维拉帕米对失血性休克犬心脏的保护作用及机制

杂种犬１１只，由股动脉放血使平均动脉压（ＭＡＰ）维持在６．０ｋＰａ９０ｍｉｎ后回输全部血液，继续观察１５０ｍｉｎ。在休克３０ｍｉｎ后，对照组和维拉帕米处理组（Ｖｅｒ组）分别静脉滴注生理盐水和Ｖｅｒ溶液［（１０μｇ／ｋｇ·ｍｉｎ）１５ｍｉｎ］，液体总量为３ｍｌ／ｋｇ。对照组犬在失血后心率（ＨＲ）加快，左室ｄｐ／ｄｔｍａｘ显著降低，回输血液后ＭＡＰ虽有回升，但仍低于基础值，左室ｄｐ／ｄｔｍａｘ无明显改善；Ｖｅｒ使休克犬ＨＲ减慢，血液回输后ＭＡＰ缓慢恢复至基础值，左室ｄｐ／ｄｔｍａｘ显著高于对照组；电镜观察可见对照组心肌肌原纤维和线粒体等有明显的损伤，而Ｖｅｒ组心肌超微结构基本正常。结果还显示：Ｖｅｒ组犬心肌中丙二醛含量、黄嘌呤氧化酶活性低于对照组，而超氧化物歧化酶活性高于对照组。结果表明：Ｖｅｒ对失血性休克犬的心脏具有保护作用，其机制可能与其阻滞膜Ｃａ２＋内流、抑制脂质过氧化有关。

Benefial Effects of Verapamil on Myocardium in Canine Hemorrhagic Shock

Anesthetized mongrel dogs were rapidly bled to a mean arterial pressure (MAP) of 6 .0kpa and maitained at that level for 90min followed by resuscitation with all shed blood. At 30min into hemorrhagic shock verapamil(10μg/kg.min,15min, n= 6) or same volume of saline (3ml/kg, n=5)was infused intravenously over 15min. At the end of experiment (240min after hemorrhage and resuscitation), the dogs were euthnized by pentobarbital overdose and myocardial samples were obtained and analyzed.The results demonstrated: Resuscitation with shed blood alone did not restore MAP and left venticular dp/dtmax completely. Verapemil treatment significantly facitated the normalization of MAP and left venticular dp/dt max and also remarkably ameliorated myocardial ultrastructure damage. Further more. myocardial of verapamil treatment dogs exhibited less malonyldialdehyde, lower xanthine oxidative activity and higher activity of superoxide dismutase as compared with those of control dogs. These data suggest that verapamil has a beneficial effect on myocardium of dogs with hemorrhagic shock, which is associated with its calcium channel blockage and antioxidant activity.