阿片δ受体诱导大鼠心脏预处理延迟保护效应及其机制的探讨

目的探讨以阿片δ受体激动剂能否诱导心脏缺血预处理的延迟保护效应及其保护机制.方法 健康成年雄性大鼠随机分4组,A和B组以阿片δ受体激动剂DADLE处理(2 mg/kg),C和D组注射生理盐水,24 h后4组都制成离体心脏,低温缺血3 h,复灌1 h.观测心功能、ATP等.其B和D组在缺血前以优降糖阻止心肌ATP敏感性钾通道的开放.结果 A左室压力变化最大速率恢复率和心肌ATP含量都高于B,C和D组,差异有显著性(P＜0.01 or P＜0.05),而B,C和D组间无明显差异.A组心肌丙二醛含量与CK-MB漏出活性明显低于B,C和D组(P＜0.01 or P＜0.05).结论阿片δ受体可以诱导健康成年大鼠产声预处理延迟保护效应,而ATP敏感性钾通道参与介导其效应机制.

Experimental study ofδopiod receptor-induced delayed preconditioining rat heart and its mechanism

Obyective:To study the effect of the delayed preconditioning in rat heart triggered by opioid δ receptor and its mechanism with ATP sensitive potassium channel. Methods: Wistar rats were randomly divided into A,B, C and D groups, and then opioid δ receptor, D-Ala2-D-Leu5-enkephin (DADLE) was used to induce delayed preconditioning in A and B, while the rats in C and D were injected with saline. 24 h later, the hearts in all groups were subjected to 180 min of hypothermal ischemia, and 60 min of normothermial reperfusion with Langendorff-peffused isolated heart model, ±dp/dtmax of left ventricle, myocardial ATP and MDA content and CK-MB leakage were measured. Glibenclamide was used in B and D groups to inhibit ATp-sensitive potassium channels before ischemia.Results: The recovery rate of ±dp/dtmax in A group was better than that in B, C and D groups (P ＜0.01 or P ＜0.05).similarly, ATP content in A was higher than that in B, C and D (P ＜0.01), and MDA content in A was much less than that in B, C and D (P ＜0.05 or P ＜0.01), while no difference was observed among B, C, D group. Conclusion:This study shows that opioid δ receptor could induce delayed preconditioning in healthy adult male rat, and ATP sensitive potassium channel may mediate this cardioprotection.