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

NMDA 激动剂和 α2 肾上腺素能激动剂对脊髓和大脑微循环的影响 - 使用闭合脊柱和颅窗技术进行评估 -。

基本信息

批准号：
09671555
负责人：
IIDA Hiroki
金额：
$ 1.47万
依托单位：
GIFU UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1997
资助国家：
日本
起止时间：
1997 至 1999
项目状态：
已结题

项目摘要

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.

准备戊巴比妥麻醉动物，以测量颅骨和脊柱窗户制备中的脑和脊柱血管直径。我们根据以下方案研究了实验。（1）研究右美托咪定对全身性预处理对异氟烷和Sevoflurane的脑血管反应的影响。异氟烷和七氟烷诱导的脑丘脑血管的血管舒张可能会通过右美托咪定的系统给药而减弱，右美托咪定的这种相互作用与右美托咪定与挥发性麻醉药之间的这种相互作用没有显示出剂量依赖性的证据。和Sevoflurane。氯胺酮本身不会诱导脑血管扩张。氯烷和七氟烷诱导诱导的脑pial血管的血管舒张可能会被氯胺酮的全身施用减弱，而氯胺酮对PIAL血管对PACO2的反应也会减弱。（3）研究α1和alpha2-腺能激动剂的影响。脑血管：以浓度依赖性方式右美托咪定和可乐定收缩血管，但是这种血管收缩小于苯肾上腺素和肾上腺素诱导的血管收缩。在脑血管中，与苯肾上腺素和肾上腺素诱导的那些诱导的右中性托咪定和可乐定诱导的收缩更大。（4）研究脊柱α2-α2-肾上腺素能激动剂对脑血管反应对甲状腺素和低氧的脑血管反应的影响。固定地进入腰脊柱区域会减弱过度cap，但不能通过刺激中枢神经系统的中央α2-肾上腺素能受体刺激。