls. From euthermy to hibernation, the temperature coefficient of pH was lowest in blood plasma and brain, intermediate in striated muscles (thigh muscles and diaphragm), and highest in heart and liver (Fig. 1). Correspondingly, the estimated dissociation ratio of the protein imidazole buffer groups, alpha Im, decreased markedly in plasma and brain, denoting an acid titration, but varied little in liver and heart. Striated muscles were intermediate (Fig. 2). Like in other mammals, intracellular responses to short-term euthermic respiratory acidosis were characterized by a partial metabolic compensation in the brain and a small metabolic acidification in striated muscles. In hibernation, a powerful metabolic compensation took place in liver and heart, nearly restoring alpha Im, but none occurred in brain (Figs. 3 to 5). The existence of an intracellular acidosis in brain and striated muscles during hibernation is in keeping with an inhibitory role of acidosis, whereas the homeostasis of intracellular alpha Im in liver and heart would subserve the eurythermal functioning of metabolic regulations in these organs, like in most organs of ectotherms.
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PMID:Intracellular pH in hibernation and respiratory acidosis in the European hamster. 383 35

The influence of hypercapnic acidosis upon the heart was examined in four vertebrate species. The CO2 in the tissue bath was increased from 2.7 to 15% at 12 degrees C for flounder (Platichthys flesus) and cod (Gadus morhua) and from 3 to 13% at 22 degrees C for turtle (Pseudemys scripta) and rainbow trout (Salmo gairdneri). During hypercapnia, as previously described, there was a decline and recovery of contractility in heart strips of flounder and turtle, and a sustained decrease in cod and rainbow trout. At high CO2 the increase in contractile force following increases in the extracellular Ca-concentration were smaller for the cod myocardium than for the other myocardia. The intracellular pH (pHi), measured with the DMO method, in heart strips of turtle and trout was significantly lower at high than at low CO2. This acidifying effect expressed as the increase in the intracellular concentration of hydrogen ions was larger in the turtle than in the trout myocardium. Intracellular Ca-activity, measured by efflux of 45Ca from preloaded heart strips, was unaffected by high CO2 in trout, but was raised in the other three species. Thus the ability to counteract the negative inotropic effect of hypercapnia is apparently not due to cellular buffering or extrusion of hydrogen ions. More probably it involves (a) a release of intracellular Ca; (b) a positive inotropic effect of an increase in intracellular Ca-activity.
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PMID:pHi, contractility and Ca-balance under hypercapnic acidosis in the myocardium of different vertebrate species. 680 89

We used the transmembrane distribution of 5,5-[2-14C]dimethyloxazolidine-2,4-dione ([14C]DMO) and 31P magnetic resonance spectroscopy (NMR) to investigate the effects of hypercapnia on intracellular pH (pHi) in brain and skeletal muscle of two lizard species: Anolis equestris and Dipsosaurus dorsalis. In control animals (normocapnic), plasma PCO2 (3.3 +/- 0.1 kPa) and plasma pH (7.52 +/- 0.01) for D. dorsalis were not significantly different from the values for A. equestris (2.8 +/- 0.2 kPa and 7.59 +/- 0.02, respectively). Furthermore 60 min of 5% CO2 increased plasma PCO2 and decreased plasma pH by the same amounts in both species. Brain pHi values determined with the DMO method were not significantly different from values determined with NMR. Control values of brain pHi (DMO, 7.16 +/- 0.01; NMR, 7.11 +/- 0.02) and muscle pHi were significantly higher for D. dorsalis (DMO, 7.15 +/- 0.03) than for A. equestris (DMO, 6.99 +/- 0.03; NMR, 7.02 +/- 0.02 for brain; DMO, 6.97 +/- 0.03 for muscle). In addition, changes in tissue pHi after 60 min of 5% CO2 were significantly different for the two species. In D. dorsalis muscle and brain pHi decreased significantly after hypercapnia, whereas in A. equestris muscle pHi decreased significantly but brain pHi was unchanged. Our findings were independent of the methods used to determine pHi. The smaller change in brain and muscle pHi than in plasma pH for A. equestris is consistent with the view that pHi regulation involves active processes such as transmembrane ion transport.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intracellular pH in lizards after hypercapnia. 773 98