Brain injury induced by ischemia-reperfusion of rat hindlimbs and its mechanisms
- VernacularTitle:大鼠肢体缺血再灌注所致脑损伤及其机制探讨
- Author:
Zhongli SHI
;
Yiling LING
;
Yuxia YAO
;
Aizi ZHANG
;
Junlin ZHOU
;
Zhenyong GU
;
Xinli HUANG
- Publication Type:Journal Article
- Keywords:
Brain;
Extremites;
Ischemia;
Reperfusion injury;
Nitric oxide
- From:
Chinese Journal of Pathophysiology
1989;0(05):-
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To investigate the pathologic changes in the brain and its underlying mechansims during ischemia-reperfusion of rat hindlimbs.METHODS: SD rats were divided into the normal(N), sham(S), 4 h ischemia without reperfusion(I), and 4 h ischemia-2, 6,12,18 or 24 h reperfusion (I-R) groups at random. Ischemia and ischemia-reperfusion were established with the occlusion or/and re-opening of the terminal of abdominal aorta, respectively. The pathologic changes in the brain tissue were morphologically observed. The expression of inducible nitric oxide synthase ( iNOS ) mRNA, and iNOS protein and the nitrotyrosine, a marker of peroxynitrite (ONOO -),in the brain tissue were detected with RT-PCR and immunohistochemical technique, respectively. The brain superoxide dismutase (SOD) activity and malondialdehyde (MDA) contents were spectraphotometrically measured.RESULTS: Hydropic degeneration and severe injury to neurons were only showed in I-R group. Expressions of iNOS mRNA and protein were demonstrated in I-R, I and S groups, which were maximal in I-R 6 h group. iNOS positive neurons and microglias were more spread in I-R 6 h group than those in S and I groups. NT positive neurons were localized in the cerebral cortex and hippcampus of I-R 6 h group. The contents of MDA markedly increased, while the activity of SOD significantly decreased in I-R 6 h group compared to the N, S and I groups. There were no significant changes in MDA and SOD in N, S and I groups.CONCLUSION: Severe ischemia-reperfusion of rat hindlimbs could induce brain injury, and its mechanisms might be related to enhanced expression of iNOS -NO-ONOO - in the brain.
