Chronic respiratory alkalosis. The effect of sustained hyperventilation on renal regulation of acid-base equilibrium.
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BACKGROUND: In normal subjects, chronic hyperventilation lowers plasma bicarbonate concentration, primarily by inhibiting the urinary excretion of net acid. The quantitative relation between reduced arterial carbon dioxide tension (PaCO2) and the plasma bicarbonate concentration in the chronic steady state has not been studied in humans, however, and the laboratory criteria for the diagnosis of chronic respiratory alkalosis therefore remain undefined. We wished to provide such reference data for clinical use. Moreover, because chronic hyperventilation paradoxically lowers blood pH still further in dogs with metabolic acidosis, we desired to study the effect of chronic hypocapnia on the plasma bicarbonate concentration (and blood pH) in normal human subjects in whom acidosis had been induced with ammonium chloride. METHODS: Under metabolic-balance conditions, we used altitude-induced hypobaric hypoxia to produce chronic hypocapnia in nine normal young men, five of whom received ammonium chloride daily to cause metabolic acidosis (the mean [+/- SE] steady-state plasma bicarbonate level in these five was 12.0 +/- 0.5 mmol per liter). RESULTS: For each decrease of 1 mm Hg (0.13 kPa) in the PaCO2, the plasma bicarbonate concentration decreased by 0.41 mmol per liter in the subjects who started with a normal plasma bicarbonate concentration and by 0.42 mmol per liter in the subjects with acidosis. In contrast to the findings in previous studies of dogs, hypocapnia increased blood pH similarly in both groups; the blood hydrogen ion concentration decreased by about 0.4 nmol per liter for every decrease of 1 mm Hg (0.13 kPa) in PaCO2. CONCLUSIONS: These results provide reference data for the diagnosis of chronic respiratory alkalosis in humans. Although chronic hypocapnia decreased plasma bicarbonate levels similarly in normal subjects with acidosis and without acidosis, the percent reduction in PaCO2 was always greater than the corresponding percent reduction in the plasma bicarbonate concentration. Therefore, as was not true of the response in dogs, the subjects' blood pH always increased with hyperventilation, regardless of the initial plasma bicarbonate concentration. (+info)
Delivery dependence of early proximal bicarbonate reabsorption in the rat in respiratory acidosis and alkalosis.
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In the intact rat kidney, bicarbonate reabsorption in the early proximal tubule (EP) is strongly dependent on delivery. Independent of delivery, metabolic acidosis stimulates EP bicarbonate reabsorption. In this study, we investigated whether systemic pH changes induced by acute or chronic respiratory acid-base disorders also affect EP HCO3- reabsorption, independent of delivery (FLHCO3, filtered load of bicarbonate). Hypercapnia was induced in rats acutely (1-3 h) and chronically (4-5 d) by increasing inspired PCO2. Hypocapnia was induced acutely (1-3 h) by mechanical hyperventilation, and chronically (4-5 d) using hypoxemia to stimulate ventilation. When compared with normocapneic rats with similar FLHCO3, no stimulation of EP or overall proximal HCO3 reabsorption was found with either acute hypercapnia (PaCO2 = 74 mmHg, pH = 7.23) or chronic hypercapnia (PaCO2 = 84 mmHg, pH = 7.31). Acute hypocapnia (PaCO2 = 29 mmHg, pH = 7.56) did not suppress EP or overall HCO3 reabsorption. Chronic hypocapnia (PaCO2 = 26 mmHg, pH = 7.54) reduced proximal HCO3 reabsorption, but this effect was reversed when FLHCO3 was increased to levels comparable to euvolemic normocapneic rats. Thus, when delivery is accounted for, we could find no additional stimulation of proximal bicarbonate reabsorption in respiratory acidosis and, except at low delivery rates, no reduction in bicarbonate reabsorption in respiratory alkalosis. (+info)
Pulmonary O2 uptake and leg blood flow kinetics during moderate exercise are slowed by hyperventilation-induced hypocapnic alkalosis.
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