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在休克过程中，体内活性氧代谢与细胞内钙超负荷存在着相互影响。为了研究林克和复苏过程中钙拮抗剂对脂质过氧化的影响，用１７只杂种犬快速放血使平均动脉压为５．３２ｋｐｄ，并维持９０ｍｉｎ。然后回输全部失血。在休克３０ｍｉｎ时，各组别静脉注射（１５ｍｉｎ内）硫氮酮（４０ｇ／ｋｇ·ｍｉｎ￣（－１）），异搏定（１０μｇ／ｋｇ·ｍｉｎ￣（－１）），或等量生理盐水。复苏后１５０ｍｉｎ处死动物，取心、肝、肺、肾、胰和小肠组织备检。结果显示，用硫氮酮和异搏定治疗组，各主要脏器组织中黄嘌呤氧化酶活性和丙二醛含量均显著低于休克对照组。而各检测组织中超氧化物歧化酶活性变化不一。这些资料显示钙拮抗剂抗休克的机制与其阻滞Ｃａ２＋内流，降低组织中黄嘌呤氧化酶活性，抑制脂质过氧化有密切关系。
During shock, there is an interaction between reactive oxygen species metabolism and intracellular calcium overload. To investigate the effects of lincomycin and calcium antagonists on lipid peroxidation during revolving and resuscitation, 17 dogs were rapidly bled to a mean arterial pressure of 5.32kpd for 90 min. Then return to lose all the blood. After 30 min of shock, all the groups received intravenous (within 15 min) of diltiazem (40 g / kg · min -1), verapamil (10 μg / kg · min -1) or equivalent physiology brine. Animals were sacrificed 150 minutes after resuscitation, heart, liver, lung, kidney, pancreas and small intestine tissue preparation. The results showed that the use of diltiazem and verapamil treatment group, the major organs of xanthine oxidase activity and malondialdehyde content were significantly lower than the shock control group. However, the activity of superoxide dismutase varied in different tissues. These data show that calcium antagonist anti-shock mechanism and its block Ca2 influx, reduce tissue xanthine oxidase activity, inhibition of lipid peroxidation are closely related.