The effect of reducing cerebral oxygen consumption (CMR(O)2) on the cerebral blood flow (CBF) responses to isocapnic hypoxic hypoxia and hypotension was examined in sheep. Newborn and adult animals were studied because of their different base-line CMR(O)2. Microsphere-measured CBF responses during pentobarbital coma (i.e., electroencephalographic silence) were compared with responses in conscious or lightly sedated animals. Induction of barbiturate coma reduced both CMR(O)2 and CBF by 50% from the awake value and by 25% from the value obtained in animals sedated with pentobarbital. The CBF response to 30 and 50% reductions in arterial O2 content (Ca(O)2) was attenuated during coma, but only in proportion to the decrease in CMR(O)2. Whether CMR(O)2 was normal or reduced, the normoxic cerebral O2 delivery (CA(O)2 x CBF) was maintained during hypoxia in both newborns and adults. The relative autoregulatory index (fractional change in CBF ./. fractional change in perfusion pressure) was determined during graded hemorrhage. The index was not significantly different from zero (which represents perfect autoregulation) in awake, lightly sedated, or comatose animals. The data demonstrate that both base-line CBF and responses to hypoxia are closely tied to CMR(O)2 and that 50% reduction of CMR(O)2 does not impair cerebrovascular autoregulation.
|Original language||English (US)|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|State||Published - 1985|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Physiology (medical)