实验性大鼠血栓栓塞性脑梗死出血性转换的机制研究

目的研究大鼠血栓栓塞性脑梗死后并发出血性转换(hemorrhagic transformation,HT)的自然发生率、特点及溶栓治疗对其影响,探讨HT的可能机制.方法采用单一血栓大脑中动脉栓塞模型,通过伊文(氏)蓝、红四氮唑染色、病理观察以及动态MR扫描比较HT组和非HT组血-脑脊液屏障破坏范围、梗死体积、出血类型和部位以及栓塞后30、90 min开始溶栓对其影响.结果HT自然发生率为27.27%,30 min溶栓组为9.09%,有降低趋势.晚期溶栓不增加其发生率,但多发性血肿增多.HT组血-脑脊液屏障破坏范围、梗死体积[(207.33±15.42)和(178.00±54.91)mm3]均大于非HT组[(141.22±48.88)和(113.25±43.08)mm3,均P＜0.05].结论血栓栓塞性脑梗死HT发生率高,早期溶栓不增加其发生率,但溶栓治疗使多发性血肿的发生率增加.大面积梗死后血栓迁移、延迟再通与栓塞性脑梗死并发HT有关.

The Mechanism of Hemorrhagic Transformation in a Rat Cerebral Infarction Model Embolized by Autologous Blood Clot

Objective To examine the characteristics and the natural frequency of hemorrhagic transformation (HT) in a rat embolic stroke model and the effect of thrombolysis therapy. Methods The middle cerebral artery (MCA) occlusion model was established in rats by single autologous clot. The animals with embolic stroke were divided into 3 groups:the control one. had no any treatment, the second treated by UK at 30 min after embolised and the third accepted UK at 90 min. The HT was investigate by pathology and MR at 12 hours. We compared both HT rate and its subtypes in these groups, and then the blood-brain barrier(BBB) disruption examined by Evan blue staining, the infarct volume confirmed by TTC and the neurologic deficit score evaluated between HT and non-HT rats. Results The rate of HT was 27. 27% naturally and 9. 09% in UK treated group at 30 min, which was not decreased significantly ( P >0. 05). Some rats treated by UK got multiple parenchyma hematomas(PH). Both the infarct volume and BBB damaged area in HT group were larger than those in non- HT ( P <0. 05, respectively). Conclusions Embolic stroke by single clot had a high rate of HT. Though it was not increaseed, multiple PH was seen frequently after administration of UK. The migration of clot and delayed recanalization after embolization are the possible mechanism of complicated HT.