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

Acidosis has often been reported in inflamed tissues, and changes in strong relevant ions at the site of inflammation may provoke alterations in blood acid-base status. We measured changes in blood acid-base variables during carrageenan-induced inflammation in rats. We found a mixed acid-base disorder in rat blood during acute inflammation (12, 24, and 48 h). A metabolic acid contribution was found during the first 12 h and maintained further, as revealed by a decrease in plasma strong ion concentration difference ([SID]) and an increase in plasma weak acid concentration due to a rise in inorganic phosphate ([ATOT]P(i)). Plasma [SID] and [ATOT]P(i) changes were probably due to exchange of Na+ and P(i) between the inflammatory exudate and rat blood. A secondary respiratory compensation for the metabolic acid changes occurred in the blood of inflamed rats, resulting in significant hypocapnia. Furthermore, a progressive decrease in the total weak acid buffer concentration due to a decrease in plasma albumin ([ATOT]Alb) also counteracted the impact of changes in [SID] and P(i) to increase blood acidity. Therefore, despite the metabolic acid-base disorders induced by inflammatory processes, hydrogen ion (H+) homeostasis was maintained, and blood pH remained essentially unchanged in the inflamed rats.
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PMID:Blood acid-base changes during acute experimental inflammation in rats. 877 12

This study examined the role of pregnancy-induced changes in wakefulness (or non-chemoreflex) and central chemoreflex drives to breathe, acid-base balance and female sex hormones in the hyperventilation of human pregnancy. Thirty-five healthy women were studied in the third trimester (TM(3); 36.3+/-1.0 weeks gestation; mean+/-S.D.) and again 20.2+/-7.8 weeks post-partum (PP). An iso-oxic hyperoxic rebreathing procedure was used to evaluate wakefulness and central chemoreflex drives to breathe. At rest, arterialized venous blood was obtained for the estimation of arterial PCO(2) (PaCO(2)) and [H(+)]. Blood for the determination of plasma strong ion difference ([SID]), albumin ([Alb]), as well as serum progesterone ([P(4)]) and 17beta-estradiol ([E(2)]) concentrations was also obtained at rest. Wakefulness and central chemoreflex drives to breathe, [P(4)] and [E(2)], ventilation and V CO(2) increased, whereas PaCO(2) and the central chemoreflex ventilatory recruitment threshold for PCO(2) (VRTCO(2)) decreased from PP to TM(3) (all p<0.01). The reductions in PaCO(2) were not related to the increases in [P(4)] and [E(2)]. The alkalinizing effects of reductions in PaCO(2) and [Alb] were partly offset by the acidifying effects of a reduced [SID], such that arterial [H(+)] was still reduced in TM(3) vs. PP (all p<0.001). A mathematical model of ventilatory control demonstrated that pregnancy-induced changes in wakefulness and central chemoreflex drives to breathe, acid-base balance, V CO(2) and cerebral blood flow account for the reductions in PaCO(2), [H(+)] and VRTCO(2). This is the first study to demonstrate that the hyperventilation and attendant hypocapnia/alkalosis of human pregnancy results from a complex interaction of pregnancy-induced changes in wakefulness and central chemoreflex drives to breathe, acid-base balance, metabolic rate and cerebral blood flow.
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PMID:Physiological mechanisms of hyperventilation during human pregnancy. 1828 46