Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes in body fluid homeostasis during acute hypoxaemia suggest a crucial role of renal function in acclimatization processes. Hypoxaemia stimulates sympathetic nervous activity, and also the cardiovascular system is affected with increases in heart rate and cardiac output. In most subjects, a hypoxic ventilatory response produces hypocapnia and respiratory alkalosis. Acute hypoxaemia depresses aldosterone secretion secondary to a direct effect on adrenal cells. Also plasma renin is decreased in resting hypoxaemic conditions, but the mechanism remains unknown. These hormonal changes may have the advantage of opposing excessive sodium and water retention, which characterizes acute mountain sickness. Short-term isocapnic or hypocapnic hypoxaemia in spontaneously breathing humans causes moderate if any increases in renal blood flow and only minor changes in GFR. In contrast, renal blood flow and GFR decreases during hypercapnic hypoxaemia. Renal clearance studies in humans after 24-48 hours in altitude hypoxia (4,350 m) demonstrate that glomerular and tubular function is only slightly changed in spite of marked depression of the renin-aldosterone system and increased plasma levels of norepinephrine. However, renal vascular tone may increase most probably secondary to the increased adrenosympathetic activity. In the first hours, acute hypoxaemia may induce an increased excretion of sodium and water. Previous studies suggest that the natriuretic response is caused by decreased reabsorption of sodium and bicarbonate in the proximal tubules secondary to the associated hyperventilation and hypocapnia. After 6 hours, sodium and water excretion is normalized or even depressed, dependent on the severity of acute mountain sickness. In view of the prompt increase in sodium and water excretion found during short-term hypoxaemia, the absence of such a response to more prolonged hypoxaemia suggests an adaptive time-dependent course of renal functional changes in hypoxaemia. Taken together, previous studies suggest that effects of acute hypoxaemia on renal haemodynamics are minor compared with effects on cerebral and coronary circulation. This might be the result of an appropriate resetting of autoregulatory mechanisms that would maintain the role of the kidney as a major sense organ to hypoxaemia and, subsequently, as a mediator of plasma volume regulation and erythropoietin synthesis.
 ...
PMID:Effect of hypoxaemia on water and sodium homeostatic hormones and renal function. 859 71

This study investigated the human erythropoietin (EPO) response to short-term hypocapnic hypoxia, its relationship to a normoxic or hypoxic increase of the haemoglobin oxygen affinity, and its suppression by the addition of CO2 to the hypoxic gas. On separate days, eight healthy male subjects were exposed to 2 h each of hypocapnic hypoxia, normocapnic hypoxia, hypocapnic normoxia, and normal breathing of room air (control experiment). During the control experiment, serum-EPO showed significant variations (ANOVA P = 0.047) with a 15% increase in mean values. The serum-EPO measured in the other experiments were corrected for these spontaneous variations in each individual. At 2 h after ending hypocapnic hypoxia (10% O2 in nitrogen), mean serum-EPO increased by 28% [baseline 8.00 (SEM 0.84) U.l-1, post-hypoxia 10.24 (SEM 0.95) U.l-1, P = 0.005]. Normocapnic hypoxia was produced by the addition of CO2 (10% Co2 with 10% O2) to the hypoxic gas mixture. This elicited an increased ventilation, unaltered arterial pH and haemoglobin oxygen affinity, a lower degree of hypoxia than during hypocapnic hypoxia, and no significant changes in serum-EPO (ANOVA P > 0.05). Hypocapnic normoxia, produced by hyperventilation of room air, elicited a normoxic increase in the haemoglobin oxygen affinity without changing serum-EPO. Among the measured blood gas and acid-base parameters, only the partial pressures of oxygen in arterial blood during hypocapnic hypoxia were related to the peak values of serum-EPO (r = -0.81, P = 0.01). The present human EPO responses to hypoxia were lower than those which have previously been reported in rodents and humans. In contrast with the earlier rodent studies, it was found that human EPO production could not be triggered by short-term increases in pH and haemoglobin oxygen affinity per se, and the human EPO response to hypoxia could be suppressed by concomitant normocapnia without acidosis.
 ...
PMID:Human erythropoietin response to hypocapnic hypoxia, normocapnic hypoxia, and hypocapnic normoxia. 895 96