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目的建立大鼠脑心综合征模型。方法采用线栓法栓塞大鼠右侧大脑中动脉,连续监测大鼠标准Ⅱ导联心电图,观察记录心律失常出现情况;大鼠右侧大脑中动脉栓塞后30 min、2h、24h及缺血2 h再灌6 h分别取左心室心肌,透射电镜观察心肌细胞受损程度;TTC染色测定脑梗死率。结果大鼠右侧大脑中动脉栓塞后(14.9±11.4)min内0.71大鼠出现室性早搏(0.38)、房性早搏(0.27)、室性心动过速(0.05)、窦性心动过速(0.01)等心律失常,心律失常持续时间为(29.0±23.2)min。电镜下见心肌细胞有明显损伤:线粒体嵴紊乱、断裂,细胞核膜下染色质聚集,胞质内糖原颗粒沉着等。脑组织TTC染色结果显示,大鼠右侧大脑中动脉栓塞后30min、2h、24h脑梗死率分别达到0.087±0.011、0.114±0.023和0.137±0.031。结论采用线栓法栓塞大鼠右侧大脑中动脉,能制得稳定的脑心综合征模型;大鼠右侧大脑中动脉栓塞引起的心律失常是脑缺血致心肌组织的病理损害所致。
Objective To establish a rat brain-heart syndrome model. Methods The right middle cerebral artery was embolized by thread occlusion. The electrocardiogram of standard Ⅱ lead of rats was continuously monitored. The occurrence of arrhythmia was recorded. The right middle cerebral artery occluded 30 min, 2 h, 24 h and ischemia 2 h after 6 h of reperfusion, left ventricular myocardium were taken, the damage of myocardial cells was observed by transmission electron microscopy; TTC staining was used to determine the infarction rate. Results Compared with the control group, the incidence of ventricular premature beats (0.38), atrial premature beats (0.27), ventricular tachycardia (0.05), sinus tachycardia (0.38), sinus tachycardia 0.01) arrhythmias, arrhythmia duration was (29.0 ± 23.2) min. Electron microscope, myocardial cells showed obvious damage: mitochondrial ridge disorders, rupture, nuclear chromatin chromatin aggregation, cytoplasmic glycogen granules and so on. TTC staining of brain tissue showed that the cerebral infarction rates at 30 min, 2 h and 24 h after right middle cerebral artery occlusion were 0.087 ± 0.011, 0.114 ± 0.023 and 0.137 ± 0.031, respectively. Conclusion The model of brain-heart syndrome can be obtained by embolizing the right middle cerebral artery by thread occlusion. The arrhythmia caused by middle cerebral artery occlusion is the pathological damage of myocardial tissue caused by cerebral ischemia.