凝血酶致脑水肿的实验观察

目的：探索凝血酶是否产生或促进水肿形成,以及由凝血酶引起的水肿能否被加入其特异性抑制剂水蛭素或钙拮抗剂尼莫地平所防止。方法：成熟SD大鼠分别接受立体定向尾状核注射,在指定时间点被断头处死,取出大脑作冠状切片,用于湿重法和显微镜(HE染色)观察脑水肿情况。结果：大剂量凝血酶注射后4小时即可产生明显脑水肿,与其余各组比水蛭素或尼莫地平治疗鼠脑水含量减少,脑肿胀减轻。结论：凝血酶直接涉及脑出血水肿形成的过程,水蛭素对脑出血后脑水肿治疗的有效性提供进一步依据证明凝血酶在实质性血块产生水肿病因中占重要地位,因而代表着治疗干预的潜在目标。钙离子拮抗剂尼莫地平能减缓凝血酶对脑细胞的毒性,起保护神经的作用。

Experimental observation of brain edema induced by thrombin

Objective This study sought to determine whether or not thrombin cause edema formation or contribute to it, and to see if the edema response to thrombin could be prevented by adding a specific thrombin inhibitor, hirudin, or a calcium antagonist, nimodipine. Methods Adult SD rats were subjected differently to stereotaxic caudate nucleus injections. The rats were sacrificed by decapitation at the pointed time course. The brains were removed and a coronal slice was cut. Brain edema was observed using a "dry-wet-weighing technique" and a microscopy(HE staining). Results High dose thrombin resulted in obvious brain edema as early as 4hrs after injection. Brain water content in brain tissue were reduced in the hirudin or nimodipine treated rats as compared to other groups, and brain swelling were alleviated. Conclusion Thrombin is directly involved in the process of brain edema formation following ICH. The effectiveness of hirudin as an inhibitor of brain edema from intracerebral hematomas provides further evidence that thrombin plays an important role in the pathogenesis of edema resulting from a parenchymal clot, and therefore represent potential targets for therapeutic intervention. The calcium antagonist, nimodipine, its neuroprotection may be indicated by alleviating toxicity of thrombin.