摘要
本实验采用光化学诱导大鼠大脑中动脉闭塞及再通模型,观察了PAF受体拮抗剂海风藤酮对实验性脑缺血的脑保护作用。结果显示海风藤酮可明显改善缺血区rCBF,增加脑缺血再灌注期脑组织SOD活性,明显减轻缺血脑组织水肿及神经元的坏死。本研究结果提示PAF为脑缺血病理损害过程中的一个重要活性介质;其对脑缺血继发病理损害诸多重要环节有明显的活化及调节作用。PAF受体拮抗海风藤酮对实验性脑缺血组织有明确的脑保护作用。
Institution of Neurology, Chongqing Medical UniversityPlatelet activation factore(PAF)is an endogenous potent mediator in stroke and a contributor to postischemia microcirculatory failure, Blood-brain barrier damage as well as edema formation. To determine whether the specific PAF recetor antagonist might inproved cerebral metabolism and protcet the brain in the post-is chemic and reperfusion phase, Kadsurenone was used in cerebralischemic model in rats by occlusion of photochemical induced. The results showed that Kadsurenone significiantly improved the rCBF of cortex in the ischemic region and the SOD activity, and supressed the formation of brain edema, In the same time, Kadsurenone reduced ischemic neuronal neurosis markedly also. The results suggested that PAF receotor antagonist Kadsurenone has apotent neuroprotective effect on cerebral ischemia.
出处
《卒中与神经疾病》
1996年第1期8-12,共5页
Stroke and Nervous Diseases
关键词
脑缺血
血小板活化因子
海风藤酮
病理
Platelet activating foctor
Kadsurenone
Cerebral ischemia
Brain edema
Rat