Experimental study on the toxicity from PMNLs during ischemia reperfusion cerebral injury
- VernacularTitle:缺血再灌注脑损伤中PMNLs毒性机制的实验研究
- Author:
Xiaodan JIANG
;
Wenguang SONG
;
Sheng TAN
- Publication Type:Journal Article
- Keywords:
Cerebral ischemia reperfusion PMNLs Superoxide
- From:
Journal of Clinical Neurology
1988;0(02):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the change of activity and toxicity of superoxide (O - 2 ) produced in polymorphonuclear leukocytes(PMNLs) during ischemia reperfusion cerebral injury.Methods The rats were administrated by both PMA (an activator of single transduction of O - 2 produced in alkaline phosphatase(ALPase) positive granules of PMNLs) and the inhibitor BCA respectively; the model of middle cerebral artery (MCA) occlusion was made by suture cleat mothod,the activity changes of both myeloperoxidease (MPO) and O - 2 were measured at 6, 12, 24, 48, 72 and 168h reperfusion following ischemia 1h, and the pathological ultrastructural changes were observed. Results The MPO activity of both PAM group and BCA group reached the peaks at 24h after reperfusion; however,there were no remarkable differences in MPO activity between these two groups in the same time point. The O - 2 activity in the PAM group was significantly higher than those in the BCA group. The O - 2 activity reached the peak at 72h of ischemia reperfusion. In the same experimental time point, the pathological changes of the ultrastructure in ischemic reperfusive injury brain of the PAM group were much more serious than the those of the BCA group, which showed obviously the neurons edema, the abnormal structures of nerve felt and synapse in the ischemia reperfusion injured brain.Conclusion The increase of brain O - 2 activity from PMNLs during cerebral ischemia reperfusion injury was direct ratio to the degree of cerebral injury. BCA might depress the activity and the toxicity of the O - 2.
