论文部分内容阅读
目的 观察凝血酶与脑水肿的关系及使用凝血酶抑制剂 (如水蛭素 )、钙离子拮抗剂(尼莫地平 )是否能减轻凝血酶对脑细胞的毒性损伤 ,是否存在治疗的有效时间。方法 分别以不同剂量的凝血酶注入SD大鼠尾状核 ,建立SD大鼠模型 ,采用干湿重法及普通光镜 (HE染色 )观察脑水肿情况。SD大鼠随机分为 6组。 1组 :生理盐水组 ;2组 :小剂量凝血酶组 ;3组 :大剂量凝血酶组 ;4组 :小剂量凝血酶与小剂量水蛭素同时注入组 ;5组 :大剂量凝血酶与大剂量水蛭素同时注入组 ;6组 :尼莫地平组。每组每时相 (4h、2 4h、48h、3d、7d)各 5只SD大鼠。结果 大剂量凝血酶组脑含水量与其余各组比P <0 0 1,尼莫地平组与其余各组比P <0 0 5 ,大剂量凝血酶组与尼莫地平比P <0 0 5 ,而 3d和 7d二个时相点 6组组间无明显差异P >0 0 5。结论 大剂量凝血酶可早期 (4h)引起明显脑水肿 ,其高峰时间为 2 4～ 48h ,3至 7天后水肿逐渐消褪且趋于正常 ,凝血酶致脑水肿作用可被其特异性抑制剂水蛭素有效抑制 ,钙离子拮抗剂 (尼莫地平 )早期即能减轻凝血酶致脑水肿作用。研究提示如能在脑出血早期 (特别是 4～ 2 4h ,这一时期可能是治疗脑出血的关键时期 )有效抑制凝血酶致水肿的作用 (如使用水蛭素及尼莫地平等 ) ,将会明显减轻脑出血后脑?
Objective To investigate the relationship between thrombin and cerebral edema and whether thrombin inhibitors (such as hirudin) and calcium antagonists (nimodipine) can reduce the toxic damage of thrombin to brain cells and whether there is effective time for treatment. Methods Sprague - Dawley rats were injected with thrombin of different doses respectively to establish a rat model of SD. The cerebral edema was observed by HE staining and wet - dry method. SD rats were randomly divided into 6 groups. 1 group: saline group; 2 groups: low dose thrombin group; 3 groups: high dose thrombin group; 4 groups: small dose thrombin and low dose hirudin simultaneously injected group; The dose of hirudin injected into the group at the same time; 6 groups: nimodipine group. Each group each time phase (4h, 2 4h, 48h, 3d, 7d) each 5 SD rats. Results The brain water content of the high-dose thrombin group was significantly lower than that of the other groups (P <0.01), that of the nimodipine group (P <0 05), and that of the high-dose thrombin group and nimodipine , But there was no significant difference between the 6 groups at 3d and 7d (P> 0.05). Conclusion High-dose thrombin can cause obvious brain edema in early phase (4h), with peak time of 24-48h. After 3-7 days, edema gradually faded and became normal. Thrombin-induced brain edema could be inhibited by its specific inhibitor Hirudin effective inhibition, calcium antagonists (nimodipine) early that can reduce the role of thrombin-induced brain edema. The study suggests that if the effect of thrombin-induced edema (such as hirudin and nimodipine) is effectively inhibited during the early stages of ICH (especially 4 ~ 24 h, which may be the key period for the treatment of ICH during this period) Obviously reduce the brain after cerebral hemorrhage?