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高血糖与脑梗死出血转化:一种宏观出血转化大鼠模型

Hyperglycemia and hemorrhagic transformation of cerebral infarction: a macroscopic hemorrhagic transformation rat model.

作者信息

Tsubokawa Tamiji, Joshita Hiroo, Shiokawa Yoshiaki, Miyazaki Hiroshi

机构信息

Department of Neurosurgery, Saitama Cardiovascular and Respiratory Center, Kumagaya, Saitama, Japan.

出版信息

Acta Neurochir Suppl. 2011;111:43-8. doi: 10.1007/978-3-7091-0693-8_8.

Abstract

The recombinant tissue plasminogen activator (t-PA) is a useful therapy for acute ischemic stroke patients, but there is a major risk factor of hemorrhagic transformation. Hyperglycemic patients are not able to admit t-PA because hyperglycemia exaggerates ischemic brain and vascular damage following transient focal cerebral ischemia and frequently induces hemorrhagic transformation of the infarct during reperfusion. However, the mechanisms underlying hemorrhagic transformation induced by hyperglycemia are still unknown. Furthermore, previous reports focused upon microscopic hemorrhage rather than macroscopic hemorrhagic transformation. In order to make these problems clear, it is necessary to establish an experimental model that induces constant macroscopic hemorrhagic transformation in the infarct area caused by middle cerebral artery occlusion and the reperfusion model on the hyperglycemic rat. This experimental study can establish the model in which macroscopic hemorrhagic transformation occurs following 1.5 h occlusion and 24 h reperfusion by using the intraluminal thread method on hyperglycemic rats. It might be useful to determine the mechanisms and understand why hyperglycemia exaggerates the causes inducing macroscopic hemorrhagic transformation in the infarct area, and this reproducible model provides a platform for evaluating treatment strategies.

摘要

重组组织型纤溶酶原激活剂(t-PA)对急性缺血性中风患者是一种有效的治疗方法,但存在出血性转化的主要危险因素。高血糖患者不能接受t-PA治疗,因为高血糖会加剧短暂性局灶性脑缺血后的缺血性脑和血管损伤,并在再灌注期间频繁诱发梗死灶的出血性转化。然而,高血糖诱导出血性转化的潜在机制仍不清楚。此外,先前的报告侧重于微观出血而非宏观出血性转化。为了弄清楚这些问题,有必要建立一种实验模型,该模型能在高血糖大鼠大脑中动脉闭塞和再灌注模型所致梗死区域诱导持续的宏观出血性转化。本实验研究通过对高血糖大鼠采用腔内穿线法,可建立在闭塞1.5小时和再灌注24小时后发生宏观出血性转化的模型。这对于确定机制以及理解为何高血糖会加剧梗死区域诱导宏观出血性转化的原因可能是有用的,并且这种可重复的模型为评估治疗策略提供了一个平台。

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