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

This study was designed to establish the relationship between urinary pCO2 and systemic blood pCO2 during acute hypercapnia and to investigate the significance of this relationship to collecting duct hydrogen ion (H+) secretion when the urine is acid and when it is highly alkaline. In rats excreting a highly alkaline urine, an acute increase in blood pCO2 (from 42 +/- 0.8 to 87 +/- 0.8 mmHg) resulted in a significant fall in urine minus blood (U-B) pCO2 (from 31 +/- 2.0 to 16 +/- 4.2 mmHg, P less than 0.005), a finding which could be interpreted to indicate inhibition of collecting duct H+ secretion by hypercapnia. The urinary pCO2 of rats with hypercapnia, unlike that of normocapnic controls, was significantly lower than that of blood when the urine was acid (58 +/- 6.3 and 86 +/- 1.7 mmHg, P less than 0.001) and when it was alkalinized in the face of accelerated carbonic acid dehydration by infusion of carbonic anhydrase (78 +/- 2.7 and 87 +/- 1.8 mmHg, P less than 0.02). The finding of a urinary pCO2 lower than systemic blood pCO2 during hypercapnia suggested that the urine pCO2 prevailing before bicarbonate loading should be known and the blood pCO2 kept constant to evaluate collecting duct H+ secretion using the urinary pCO2 technique. In experiments performed under these conditions, sodium bicarbonate infusion resulted in an increment in urinary pCO2 (i.e., a delta pCO2) which was comparable in hypercapnic and normocapnic rats (40 +/- 7.2 and 42 +/- 4.6 mmHg, respectively) that were alkalemic (blood pH 7.53 +/- 0.02 and 7.69 +/- 0.01, respectively). The U-B pCO2, however, was again lower in hypercapnic than in normocapnic rats (15 +/- 4.0 and 39 +/- 2.5 mmHg, respectively, P less than 0.001). In hypercapnic rats in which blood pH during bicarbonate infusion was not allowed to become alkalemic (7.38 +/- 0.01), the delta pCO2 was higher than that of normocapnic rats which were alkalemic (70 +/- 5.6 and 42 +/- 4.6 mmHg, respectively, P less than 0.005) while the U-B pCO2 was about the same (39 +/- 3.7 and 39 +/- 2.5 mmHg). We further examined urine pCO2 generation by measuring the difference between the urine pCO2 of a highly alkaline urine not containing carbonic anhydrase and that of an equally alkaline urine containing this enzyme. Carbonic anhydrase infusion to hypercapnic rats that were not alkalemic resulted in a fall in urine pCO(2) (from 122+/-5.7 to 77+/-2.2 mmHg) which was greater (P <0.02) than that seen in alkalemic normocapnic controls (from 73+/- 1.9 to 43+/-1.3 mmHg) with a comparable urine bicarbonate concentration and urine nonbicarbonate buffer capacity. CO(2) generation, therefore, from collecting dust H(+) secretion and titration of bicarbonate, was higher in hypercapnic rats that in normocapnic controls. We conclude that in rats with actue hypercapnia, the U-B p(CO(2)) achieved during bicarbonate loading greatly underestimates collecting duct H(+) secretion because it is artificially influenced by systemic blood pCO(2). the deltapCO(2) is a better qualitative index of collecting duct H+ secretion that the U-B pCO(2), because it is not artificially influenced by systemic blood pCO(2) and it takes into account the urine PCO(2) prevailing before bicarbonate loading.
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PMID:Relationship of urinary and blood carbon dioxide tension during hypercapnia in the rat. Its significance in the evaluation of collecting duct hydrogen ion secretion. 298 5

To study both temporal and quantitative effects of hypercapnia on the extent of pH compensation in the arterial blood, specimens of carp (Cyprinus carpio) were exposed to a PCO2 of about 7.5 mmHg (1 mmHg = 133.3 Pa) (1% CO2) in the environmental water for several weeks, and a second group of animals was subjected to an environmental PCO2 of about 37 mmHg (5% CO2) for up to 96 h. A third series of experiments was designed to test the possibility that infusion of bicarbonate would increase the extent of plasma pH compensation. Dorsal aortic plasma pH, PCO2 and [HCO3-], as well as net transfer of HCO3- -equivalent ions, NH4+, Cl- and Na+, between fish and ambient water, were monitored throughout the experiments. Exposure to environmental PCO2 of 7.5 mmHg resulted in the expected respiratory acidosis with the associated drop in plasma pH, and subsequent compensatory plasma [HCO3-] increase. The compensatory increase of plasma bicarbonate during long-term hypercapnia continued during 19 days of exposure with plasma bicarbonate finally elevated from 13.0 mmoll-1 during control conditions to 25.9 mmoll-1 in hypercapnia, an increase equivalent to 80% plasma pH compensation. Exposure to 5% hypercapnia elicited much larger acid-base effects, which were compensated to a much lesser extent. Plasma pH recovered to only about 45% of the pH depression expected at constant bicarbonate concentration. At the end of the 96-h exposure period, plasma [HCO3-] was elevated by a factor of 2.5 to about 28.2 mmoll-1. The observed increase in plasma bicarbonate concentration during 5% hypercapnic exposure was attributable to net gain of bicarbonate equivalent ions from (or release of H+-equivalent ions to) the environmental water. Quantitatively, the gain of 15.6 mmol kg-1 was considerably larger than the amount required for compensation of the extracellular space, suggesting that acid-base relevant ions were transferred for compensation of the intracellular body compartments. The uptake of bicarbonate-equivalent ions from the water was accompanied by a net release of Cl-and, to a smaller extent, by a net uptake of Na+, suggesting a 75% contribution of the Cl-/HCO-3 exchange mechanism. Infusion of bicarbonate after 48 h of exposure to 7.5 mmHg PCo2 had only a transient effect on further pH compensation. The infused bicarbonate was lost to the ambient water, and pre-infusion levels of bicarbonate were reattained within 24 h. Repetition of the infusion did not result in a notable improvement of the acid-base status.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acid-base regulation and ion transfers in the carp (Cyprinus carpio): pH compensation during graded long- and short-term environmental hypercapnia, and the effect of bicarbonate infusion. 302 33

The effects of body temperature and hypercapnia (7% inspired CO2) on arterial blood gases, plasma pH, and the characteristics of the blood oxygen dissociation curve were determined in Tegu lizards (Tupinambis nigropunctatus). Arterial pH fell from 7.59 to 7.50 when body temperature was increased from 25 to 35 degrees C. The pH/temperature coefficient (delta pH/delta t = -0.009 U/degrees C) was half of that predicted on the basis of 'constant relative alkalinity' and the alphastat hypothesis. The fall in plasma pH resulted from a decrease in plasma [HCO3-], and a rise in plasma Pco2. The O2 affinity of Tegu blood, expressed by the partial pressure at half saturation (P50), decreased with temperature in vitro from 42.3 to 49.6 torr at pH 7.4. The apparent enthalpy (delta H = -3.1 kcal/mol) is about 1/4 of that of human blood. In vivo, the arterial blood oxygen saturation decreased from 89% at 25 degrees to 82% at 35 degrees C. Arterial Po2 increased from 61 to 71 torr as expected from the right-shift of the oxygen dissociation curve. During environmental hypercapnia (7% CO2, 21% O2, 72% N2 inspired concentrations), arterial pH decreased to 7.28. Arterial O2 saturation remained constant and arterial Po2 increased from 61 to 85 torr due to the right-shift of the oxygen dissociation curve. The comparatively small effect of changes in temperature on the oxygen affinity of Tegu blood (directly according to the delta H value, and indirectly via changes in blood pH) results in a relatively small right shift of the oxygen dissociation curve, and accordingly in relatively high arterial and tissue Po2 values also at higher temperatures.
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PMID:Respiratory properties of blood and arterial blood gases in the tegu lizard: effects of temperature and hypercapnia. 311 84

The present study was undertaken to examine the effects of changes in PaCO2 and pHa on myocardial blood flow and central hemodynamics during acute ischemic left ventricular failure. Six closed-chest dogs anesthetized with pentobarbital were hyperventilated, and CO2 was added to the inspiratory gas to induce: a) normocapnia, b) hypocapnia, c) hypercapnia, and d) hypercapnia with sodium carbonate given to correct pH. Embolization of the left coronary artery with 50-microns microspheres resulted in deterioration of left ventricular function, as indicated by increased left ventricular end-diastolic pressure and mean pulmonary arterial pressure, while cardiac output decreased. During hypocapnia with left ventricular failure, the central hemodynamics remained unchanged, while a minor but nonsignificant decrease in myocardial blood flow was observed. Hypercapnia aggravated the heart failure, as indicated by increased left ventricular end-diastolic pressure, mean right atrial pressure, and mean pulmonary arterial pressure; however, the pump function of the heart was unchanged, as demonstrated by the unaltered cardiac output, heart rate, and mean aortic blood pressure. The changes in the central hemodynamics were reversed when pH was normalized during hypercapnia. Thus, in the present study pH, and not PaCO2, was responsible for the hemodynamic deterioration observed during hypercapnia in the failing heart.
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PMID:Effects of carbon dioxide and pH on myocardial function in dogs with acute left ventricular failure. 311 92

An inhibitor of the HCO3-/Cl- exchange carrier protein, 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) or vehicle was infused in mock cerebrospinal fluid (CSF) via the cisterna magna in conscious rabbits at 10 mumol/l for 40 min at 10 microliter/min. Neither treatment had any effect over 2-5 h on the non-CO2-stimulated CSF ion values or blood gases. With CO2 stimulation such that arterial PCO2 (PaCO2) was increased 25 Torr over 3 h, DIDS treatment significantly decreased the stoichiometrically opposite changes in CSF [HCO3-] and [Cl-] that normally accompany hypercapnia and reflect ionic mechanisms of CSF pH regulation. Expressed as delta CSF [HCO3-]/delta PaCO2, DIDS treatment decreased the CSF ionic response by 35%. In a separate paired study design DIDS administration via the same protocol had no effect on resting ventilation but significantly increased the ventilation and tidal volume responses to a 28-Torr increase in PaCO2. Expressed as change in minute ventilation divided by delta PaCO2, DIDS treatment produced a 39.6% increase. The results support the concept of a DIDS-inhibitable anion exchange carrier being involved in CSF pH regulation in hypercapnia and suggest a DIDS-related effect on the ventilatory response to CO2.
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PMID:DIDS decreases CSF HCO3- and increases breathing in response to CO2 in awake rabbits. 312 29

Specimens of Bufo marinus were exposed to aerial and aquatic hypercapnia (5% CO2) in a closed, water recirculation system to evaluate mechanisms involved in the compensation of a respiratory acidosis in these animals. Arterial PCO2 was elevated from about 9 mmHg (1 mmHg = 133.3 Pa) to 35 (1 h) and 37 mmHg (2 h), and gradually approached about 40 mmHg (24 h of hypercapnia). The typical hypercapnia-induced reduction in plasma pH from about 7.9 to below 7.4 was partially offset, at least during the first hours of hypercapnia, by a reduction in the inspired/arterial PCO2 difference, presumably brought about by pulmonary hyperventilation. The predominant contributor to extracellular pH compensation, however, was a net gain of bicarbonate from the environment, mainly facilitated by ammonia excretion. Bicarbonate originating from the environment was accumulated in the body fluids, increasing the plasma concentration from the control of about 9 to 36 mmol l-1 after 24 h. Extracellular pH was compensated to only about 30% of the shift expected at constant bicarbonate level and, according to the steady reduction of pH, non-bicarbonate buffering of CO2 also contributed significantly to the elevation of bicarbonate. This relatively poor pH compensation (compared with fishes) could not be improved either by direct administration of bicarbonate into the bloodstream or by increased environmental ion concentrations. It is concluded that the availability of bicarbonate is not a limiting factor for pH compensation during hypercapnia, and that the inability of Bufo to accumulate bicarbonate to concentrations sufficient for better hypercapnia compensation is based on a constitutional 'bicarbonate threshold' of the resorbing and retaining structures for acid-base-relevant ions.
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PMID:Acid-base regulation and blood gases in the anuran amphibian, Bufo marinus, during environmental hypercapnia. 312 28

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

When exposed to hypercapnia, several muscles deteriorate with respect to their mechanical performance. Exposure to metabolic acidosis and, perhaps surprisingly, to compensated metabolic acidosis has the same effect on the diaphragm. The mechanisms involved in these effects remain unclear. If the diaphragmatic intracellular pH (pHi) is assumed to decrease with hypercapnia, to remain unchanged during metabolic acidosis, and to increase during compensated metabolic acidosis, it would appear that different mechanisms must be responsible for the depreciation in the diaphragm's mechanical performance. The present experiments using 31P nuclear magnetic resonance (31P-NMR) spectroscopy were undertaken to determine the effect of metabolic acidosis and compensated metabolic acidosis on pHi and on high-energy phosphate metabolites in the resting rat diaphragm. A whole diaphragm was slightly stretched while being stitched onto a fiberglass mesh. The area approximated that at functional residual capacity. It was superfused in the NMR sample tube with a phosphate-free Krebs-Ringer bicarbonate solution [( HCO3-] = 6 meqO equilibrated with either 95% O2-5% CO2 or 98.75% O2-1.25% CO2). Spectra were acquired during 15-min intervals for control (30 min of normal Krebs-Ringer bicarbonate superfusate, equilibrated with 95% O2-5% CO2), for 120 min of exposure to either form of acidosis and for 60 min of recovery with normal superfusate. The pHi decreased rapidly during metabolic acidosis but did not change significantly during compensated metabolic acidosis. In both forms of acidosis, phosphocreatine declined gradually but not significantly, whereas ATP and inorganic phosphate did not change at all. The results suggest that HCO3- passes freely through the diaphragmatic sarcolemma, very much like the cardiac sarcolemma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:NMR study of rat diaphragm exposed to metabolic and compensated metabolic acidosis. 320 72

We evaluated to what extent acidosis and alkalosis and their respiratory and metabolic components during the first 12 hours of life occurred prior to early neonatal death and postnatal intracranial hemorrhage among 206 low birth weight, intubated premature babies participating in a clinical trial of phenobarbital prophylaxis for intracranial hemorrhage. Time-weighted indices included the time each baby spent with abnormal values of pH, PaCO2 and HCO3-. Babies whose birth weight was less than 1 kg suffered adversities associated with prolonged pH less than 7.35. Heavier birth weight babies were at increased risk of adversity if their pH fell below 7.2. Babies who were not severely acidotic initially, but became so within hours, were at prominently increased risk of death and hemorrhage. Babies who had a mild increase of PaCO2 between 45 and 60 mmHg were less likely to develop germinal matrix hemorrhage than their peers who had more severe hypercapnia. A time-weighted measure of metabolic deficit correlated with death, but not with hemorrhage. Prolonged exposure to pH greater than 7.55 was associated with reduced risk of subependymal/intraventricular hemorrhage and death, especially in babies below 1 kg birth weight. We conclude that acidosis is an antecedent of intracranial hemorrhage in low birth weight premature babies, that duration of exposure might convey important risk information, and that birth weight is a correlate of vulnerability to some pH disturbances.
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PMID:Arterial blood gas derangements associated with death and intracranial hemorrhage in premature babies. 323 3

Amiloride (10(-3) M), a Na+-H+ countertransport inhibitor, infused into the cisterna magna (10 microliter/min for 40 min) of ketamine-xylazine-anesthetized rabbits decreased the cerebrospinal fluid (CSF) HCO3- response to 3 h of hypercapnia [arterial PCO2 (PaCO2) = 60 Torr] by 21.6% (mean delta CSF [HCO3-]/delta PaCO2 0.232 vs. 0.296 mmol.l-1.Torr-1, P less than 0.05). Diethyl pyrocarbonate (DEPC, 10(-3) M), a histidine-blocking agent, infused into the cisterna magna decreased the CSF HCO3- response to hypercapnia by 25.3% (mean delta CSF [HCO3-]/delta PaCO2, 0.230 vs. 0.308 mmol.l-1.Torr-1, P less than 0.02). DEPC is known to inhibit the ventilatory response to hypercapnia (E. Nattie. Respir. Physiol. 64: 161-176, 1986) by a direct effect at the ventrolateral medulla (E. Nattie. J. Appl. Physiol. 61: 843-850, 1986). In this study amiloride had no significant effect on the ventilatory response to hypercapnia. The interpretation is that a Na+-H+ countertransport protein, perhaps with a histidine at a key location, is involved in CSF acid-base regulation and that amiloride appears to have no effects on the chemoreception process. DEPC appears to have effects on chemoreception and on CSF acid-base regulation.
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PMID:Effects of amiloride and diethyl pyrocarbonate on CSF HCO-3 and ventilation in hypercapnia. 340 66


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