Endothelin-1诱导的大鼠局灶性脑缺血再灌注模型

目的　研究Endothelin 1(ET 1)诱导的大鼠局灶性脑缺血再灌注模型。方法　将ET 1注入大脑中动脉 (MCA)附近 ,ET 1强烈的缩血管作用可使脑血流 (CBF)降低造成缺血性脑损伤 ,采用氢清除法监测缺血过程中大鼠纹状体脑血流的变化 ,于缺血后 6h进行神经功能评分 ,并采用TTC染色法观察脑梗死面积的变化。结果　ET 1可使纹状体血流呈现浓度依赖性的降低 ,10min时CBF降至最低 ,分别为 :ET 130 0 pmol组 (2 7 1± 2 9) %、36 0pmol组 (12 7±2 1) %、4 0 0pmol组 (11 9± 1 8) %、5 0 0 pmol组 (9 5±1 6 ) % ;神经功能评分显示ET 1可造成大鼠不同程度的神经功能损伤 ;MCAO后 2 4h ,脑梗死面积百分率随ET 1浓度的增加而呈上升趋势 ,并显示出良好的浓度依赖关系 :30 0pmol组 (3 9± 0 3) %、36 0 pmol组 (7 4± 0 5 ) %、4 0 0 pmol组 (11 3± 1 3) %、5 0 0 pmol组 (16 2± 1 8) % ;r =0 992 6(P <0 0 5 )。结论　该模型操作简单 ,造成的脑梗死范围稳定、重现性好 ,是一种更接近人类卒中具体情况的较理想的局灶性脑缺血再灌注模型

The focal cerebral ischemia and reperfusion model induced by Endothelin-1 in rat

AIM To establish an Endothelin 1 induced focal cerebral ischemia and reperfusion model. METHODS Endothelin 1(ET 1), a potent vasoconstrictor, was injected near the middle cerebral artery to induce reduction in cerebral blood flow and ischemic neuronal damage. The changes of cerebral blood flow in striatum were characterised using hydrogen clearance technique. The neurologic scores were performed and the infarct volume was identified by TTC staining at 6 h and 24 h after ET 1 application, respectively. RESULTS ET 1 induced a dose dependent reduction of cerebral blood flow in striatum and the CBF at 10 min after ET 1 injection were the lowerest. CBF at 10 min post injection was (27 1±2 9)% in group 300 pmol, (12 7±2 1) % in group 360 pmol, (11 9±1 8)% in group 400 pmol and (9 5±1 6)% in group 500 pmol , respectively. Neurologic score showed that ET 1 could induce variable grade neurologic deficit. The infarct volume were increased with the increment of ET 1 concentration and showed a close correlation, which were (3 9±0 3)% in group 300 pmol, (7 4±0 5)% in group 360 pmol, (11 3±1 3)% in group 400 pmol, and (16 2±1 8)% in group 500 pmol respectively, r =0 992 6 ( P <0 05). CONCLUSION The ET 1 induced focal cerebral ischemia and reperfusion model is a relatively ideal animal model of focal cerebral ischemia and reperfusion, which is simple, reproducible and similar to the condition in human stroke.