Effect of different doses of naloxone postconditioning on focal cerebral ischemia-reperfusion injury in rate
10.3760/cma.j.issn.0254-1416.2010.01.028
- VernacularTitle:不同剂量纳洛酮后处理对大鼠局灶性脑缺血再灌注损伤的影响
- Author:
Yi LIU
;
Fushan XUE
;
Xu LIAO
;
Jiaxun ZHAO
;
Yachao XU
;
Jun XIONG
;
Yanming ZHANG
;
Jianhua LIU
- Publication Type:Journal Article
- Keywords:
Naloxone;
Brain;
Reperfusion injury;
Ischemic postconditioning
- From:
Chinese Journal of Anesthesiology
2010;30(1):97-100
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate whether naloxone postconditioning could attenuate the focal cerebral ischemia-reperfusion (I/R) injury in rats. Methods Eighty-eight adult male SD nits weighing 270-330 g were randomly divided into 4 groups (n = 22 each) : group I sham operation (S); group Ⅱ I/R; group Ⅲ , Ⅳ I/R + low and high dose naloxone ( N_1, N_2). Focal cerebral I/R was produced by occlusion of right middle cerebral artery for 90 min followed by 24 h reperfusion. In group N_1, and N_2 naloxone 1 and 10 mg/kg were injected intraperitoneally at initiation of reperfusion respectively. In group I/R normal saline was injected instead of naloxone. HR, MAP and EKG were continuously monitored throughout the experiment. He neurological deficits were scored (0 = no deficit, 4 = unable to crawl, mental dysfunction) at 2 h and 24 h of reperfusion. The animals were then decapitated. The brains were immediately removed for determination of infarct size ( n = 10) and the expression of microtubule-associated protein-2 ( MAP-2) in brain tissue ( n = 6) . In the other 6 rats in each group FICT-dextran 1 ml (50 mg/ml) was injected iv at 1 min before decapitation. The cerebral plasma volume and diameter and segment length of cerebral microvessels on the I/R side were measured using laser scanning confocal microscopy (LSCM). Results Focal cerebral I/R significantly increased neurological deficit scores, induced cerebral infarct, and decreased MAP-2 expression in the brain tissue, cerebral plasma volume and the diameter and segment length of cerebral microvessels on the I/R side. Postconditioning with 10 mg/kg naloxone significantly attenuated the above-mentioned focal cerebral I/R-induced changes. Conclusion Postconditioning with naloxone can attenuate focal cerebral I/R injury in a dose-dependent manner.
