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

本实验将五指肠麻醉动物制备成颅窗和脊髓窗，分别测量脑血管和脊髓软膜血管直径。我们按照以下方案进行了实验研究：(1)全身注射右美托咪定对异氟醚和七氟醚所致脑血管反应的影响。全身注射右旋美托咪定可减弱异氟烷和七氟醚所致的脑血管扩张，右旋美托咪定和挥发性麻醉剂之间的这种相互作用没有剂量依赖性。(2)研究氯胺酮对异氟烷和七氟醚脑血管反应的影响；氯胺酮本身不诱导脑血管扩张。全身氯胺酮可减弱异氟醚和七氟烷所致的软脑膜血管扩张作用，并减弱软脑膜血管对PaCO2的反应。(3)研究α1和α2肾上腺素能激动剂对脊髓和脑软脑膜血管的作用：右美托咪啶和可乐定以浓度依赖的方式收缩脊髓血管，但收缩幅度小于苯肾上腺素和肾上腺素。在脑血管中，右美托咪啶和可乐定比苯肾上腺素和肾上腺素引起的收缩更大。(4)研究脊髓α2-肾上腺素能激动剂对高碳酸血症和低氧脑血管反应性的影响。鞘内注射α2-肾上腺素能激动剂可减轻高碳酸血症，但不能减轻缺氧性脑血管扩张，这可能是通过刺激中枢中枢α2-肾上腺素能受体来实现的。

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.