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实验性脑出血急性期凝血酶致病机制的探讨 被引量:4

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摘要 目的通过观察凝血酶特异性抑制剂水蛭素对脑出血后血肿周围组织微管相关蛋白2(MAP2)表达及脑组织含水量变化的影响,探讨凝血酶在脑出血后继发性损伤中的致病机制。方法采用自体未抗凝动脉血注入法,制作实验性脑出血动物模型。将大鼠随机分为正常对照组、单纯脑出血组、水蛭素组。采用干湿比重法定量测定脑组织含水量;免疫组化染色观察脑出血后MAP2的变化。结果脑出血后6h开始MAP2表达逐渐减弱(P<0.05),3d达到最低(P<0.05)。脑出血后脑组织含水量逐渐增加,从1d开始增加显著(P<0.05),3d达高峰(P<0.05)。水蛭素组,均较相应时间点单纯出血组脑组织含水量降低(P<0.05);MAP2阳性细胞数目增多(P<0.05),变形程度减轻,染色加深。直线回归分析表明,脑出血后1周内MAP2的变化与脑组织含水量变化呈负相关关系。结论脑出血急性期凝血酶可能通过MAP2的破坏发挥其致病作用;血肿局部应用水蛭素具有保护作用。
出处 《中国神经精神疾病杂志》 CAS CSCD 北大核心 2006年第1期60-62,共3页 Chinese Journal of Nervous and Mental Diseases
基金 ☆卫生部临床学科重点项目资助(编号:20013144)
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