钙通道阻滞剂抗肝缺血-再灌注损伤作用机制的实验研究

Experimental study on mechanism of calcium channel entry blockers in protecting liver from ischemia-reperfusion injury

目的 探讨钙通道阻滞剂（ＣＣＥＢ）对肝缺血一再灌注损伤（ＨＩＲＩ）防治作用的机制。方法制备家兔ＨＩＲＩ模型，动态观察维拉帕米（ＶＰ）和地尔硫卓（ＤＴ）对肝组织及血中黄嘌呤氧化酶（ＸＯ）、超氧化物歧化酶（ＳＯＤ）活性及脂质过氧化物（ＬＰＯ）浓度的影响。结果 ＶＰ组和ＤＴ组ＯＸ活性及ＭＤＡ含量分别显著低于对照组（均Ｐ＜０．０１），而ＳＯＤ活性与对照组比较均无显著性差异（均 Ｐ＞ ０．０５）。结论 ＣＣＥＢ抗 ＨＩＲＩ的机制与其降低 ＸＯ活性、抑制脂质过氧化反应密切相关。

The mechanism of calcium channel entry blockers (CCEB) in protecting the liver from ischemia-reperfusion injury was to be explored. Methods With establishment of hepatic ischemia-reperfusion injury (HIRI) model, the effects of verapamil (VP) and diltiazem(DT) on xanthine oxidase (XO), superoxide dismutase (SOD) activities and concentration of lipid peroxides (LPO) in the liver tissue and plasma during HIRI were dynamically observed in rabbits. Results The group treated with VP or DT, as compared with the control group, showed that XO activity and LPO content all decreased significantly (all P< 0.01), but there was no difference for SOD activity between VP group and control group or DT group and control group (all P> 0.05),. Conclusion It is indicated that mechanism of the protection afforded by CCEB was closely related to its decreasing XO activity and inhibiting lipid peroxidation during HIRI.