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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。
11 hybrid dogs, the femoral artery blood pressure so that the average arterial pressure (MAP) maintained at 6.0kPa90min after the return of all blood, continue to observe 150min. After 30 minutes of shock, the control group and verapamil treatment group (Ver group) were given intravenous infusion of normal saline and Ver solution [(10μg / kg · min) 15min], the total amount of liquid 3ml / kg. In the control group, the heart rate (HR) and the dp / dtmax of the left ventricle decreased significantly after the blood loss. The MAP even after the blood was transfused was still lower than the baseline values, but the dp / dtmax of the left ventricle did not improve obviously. Ver Slowed down and returned to the basal level after MAP. The dp / dtmax of left ventricle was significantly higher than that of control group. Electron microscopy showed obvious damage of myocardial myofibrils and mitochondria, while the myocardial ultramicrostructure of Ver group normal. The results also showed that the malondialdehyde content and xanthine oxidase activity of Ver dogs were lower than those of the control group, while the activity of superoxide dismutase was higher than that of the control group. The results showed that Ver had a protective effect on the heart of hemorrhagic shock dogs, which may be related to the inhibition of membrane Ca2 + influx and inhibition of lipid peroxidation.