摘要
目的:探讨酸敏感离子通道(ASICs)阻断剂阿米洛利(amiloride)对脑缺血/再灌注(ischemia/reperfusion,I/R)大鼠神经行为学和梗死体积的影响。方法:参照ZeaLonga线栓法建立SD大鼠局灶性脑I/R模型。将32只大鼠随机分为4组,即假手术组、I/R模型对照组、amilorideⅠ组和amilorideⅡ组,每组8只,再灌注24h时间点行神经功能缺损评分,之后进行脑梗死灶体积测定和组织细胞HE染色。结果:I/R模型对照组神经功能缺损评分和脑梗死灶体积均明显大于amilorideⅠ组和amilorideⅡ组(P<0.05),amilorideⅠ组明显大于amilo-rideⅡ组(P<0.05)。结论:ASICs阻断剂amiloride对大鼠脑I/R损伤具有保护作用,其作用机制可能主要为amiloride阻断ASICs,抑制Ca2+超载,减轻脑I/R损伤。amiloride药理作用具有剂量效应关系。
Objective： To investigate changes of ethology and cerebral infarct volume in ASICs blocker on ischemia-reperfusion injury in rats. Methods： The model of focal cerebral ischemia-reperfusion in SpragueDawley （SD） rats was established with sutured-occluded method invented by Zea Longa. Thirty-two SD rats were randomly divided into four groups including sham operated group, focal cerebral ischemia-reperfusion model group, amiloride Ⅰ group and amiloride Ⅱ group, and each group was eight rats. The rats were randomly taken for the evaluation of neurological deficit score, the determination to cerebral infarct volume and HE stain of brain tissue at twenty-four hours reperfusion after two hours focal brain ischemia. Results： Compared with amiloride Ⅰ and amiloride Ⅱ group, the score of neurological deficit and cerebral infarct volume were significantly higher in the focal cerebral ischemia-reperfusion model group （P d0.05）, and the amiloride Ⅰ group was higher than the amiloride Ⅱ （P d0. 05）. Conclusions： ASICs blocker amiloride can protect brain ischemia-reperfusion injury in rats and its mechanism of neuroprotection is chiefly due to amiloride blocking ASICs leading to alleviating Ca^2＋ overloaded and attenuating ischemiareperfusion injury. Amiloride is of dose-effect relationship.
出处
《新疆医科大学学报》
CAS
2007年第2期133-135,138,共4页
Journal of Xinjiang Medical University
