Evidence of preservation of aerobic cerebral metabolism during halothane-induced hypotension

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Abstract
✓ The effect of halothane-induced profound systemic arterial hypotension on brain ischemia was evaluated by comparison with hypotension caused by oligemia and trimethaphan as well as nonhypotensive controls. Mean cerebral tissue lactate concentrations after halothane-induced hypotension at 5, 30, and 60 minutes were 4.34, 5.92, and 7.48 mM/kg. There was no significant difference between halothane and control animals during the experimental period. At 30 and 60 minutes, both oligemic and trimethaphan groups were higher than the control and halothane series. Definite protection from cerebral ischemia is provided by halothane during induced hypotension. Exact mechanisms of protection conveyed by halothane are unclear, but are probably not related to relative increased blood flow since cerebral vasodilation is maximal in these low blood-pressure ranges irrespective of etiology.