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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Disorders of systemic acid-base balance have recently been shown to markedly alter intestinal electrolyte transport. These studies were based on earlier acid balance studies in humans and animals, data suggesting the presence of intestinal mucosal Na+-H+ and Cl-HCO-3 exchange processes and the reported effects of acid-base variables on other epithelia. In vivo studies have shown that intestinal net sodium and chloride absorption is markedly affected by systemic pH and carbon dioxide tension (Pco2). Specifically, systemic acidemia (in the rat ileum) and hypercapnia (in the rat colon) increase sodium and chloride absorption, while alkalemia and hypocapnia decrease absorption. In addition, net bicarbonate secretion (in both segments) varies directly with the plasma HCO3 concentration. The rabbit ileum has been studied both in vivo and in vitro and is affected in a similar way. The rat jejunum and rabbit distal colon and gallbladder do not respond to changes in blood pH and Pco2, consistent with the apparent absence of a mucosal Na+-H+ exchange process in these segments. Evidence suggests important roles for cellular carbonic anhydrase activity and the intracellular concentrations of hydrogen, bicarbonate, and calcium ions and calcium-calmodulin in mediating or modulating the effects of the systemic acid-base disorders. In addition, systemic pH may alter the effects of the neural and humoral mediators of intestinal transport.
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PMID:Systemic acid-base disorders and intestinal electrolyte transport. 633 Nov 93

This study examined urinary acidification shortly after recovery from chronic hypocapnia induced by hypoxemia. Distal acidification was evaluated by measuring the urinary PCO2 and urine-blood PCO2 difference (U-B PCO2) when blood PCO2 had returned to normal. In posthypocapnic rats, maximal alkalinization of the urine by acute sodium bicarbonate loading failed to increase urine PCO2 and U-B PCO2 to the level of posthypoxemic control rats and normal control rats with comparable blood pH and urine bicarbonate concentration. To test the hypothesis that decreased distal hydrogen ion secretion in posthypocapnic rats resulted from intracellular alkalosis secondary to protracted hypocarbia, posthypocapnic rats were exposed to hypercapnia of brief duration (30 min) and prolonged duration (120 min) in an attempt to restore distal acidification to normal. In posthypocapnic rats, hypercapnia of brief duration was associated with a significant increase in urine PCO2 and a fall in urine pH. Prolonged hypercapnia resulted in a marked increase in urine PCO2 and a further fall in urine pH. At any urinary bicarbonate concentration, however, the urine PCO2 and U-B PCO2 posthypocapnic rats exposed to hypercapnia were still significantly lower than in normal control rats identically subjected to prolonged hypercapnia and with comparable blood PCO2 and blood pH. Our findings indicate that distal acidification after abrupt recovery from chronic hypocapnia is decreased as if the kidneys were still under the influence of sustained hypocapnia. These findings could not be ascribed to extracellular alkalemia but could be explained by postulating that decreased urinary acidification resulted from persistence of cell alkalinity secondary to the accumulation of non-CO2 buffers generated during protracted hypocarbia. Alternatively, factors other than cell pH could mediate the adaptive decrease in distal hydrogen ion secretion of posthypocapnic rats.
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PMID:Suppression of distal urinary acidification after recovery from chronic hypocapnia. 641 9

Rats were tested in the forced swim test in 35 or 20 cm of water or in an open field to evaluate the effects of different intensities of stress on blood gases, electrolytes, and metabolic indices, compared to nontested controls. Animals tested in the open field did not differ from controls on any measure. Immersion in deep water resulted in a greater mixed metabolic and respiratory acidemia (low pH, low bicarbonate, high pCO2), higher glucose and higher lactate levels than immersion in shallow water which in turn resulted in greater metabolic acidemia (low pH, low bicarbonate), and higher glucose and lactate levels than occurred in open field or control animals. In contrast to immersion in deep water, immersion in shallow water resulted in an initial hypocapnia followed by a hypercapnia. Immersion in deep water also resulted in higher potassium levels, lower bicarbonate and total carbon dioxide levels, and a higher anion gap than immersion in shallow water, testing in the open field, or in controls. In a second study, lactate infusion resulted in a metabolic alkalemia (increased pH and bicarbonate levels) and an increase in total carbon dioxide levels. These results indicate that test parameters from forced swim testing (e.g., water depth) can significantly affect the rat's physiological response to testing. The effects of forced swim testing are not simply due to general stress; and the physiological changes seen in conjunction with forced swim testing (e.g., acidemia) are not due to lactate alone.
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PMID:A further analysis of physiological changes in rats in the forced swim test. 780 Jul 51

Hypocapnia is known to decrease blood flow and tissue oxygen tension in the brain and the splanchnic organs, but there are few and contradictory results in skeletal muscle. The aim of the present study was to investigate the effect of hypocapnia on microcirculatory blood flow, local skeletal muscle PO2 (PtO2) and pH (pHt). Blood flow was measured using laser-Doppler flowmetry (LDF) and a multichannel antimony microelectrode served for PtO2 and pHt measurements. These parameters were studied in six anesthetized and mechanically ventilated rabbits during normocapnia (arterial PCO2 4.4 kPa), hypocapnia (PCO2 2.3 kPa) and finally a second period of normocapnia (PCO2 4.5 kPa). During normocapnia the relative LDF flux was 100 +/- 53% (mean +/- SD), decreased to 80 +/- 48% (p < 0.01) during hypocapnia and returned to 103 +/- 51% during the second period of normocapnia (N.S.). The PtO2 was 3.2 +/- 1.2 kPa, 2.9 +/- 0.8 kPa (p < 0.05) and 3.2 +/- 1.0 kPa (N.S.), respectively. pHt remained unchanged, although there was a significant arterial alkalosis (pH increased 0.10 units, p < 0.01). These results show that hypocapnia induces a 20% decrease in LDF flow and a 9% reduction in PtO2 with an unchanged pHt level. In this skeletal muscle model, the decrease in microcirculatory blood flow due to vasoconstriction leads to a reduction in both tissue oxygenation and in the removal of acid metabolites, which counteract a developing tissue alkalosis.
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PMID:The effect of hypocapnia on skeletal muscle microcirculatory blood flow, oxygenation and pH. 850 Sep 73

A 92-year-old woman was admitted to our hospital due to hypertension, nausea, pain in the anterior part of the chest, epigastralgia, and tachypnea. During the initial examination of the patient in the emergency ward, she was very excited, howled, and both her hands were numb. Arterial blood gas analysis revealed a marked alkalemia (pH greater than 7.55) and hypocapnia (Pco2 24.1 mmHg). After paper bag re-breathing, the pH and Pco2 were within normal limits. Because there was no lesion in the lungs or the brain that would account for hyperventilation and convulsions, the attack was considered to be a manifestation of hyperventilation syndrome should be carefully considered in the differential diagnosis of disturbance of consciousness even in elderly patients.
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PMID:[Hyperventilation syndrome in a very old woman]. 915 99

The purpose of this study was to determine if baseline oxygen pressure (PO2), carbon dioxide pressure (PCO2), and pH in brain tissue adjacent to an arteriovenous malformation (AVM) is different from measures in control patients. In addition, PO2, PCO2, and pH changes were measured during the course of AVM resection. Two groups were studied. Group 1 (n = 8) were non-ischemic patients scheduled for cerebral aneurysm clipping. Group 2 (n = 13) were patients undergoing neurosurgery for AVM resection. Following craniotomy, the dura was retracted and a PO2, PCO2, pH sensor inserted into non-ischemic brain tissue in Group 1. In Group 2, the sensor was inserted into tissue adjacent to the AVM. Following equilibration, tissue gases and pH were measured during steady state anesthetic conditions in Group 1 and during AVM resection in Group 2. The results show that under baseline conditions before the start of surgery, tissue PO2 was decreased in AVM compared to control patients but PCO2 and pH were not changed. During AVM resection, PO2 increased, PCO2 decreased, and pH increased compared to baseline measures. These parameters did not change in control patients over a similar time period. The results suggest that chronic cerebrovascular adaptation occur in AVM patients with decreased tissue perfusion pressure as an adjustment for decreased oxygen delivery. During AVM resection, this adaptation produces a hyperemic environment with relative tissue hyperoxia, hypocapnia, and alkalosis which is not corrected by the end of surgery.
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PMID:Increased brain tissue oxygenation during arteriovenous malformation resection. 1023 2

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+]i and 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 observed during hypercapnic acidosis. The hypercapnia-induced increase in [Ca2+]i was unchanged by the removal of Ca2+ from the extracellular medium or by the depletion of thapsigargin-sensitive intracellular Ca2+ stores. Hypercapnic acidosis may thus release Ca2+ from pH-sensitive but thapsigargin-insensitive intracellular Ca2+ stores. Hypocapnic alkalosis caused a fivefold increase in [Ca2+]i compared with hypercapnic acidosis. Intracellular alkalinization at a normal extracellular pH did not affect [Ca2+]i. The hypocapnia-evoked increase in [Ca2+]i was decreased from 242 +/- 56 to 50 +/- 32 nmol/l by the removal of extracellular Ca2+. The main mechanism affecting the hypocapnia-dependent [Ca2+]i increase was thought to be the augmented influx of extracellular Ca2+ mediated by extracellular alkalosis. Hypercapnic acidosis caused little change in PGI2 production, but hypocapnic alkalosis increased it markedly. In conclusion, both hypercapnic acidosis and hypocapnic alkalosis increase [Ca2+]i in HPAECs, but the mechanisms and pathophysiological significance of these increases may differ qualitatively.
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PMID:Effects of hypercapnia and hypocapnia on [Ca2+]i mobilization in human pulmonary artery endothelial cells. 1135 71

Thirty-four dogs suffering from severe babesiosis caused by Babesia canis rossi were included in this study to evaluate acid-base imbalances with the quantitative clinical approach proposed by Stewart. All but 3 dogs were severely anemic (hematocrit <12%). Arterial pH varied from severe acidemia to alkalemia. Most animals (31 of 34; 91%) had inappropriate hypocapnia with the partial pressure of CO2 < 10 mm Hg in 12 of 34 dogs (35%). All dogs had a negative base excess (BE; mean of - 16.5 mEq/L) and it was below the lower normal limit in 25. Hypoxemia was present in 3 dogs. Most dogs (28 of 34; 82%) were hyperlactatemic. Seventy percent of dogs (23 of 33) were hypoalbuminemic. Anion gap (AG) was widely distributed, being high in 15, low in 12, and normal in 6 of the 33 dogs. The strong ion difference (SID; difference between the sodium and chloride concentrations) was low in 20 of 33 dogs, chiefly because of hyperchloremia. Dilutional acidosis was present in 23 of 34 dogs. Hypoalbuminemic alkalosis was present in all dogs. Increase in unmeasured strong anions resulted in a negative BE in all dogs. Concurrent metabolic acidosis and respiratory alkalosis was identified in 31 of 34 dogs. A high AG metabolic acidosis was present in 15 of 33 dogs. The lack of an AG increase in the remaining dogs was attributed to concurrent hypoalbuminemia, which is common in this disease. Significant contributors to BE were the SID, free water abnormalities, and AG (all with P < .01). Mixed metabolic and respiratory acid-base imbalances are common in severe canine babesiosis, and resemble imbalances described in canine endotoxemia and human malaria.
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PMID:The mixed acid-base disturbances of severe canine babesiosis. 1159 31

Respiratory alkalosis is the most frequent acid-base disturbance encountered in clinical practice. This is particularly true in critically ill patients, for whom the degree of hypocapnia directly correlates with adverse outcomes. Although this acid-base disturbance often is considered benign, evidence suggests that the alkalemia of primary hypocapnia can cause clinically significant decreases in tissue oxygen delivery. Mild respiratory alkalosis often serves as a marker of an underlying disease and may not require therapeutic intervention. In contrast, severe respiratory alkalosis should be approached with a sense of urgency and be aggressively corrected.
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PMID:Evaluation and treatment of respiratory alkalosis. 2287 Dec 40


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