Brain extracellular fluid pH and blood flow during isocapnic and hypocapnic hypoxia

Abstract

Cerebrovascular responses to 30 min of isocapnic hypoxia [arterial O2 partial pressure (PaO2) = 33 .+-. 1 torr; mean .+-. SE] were examined in 8 chloralose-urethane-anesthetized, paralyzed and artificially ventilated New Zealand White rabbits. Cerebral blood flow (.ovrhdot.Q) was measured using the radioactive microsphere technique. Vascular resistance (R) was calculated from arterial pressure and .ovrhdot.Q. Brain extracellular fluid (ECF) pH was measured continuously in the same animals using pH microelectrodes (1- to 2-.mu.m tip diameter) placed stereotaxically in the diencephalon. Diencephalon .ovrhdot.Q increased from 40 .+-. 2 to 69 .+-. 4 ml .cntdot. 100 g-1 .cntdot. min-1 (P < 0.05) as R decreased (P < 0.05) after 4-6 min of isocapnic hypoxia. Total brain .ovrhdot.Q and R changes resembled those of the diencephalon. ECF pH of the diencephalon increased by 0.016 .+-. 0.006 (P < 0.05) after 1 min of isocapnic hypoxia and remained significantly elevated through the first 20 min of hypoxia. Ten minutes after the return to normoxia, .ovrhdot.Q and R were at control levels; diencephalon ECF pH was 0.043 .+-. 0.006 below control (P < 0.05). Five additional rabbits were prepared as described above then made hypocapnic [PaCO2 = 21 .+-. 0.3 torr] for 18 min. Diencephalon and total brain .ovrhdot.Q and R remained at control levels through 12-14 min of hyperventilation; diencephalon ECG pH was elevated by 0.03 .+-. 0.006 (P < 0.05). Hyperventilation was then continued with hypoxic gas to lower PaO2 to 35 .+-. 4 torr for 30 min. Diencephalon and total brain R decreased (P < 0.05), with no change in .ovrhdot.Q after 4-6 min of hypocapnic hypoxia. Diencephalon ECF pH was not significantly different from control throughout the hypocapnic-hypoxic period. Early cerebral vasodilation during hypoxia is not mediated by increased brain ECF acidity.