目的　确定多巴胺D2、D3受体是否介导脑缺血时多巴胺的神经毒性作用。方法　用尼龙线阻断大鼠大脑中动脉制备局灶性脑缺血模型 ,用图像分析仪计算梗塞体积 ,激光多普勒血流计监测皮层半暗带脑血流。结果　E 10 1在 2mg/kg剂量时明显减小梗塞体积 ,并使皮层半暗带血流明显升高 ,U 99194A在 15mg/kg剂量时产生与前者相似的效果 ,但是其梗塞体积减小和脑血流升高的程度均较低。结论　D2受体参与介导了脑缺血时多巴胺的神经毒性作用 ,D3受体是否介导该作用仍需进一步研究证实。 Objective To determine whether dopamine D2 and D3 receptors mediate the neurotoxic effect of dopamine during cerebral ischemia. Methods The model of focal cerebral ischemia was established by blocking the middle cerebral artery of rats with nylon thread. The volume of infarction was calculated by image analyzer. The cerebral blood flow of the penumbra was detected by laser Doppler flowmetry. Results E 10 1 significantly reduced infarct volume at the 2 mg / kg dose and markedly increased cortical penumbra blood flow. U 99194A produced a similar effect at the 15 mg / kg dose as the former, but its infarct volume was reduced and Cerebral blood flow increased to a lesser extent. CONCLUSION: D2 receptor is involved in mediating the neurotoxic effect of dopamine on cerebral ischemia. Whether D3 receptor mediates this effect needs further investigation.