局灶性脑梗死出血转化模型中基质金属蛋白酶9的表达

背景：理论上来说，出血性转化可发生于任何脑梗死患者，可见于脑梗死自然演变病程的任何阶段。因此进一步从缺血时间和再灌注角度进行梗死后出血转化发病机制研究可以为临床预防和治疗梗死后出血转化提供理论依据。 目的：观察持续性脑梗死与脑缺血再灌注大鼠脑组织基质金属蛋白酶9的表达。 方法：将健康雄性成年Wistar大鼠随机分为3组：即假手术组、缺血再灌注组、持续脑梗死组。采用线栓法制成大脑中动脉闭塞模型，缺血再灌注组在相应缺血时间点(4.5，6，12，24，48 h)将线栓拔出再灌注24 h，假手术组手术过程同缺血再灌注组，但未置入栓线。持续脑梗死组制成大脑中动脉闭塞模型，但中间不取出栓线。分别于术后2 h进行模型成功评价，并于术后相应时间点进行神经功能障碍评分；TTC染色观察脑组织发生出血转化情况；用免疫组化方法测定基质金属蛋白酶9的表达。 结果与结论：脑梗死后4.5 h内血流再通神经功能评分明显提高，6 h以后尤其12 h以后血流再通将加重神经功能缺损；在缺血再灌注组内随着缺血时间的延长神经功能评分逐渐降低，缺血48 h降至最低。脑组织TTC染色可见缺血12，24，48 h再灌注大鼠均有不同程度的出血转化发生。基质金属蛋白酶9以负性因素参与再灌注损伤和出血性转化，加重缺血再灌注损伤以及促进出血性转化发病。 中国组织工程研究杂志出版内容重点：肾移植；肝移植；移植；心脏移植；组织移植；皮肤移植；皮瓣移植；血管移植；器官移植；组织工程 

Matrix-metalloproteinase-9 expression in focal cerebral infarction models experiencing hemorrhagic transformation

BACKGROUND: Theoretically, hemorrhagic transformation can appear in any patients with cerebral infarction, and occurs in any process of natural evolution of cerebral infarction. Therefore, to further study the pathogenesis of hemorrhagic transformation after infarction from the angle of ischemia time and reperfusion can provide theoretical evidence for preventing and treating hemorrhagic transformation after infarction in the clinic. OBJECTIVE: To observe matrix-metalloproteinase-9 expression in rats with persistent infarction and cerebral ischemia-reperfusion. METHODS: Healthy male adult Wistar rats were randomly assigned to three groups: sham surgery group, ischemia-reperfusion group and persistent infarction group. Suture method was used to establish models of middle cerebral artery occlusion. In the ischemia-reperfusion group, suture was pulled out at 4.5, 6, 12, 24 and 48 hours after ischemia and reperfusion were conducted for 24 hours. In the sham surgery group, the operation was the same as the ischemia-reperfusion group, but suture was not inserted. In the persistent infarction group,   models of middle cerebral artery occlusion were generated, but the suture was not pulled out. Whether the models were successful or not was evaluated at 2 hours after the surgery. Neurological disorders were scored at corresponding time points after the surgery. 2,3,5-Triphenyltetrazolium chloride staining was utilized to observe hemorrhagic transformation in brain tissue. Immunohistochemistry was applied to determine matrix-metalloproteinase-9 expression. RESULTS AND CONCLUSION: Within 4.5 hours after cerebral infarction, neurological score of blood recanalization was obviously elevated. 6 hours later, especially, 12 hours later, blood recanalization aggravated neurologic impairment. In the ischemia-reperfusion group, neurological score gradually decreased with prolonged time of ischemia. At 48 hours of ischemia, neurological score was lowest. 2,3,5-Triphenyltetrazolium chloride staining revealed that at 12, 24 and 48 hours after ischemia, hemorrhagic transformation appeared to different degrees in rats. Matrix-metalloproteinase-9 as a negative factor participates in reperfusion injury and hemorrhagic transformation, aggravated ischemia-reperfusion injury and promoted the onset of hemorrhagic transformation.