EFFECTS OF ANESTHETICS ON HYPOCAPNIA-INDUCED CONTRACTION OF ISOLATED CEREBRAL ARTERY

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Carbon dioxide is one of the most potent physiologic metabolites for regulation of cerebral blood flow. Both halothane and barbiturates have been shown to decrease cerebral matabolic rate (CMR), resulting in reduction of CO_2 production and thereby contraction of cerebral arteries. However, while barbiturates appear to maintain the normal relationship between CBF and CMR, halothane appears to possess the capacity to increase CBF.Weinvestigated the effects of anesthetics on hypocapnia-induced contraction of isolated dog cerebral artery.Arterial rings from cerebrai (basilar and middle cerebral) and mesenteric arteries were mounted in Krebs' Ringer solution aerated with 95% O_2 and 5% CO_2. Hypocapnia was induced by replacing the aerating gas mixture with 2.5% CO_2 and 97.5% O_2. Cerebral artery but not mesenteric artery contracted in response to hypocapnia. Removal of Ca^<2+> from extracellular fluid abolished the contraction. Endothelial denudation did not affect the contraction. The hypocapnia-induced contraction was attenuated by ezposure to halothane at 0.4, 0.7 and by pentobarbital only at high concectrations up to 3x10^4 M.The contraction induced by KCI 15mM was preferentially inhibited by pentobarbital rather than halothane. Isoflurane at 2.0 MAC also inhibited hypocapnia-induced contraction significantly while sevoflurane at 2 MCA failed to sffect the contraction. Among volatile anesthetics, the inhibitory effect on hypocapnia-induced contraction was in order of halothane > isoflurane > sevoflurane. It is suggested that metabolically mediated contraction of cerebral artery is inhibited during halothane to a greater extent than isoflurane and sevoflurane anesthesia, but is preserved during pentobarbital anesthesia.