内源性一氧化碳对局灶性脑缺血大鼠神经功能、梗死灶体积、脑含水量的影响

目的研究内源性CO浓度变化对局灶性脑缺血大鼠神经功能及脑组织含水量、梗死灶体积的影响.方法将48只S.D.大鼠随机分为2组(n=24), 一组为梗死灶体积组, 一组为脑含水量组.每一组又分为3小组, 分别为HO诱导剂、 HO抑制剂、生理盐水组(n=8).使用HO诱导剂、 HO抑制剂腹腔注射, 等量生理盐水腹腔注射作为对照组, 1 h后制成MCAO模型.栓塞后24 h观察局灶性脑缺血大鼠神经功能改变, 同时检测CO浓度、梗死灶体积、脑含水量.结果与生理盐水组相比, HO诱导剂组CO浓度明显升高(P＜0.01), 大鼠神经功能明显改善, 梗死灶体积、脑含水量明显降低, 各为(P＜0.01、 P＜0.01、 P＜0.05), 而HO抑制剂组CO浓度明显降低(P＜0.01), 大鼠神经功能缺失加剧, 梗死灶体积、脑含水量明显升高, 各为(P＜0.01、 P＜0.05、 P＜0.05).结论内源性CO是一种信使分子, 浓度升高对局灶性缺血的脑组织具有保护作用.

Effect of endogenous carbon monoxide on neurologic impairment、infarction size and brain water in permanent focal ischemia in rats

Objective To evaluate the effects of endougenous carbon monoxide on histochemistry of focal cerebral ischemia in SD rats.Methods 48 SD rats were divided into two groups( n =24) randomly which were infarction size group and brain water group, each group were subsequently divided into 3 sub groups( n =8) which included hemin? ZnPP group and salin group as control.Saline? hemin and ZnPP were injected intraperitoneally 1 h before middle cerebral artery occluded (MCAO) respectively.In 24 h after MCAO, the model set up.The neurologic impairment of rats was appreciated and the concentration of COHb? infarcts size and brain water were also examined.Results Contrast to saline group, in Hemin group neurologic impairment ameliorated, the concentration of COHb in blood rose and the infarct size and brain water decreased;in ZnPP group neurologic impairment deteriorated, the concentration of COHb in blood reduced, and the infarct size and brain water rose contrast to saline group.Conclusions Endogenous carbon monoxide has the protective effects on brain as a messenger gas molecular when its concentration is elevated