Halothane is a strong inhibitor of
potassium evoked spreading depression (SD) in cats. In the current study, we investigate
halothane effects on induction of perifocal SD-like depolarizations, CBF, and
infarct evolution in focal
ischemia.
Calomel and
platinum electrodes measured cortical direct current potential and CBF in ectosylvian, suprasylvian, and marginal gyri. Left
middle cerebral artery occlusion (MCAO) induced permanent focal
ischemia for 16 hours in artificially ventilated cats (30%
oxygen, 70%
nitrous oxide) under
halothane (0.75%, n = 8) or
alpha-chloralose anesthesia (60 mg/kg intravenously, n = 7). Under
alpha-chloralose, MCAO induced severe
ischemia in ectosylvian and suprasylvian gyri(mean CBF < 10 mL/100 g/min), and direct current potentials turned immediately into terminal depolarization. In marginal gyri, CBF reduction was mild (more than 20 mL/100 g/min), and in six of seven animals, frequent SD-like depolarizations turned into terminal depolarization at a later stage of the experiments. Under
halothane, MCAO induced severe
ischemia (less than 10 mL/100 g/min) and immediate terminal depolarization only in ectosylvian gyrus. In suprasylvian gyrus, residual CBF remained significantly higher (more than 10 mL/100 g/min) than under
alpha-chloralose, whereas in marginal gyri, CBF did not differ between groups. Compared with
chloralose, the number of transient depolarizations was significantly reduced in marginal gyrus, and in suprasylvian gyrus transient but significantly longer depolarizations than in marginal gyrus were recorded. Except for one animal, transient depolarizations did not turn into terminal depolarization under
halothane, and
infarct volume reduction was particularly seen in suprasylvian gyrus. We conclude that
halothane, the most commonly used
anesthetic in studies of experimental
brain ischemia, has protective properties, which may depend on both cerebrovascular and electrophysiologic influences.