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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 4 8只S .D .大鼠随机分为 2组 (n =2 4 ) ,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 ,1h后制成MCAO模型。栓塞后 2 4h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 .0 1) ,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 .0 1、P <0 .0 1、P<0 .0 5 ) ,而HO抑制剂组CO浓度明显降低 (P <0 .0 1) ,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 .0 1、P <0 .0 5、P <0 .0 5 )。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
Objective To investigate the effects of endogenous CO concentration on the neurological function, brain water content and infarct volume in focal cerebral ischemia rats. Methods 48 SD rats were randomly divided into 2 groups (n = 24). One group was infarct volume group, and the other group was brain water content group. Each group was divided into three groups, HO inducer, HO inhibitor, saline group (n = 8). Using HO inducer, HO inhibitor intraperitoneal injection, the same amount of saline intraperitoneal injection as a control group, made after 1h MCAO model. At 24 hours after embolization, the neurological function was observed in rats with focal cerebral ischemia. The CO concentration, infarct size and brain water content were also measured. Results Compared with saline group, CO concentration in HO inducer group was significantly increased (P <0.01). The neurological function was significantly improved and the volume of infarct volume and brain water content were significantly decreased (P <0. 0 1, P <0.01, P <0.05), while the concentration of CO in HO inhibitor group was significantly lower (P <0.01), the neurological deficit in rats was aggravated, the infarct volume and brain water content (P <0.01, P <0.05, P <0.05). Conclusions Endogenous CO is a messenger molecule, and elevated concentrations have a protective effect on focal ischemic brain tissue