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为探讨氯丙嗪对脑缺血的保护作用及其可能的离子通道机制,采用全细胞膜片钳技术,在急性分离的新生大鼠海马锥体细胞上研究氯丙嗪对电压门控钠通道电流(INa)的影响,利用线栓法建立大鼠脑缺血再灌注动物模型,研究氯丙嗪对脑缺血的保护作用。结果显示,大鼠缺血1h后腹腔注射氯丙嗪(10mg/kg),24h后梗塞面积明显减小。30μmol/氯丙嗪可以减小钠电流幅值及使INa激活曲线左移。实验结果提示氯丙嗪可能通过抑制INa而拮抗大鼠脑缺血所引起的损伤。
To investigate the protective effect of chlorpromazine on cerebral ischemia and its possible ion channel mechanism, whole-cell patch-clamp technique was used to study the effects of chlorpromazine on voltage-gated sodium channel currents in acutely isolated neonatal rat hippocampal pyramidal cells (INa). The animal model of cerebral ischemia-reperfusion was established by using the suture method. The protective effect of chlorpromazine on cerebral ischemia was studied. The results showed that chlorpromazine (10 mg / kg) was injected intraperitoneally in rats 1 h after ischemia, and infarct area was significantly reduced after 24 h. 30μmol / chlorpromazine can reduce the sodium current amplitude and left the INa activation curve. Experimental results suggest that chlorpromazine may antagonize the injury induced by cerebral ischemia in rats by inhibiting INa.