REGION-SPECIFIC AND AGENT-SPECIFIC DILATION OF INTRACEREBRAL MICROVESSELS BY VOLATILE ANESTHETICS IN RAT-BRAIN SLICES

Background: Volatile anesthetics are potent cerebral vasodilators. Alt hough the predominant site of cerebrovascular resistance is attributed to intracerebral arterioles, no studies have compared the actions of volatile anesthetics on intraparenchymal microvessels. The authors com pared the effects of halothane and isoflurane on intracerebral arterio lar responsiveness in hippocampal and neocortical microvessels using a brain slice preparation. Method: After Institutional Review Board app roval, hippocampal or neocortical brain slices were prepared from anes thetized Sprague-Dawley rats and placed in a perfusion-recording chamb er, superfused with artificial cerebrospinal fluid. Arteriolar diamete rs were monitored with videomicroscopy before, during, and after halot hane or isoflurane were equilibrated in the perfusate. PGF(2 alpha) pr econstricted vessels before anesthetic administration, A blinded obser ver using a computerized videomicrometer analyzed diameter changes, Re sults: Baseline microvessel diameter and the degree of preconstriction were not different between groups, In the hippocampus, the volatile a gents produced similar, concentration-dependent dilation (expressed as percent of preconstricted control +/- SEM) of 68 +/- 6% and 79 +/- 9% (1 MAC) and 120 +/- 3% and 109 +/- 5% (2 MAC) (P < 0.05) during halot hane and isoflurane, respectively, In the cerebral cortex, isoflurane caused significantly less vasodilation than did similar MAC levels of halothane (84 +/- 9% vs. 42 +/- 5% dilation at 1 MAC; 121 +/- 4% vs. 8 3 +/- 5% dilation at 2 MAC halothane vs. isoflurane, respectively). Co nclusion: Halothane and isoflurane differentially produce dose-depende nt dilation of intraparenchymal cerebral microvessels. These findings suggest that local effects of the volatile anesthetics on intracerebra l microvessel diameter contribute significantly to alterations in cere brovascular resistance and support previously described heterogeneous actions on cerebral blood flow produced by these agents.