Intracellular pH regulation during prolonged hypoxia in rats

Abstract

Conscious rats maintained for three weeks at PB 370–380 Torr were studied in a chamber where PI O2 was maintained at 68–70 Torr at ambient barometric pressure (740–750 Torr). Controls were pair-fed rats maintained at ambient barometric pressure and studied at ambient PI O2 (normoxia). In approximately half of the hypoxic and normoxic animals, hypercapnia was induced by increasing PI O2 for 4 h. Steady-state intracellular pH (pHi) of left and right ventricle, and of tibialis anterior, quadriceps and diaphragm was determined from the distribution of 5,5-dimethyl-2,4-oxazolidinedione (DMO). Apparent non-bicarbonate buffer value (βapp) was calculated as the ratio of the change in HCO 3 − concentration to the change in pH elicited by the increase in P CO 2 . βapp of plasma, tibialis anterior, quadriceps and diaphragm was approximately 2, 3, 6 and 12 times higher, respectively, in hypoxic than in normoxic rats. Neither left nor right ventricular βapp was significantly changed by prolonged hypoxia. In the hypoxic animals, bilateral nephrectomy abolished the increase in βapp of plasma, tibialis anterior and quadriceps, and moderated the increase in βapp of diaphragm. No significant effect of nephrectomy was observed in βapp of either left or right ventricle. The results indicate that in the skeletal muscles studied under conditions of an acid load in the form of increased P CO 2 , intracellular pH is better regulated in hypoxic than in normoxic rats. The effects of nephrectomy suggest that this is due, at least in part, to a more effective renal compensation in hypoxic than in normoxic rats. Prolonged hypoxia, on the other hand, does not affect the cell pH regulation of right or left ventricle.