EFFECTS OF NMDA-ATAGONISTS AND ALPHA2-ADRENERGIC AGONISTS ON SPINAL AND CEREBRAL MICROCIRCULATION -ASSESSED WITH CLOSED SPINAL AND CRANIAL WINDOW TECHNIQUE-.

经戊巴比妥麻醉的动物在颅脑和脊髓窗准备中测量脑和脊髓动脉直径。我们根据以下方案调查实验。(1)探讨右美托咪定系统预处理对异氟醚和七氟醚脑血管反应的影响；异氟醚和七氟醚诱导的脑血管舒张可通过全身给予右美托咪定而减弱，且右美托咪定与挥发性麻醉剂之间的相互作用无剂量依赖性。(2)探讨氯胺酮对异氟醚和七氟醚的脑血管反应的影响；氯胺酮本身不引起脑血管扩张。异氟醚和七氟醚所致的脑脊膜血管舒张可通过全身给药氯胺酮减弱，脑脊膜血管对PaCO2的反应也可减弱。(3)探讨肾上腺素能激动剂α 1-和α 2-对脊髓和大脑血管的影响：右美托咪定和可乐定对脊髓血管的收缩呈浓度依赖性，但其收缩程度小于苯肾上腺素和肾上腺素。右美托咪定和可乐定诱导的脑血管收缩明显大于苯肾上腺素和肾上腺素。(4)探讨脊髓α 2-肾上腺素能激动剂对高碳酸血症和缺氧时脑血管反应性的影响。腰腰椎区鞘内给予α 2-肾上腺素能激动剂，可能通过刺激中枢神经系统的中枢α 2-肾上腺素能受体，减弱了高碳酸血症，但没有减弱缺氧的脑血管舒张。

Pentobaribital anesthetized animals were prepared for measurement of cerebral and spinal pial vessel diameter in a cranial and a spinal window preparation. We investigated the experiments according to following protocols.(1) To investigate the effect of systemic pretreatment with dexmedetomidine on cerebrovascular response to isoflurane and sevoflurane.; The vasodilation of cerebral pial vessels induced by isoflurane and sevoflurane could be attenuated by the systemic administration of dexmedetomidine, and this interaction between dexmedetomidine and volatile anesthetics showed no evidence of dose dependency.(2) To investigate the effect of ketamine on cerebrovascular response to isoflurane and sevoflurane.; Ketamine itself did not induce cerebrovascular dilation. The vasodilation of cerebral pial vessels induced by isoflurane and sevoflurane could be attenuated by the systemic administration of ketamine, and the response of pial vessels to PaCO2 also attenuated.(3) To investigate the effects of alpha1- and alpha2-adrenergic agonists on spinal and cerebral pial vessels: Dexmedetomidine and clonidine constricted spinal vessels in a concentration-dependent manner, but such vasoconstrictions were smaller than those induced by phenylephrine and epinephrine. In cerebral vessels, greater constriction was induced by dexmedetomidine and clonidine than those induced by phenylephrine and epinephrine.(4) To investigate the effects of spinal alpha2-adrenergic agonists on cerebrovascular reactivity to hypercapnia and hypoxia.: The presence of alpha2-adrenergic agonist administered intrathecally into the lumbar spinal region attenuated hypercapnic, but not hypoxic cerebral vasodilation, probably via a stimulation of central alpha2-adrenergic receptors of the central nervous system.