大鼠脑心综合征模型的建立

Establishment of cerebrocardiac syndrome model in rats

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30min、2h、24h及缺血2h再灌6h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。

Aim To establish cerebrocardiac syndrome model in rats. Methods Right middle cerebral artery of rat was occluded （MCAO） with nylon thread and Ⅱ lead ECG was monitored continuously within 2 h to record the emerging of arrhythmias. 30 min, 2 h, 24 h after middle cerebral artery occlusion or 6 h reperfusion after 2 h occlusion, left ventricular myocardiums were observed with transmission electron microscope to find the morphological damage and brains were marked with TTC to locate infarction area. Results （ 14. 9 ± 11.4 ） minutes after MCAO, 71% （60/85）model rats had abnormal ECG changes including 38 % （32/85） premature ventricular contraction, 27 % （ 23/85 ） atrial premature beats, 5% （4/85） ventricular tachycardia, 1.2% （ 1/85 ） sinus tachycardia. Arrhythmias sustained （29.0 ±23.2 ） minutes. Ventricular myocardial cell injury was obvious： chaotic and broken mitoehondria ridges, aggregated chromatin under the nucleus membrane, deposited glycogen granules in the cytoplasma. 30 min, 2h, 24h after MCAO the infarction rates were 8. 7% ± 1.1%, 11.4% ± 2. 3% and 13.7% ± 3. 1% respectively. Conclusion A stable cerebrocardiac syndrome model in rat might be induced by means of occluding right middle cerebral artery and the morphological bases of cerebrogenic cardiac arrhythmias are myocardial cell injury caused by cerebral infarction.