CHANGES IN CEREBROSPINAL MLCROC1RCULATION DURING AND AFTER ABDOMINAL AORTIC CROSS-CLAMPIN : AN UNDERLYING MECHANISM

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Pentobarbital anesthetized rabbits were prepared for measurement of cerebral pial vessel diameter in a cranial window preparation. We investigated the experiments according to following protocols.(1)We studied the effect of aortic clamping and declamping on cerebral pial vessel diameter. Although infrarenal aortic cross-clamping did not affect pial vessel diameter, release of a 20-min aortic cross-clamp caused pial arterioles to dilate and then constrict. A significant constriction persisted for at least 60 mm.(2)To clarify the mechanism of changes in cerebral microcirculation during and after abdominal aortic cross-clamping, we examined whether seratorodast, a thromboxane (Tx) A2 receptor antagonist, or edaravone, a free radical scavenger, would affect the respose observed after abdominal aortic cross-clamping. Both seratrodast and edaravone significantly attenuated the constriction of pial arterioles. Thus such vasoconstriction is partly induced via a washout of the TxA2 and free radicals produced in the ischemic region during and after cross-clamp release.(3)We investigated the effect of vasoactive agents such as milrinone, colforsin daropate, or prostaglandin E1 on arteriolar constriction observed after abdominal aortic cross-clamping. Clinical dose of milrinone and colforsin daropate but not prostaglandin El attenuated the constriction of pial arterioles after cross-clamp release.