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１０ｍＡ直流电电解Ｋｒｅｂｓ液１ｍｉｎ引起兔基底动脉收缩，灌注压明显增高，血管壁组织丙二醛含量升高及兔胸主动脉，脑基底动脉内皮舒张因子（ＥＤＲＦ）释放量明显减少，卡托普利（Ｃａｐ）２５，５０，１００ｕｍｏｌ·Ｌ￣（－１）可浓度依赖性地抑制电解产生自由基诱发脑血管收缩作用，Ｃａｐ１００ｐｍｏｌ·Ｌ￣（－１）与吲哚美辛合用可完全取消Ｃａｐ的作用，此外Ｃａｐ１００ｕｍｏｌ·Ｌ￣（－１）还具有明显抑制血管壁丙二醛生成及保护内皮细胞释放ＥＤＲＦ的作用，提示Ｃａｐ对外源性氧自由基损伤脑血管保护作用可能由前列环素和ＥＤＲＰ共同中介。
In 10 mA DCs, Krebs solution elicited contraction of basilar artery, increased perfusion pressure, increased MDA content and decreased release of EDRF in rabbit aorta and basilar artery, (Cap) 25, 50, 100 μmol·L ~ (-1) inhibited the free radical induced vasoconstriction in a concentration-dependent manner. Cap100 pmol·L -1 combined with indomethacin completely abolished Cap In addition Cap100umol·L ~ (-1) also has a significant inhibition of the formation of malondialdehyde on the vascular wall and the protection of endothelial cells release of EDRF, suggesting that Cap on the exogenous oxygen free radical injury may be caused by the role of prothrombin and EDRP Common intermediary.