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杂种犬１１只，股动脉放血使平均动脉压（ＭＡＰ）维持在６．０ｋＰａ９０ｍｉｎ，回输全部血液，继续观察１５０ｍｉｎ。休克３０ｍｉｎ时，硫氮 酮（ＤｉｌｔｉａｚｅｍＤｉｌ）组（ｎ＝６）输入Ｄｉｌ［４０ｍｇ／（ｋｇ·ｍｉｎ）］，共１５ｍｉｎ，总液体量３ｍｌ／ｋｇ。休克组（ｎ＝５）于相同时间输入等量生理盐水。实验结果显示：Ｄｉｌ组在２１０ｍｉｎ和２４０ｍｉｎ时ＭＡＰ明显高于休克组，而±ｄｐ／ｄｔｍａｘ则从１２０ｍｉｎ始显著高于休克组。电镜下休克组心肌肌原纤维和线粒体均呈不同程度损伤性改变，而Ｄｉｌ组心肌超微结构基本正常。实验结果还显示，Ｄｉｌ组心肌组织中脂质过氧化产物丙二醛（ＭＤＰ）含量和黄嘌呤氧化酶（ＸＯ）活性明显低于休克组，而超氧化物歧化酶（ＳＯＤ）活性显著高于休克组。上述结果表明，硫氮 酮具有抗休克和保护心肌作用，其机制可能与其防止细胞内钙超载，抑制脂质过氧化有关。
11 hybrid dogs, the femoral artery blood let the average arterial pressure (MAP) maintained at 6.0kPa90min, all the blood back to continue to observe 150min. Shock 30min, DiltiazemDil group (n = 6) input Dil [40mg / (kg · min)], a total of 15min, the total liquid volume 3ml / kg. The shock group (n = 5) received the same amount of saline at the same time. The experimental results showed that MAP in Dil group was significantly higher than that in shock group at 210min and 240min, while ± dp / dtmax was significantly higher than that in shock group at 120min. Under electron microscope, myocardial myofibrils and mitochondria in shock group showed varying degree of lesion, while myocardial ultrastructure in Dil group was normal. The experimental results also showed that myocardial lipid peroxidation (MDP) and xanthine oxidase (XO) activity in Dil group were significantly lower than those in shock group, while superoxide dismutase (SOD) activity was significantly higher Shock group. The above results show that, diltiazem has anti-shock and myocardial protection, and its mechanism may be related to its prevention of intracellular calcium overload, inhibition of lipid peroxidation.