硫化氢对家兔肠系膜动脉血管环张力调节研究

目的:观察硫化氢(H2S)对家兔肠系膜血管环张力的调节作用,及其可能的作用机制。方法:应用离体血管环张力测定技术,用金属钩将3mm左右的动脉环悬置于含K-H液的离体器官浴槽中,观察硫化氢在血管环张力的作用,由计算机生物信号采集处理系统进行记录分析,检测血管环张力的变化,制作浓度反应曲线。结果:(1)外源性的NaHS(H2S的供体)可以剂量依赖性地舒张由氯化钾(KCL)预收缩的肠系膜动脉血管环。(2)用ATP敏感性钾通道(KA T P)通道阻断剂格列苯脲(Gli)、钙通道的开放剂1,4-二氢-2,6-二甲基-5-硝基-4-(2-三氟甲基]苯基)吡啶-3-羧酸甲酯(Bay K8644)、NO合酶的抑制剂左旋硝基精氨酸甲酯(L-NAME)和环氧合酶阻断剂吲哚美辛预处理以及去除血管内皮后,H2S的舒张效应均被显著抑制,浓度反应曲线均明显右移。(3)给予鸟苷酸环化酶的抑制剂1H-(1,2,4)恶二唑(4,3-α)喹喔啉-1-酮(ODQ)预处理后,对H2S的舒张作用没有显著改变。结论:H2S在50～800μmol/L之间浓度依赖性的舒张家兔肠系膜动脉,部分是通过开放KA T P通道和关闭L型钙通道实现的,但与3ˊ,5ˊ-环一磷酸鸟苷(cGMP)途径无关。此作用是内皮依赖性的,且与一氧化氮(NO)和前列环素(PGI2)具有协同作用。

Modulation of hydrogen sulfide on tension of isolated rabbit mesenteric artery

Objective: To observe the role of H2S for regulation of the rabbit mesenteric vascular ring tension,and to explore its possible mechanism.Methods: Isolated vascular ring tension measurement technique was applied.Artery ring(about 3 mm) was suspended in the in vitro organ perfusion bath containing K-H solution with a metal hook.The role of hydrogen sulfide in changing vascular ring tension was observed by computer biological signal acquisition and processing system.Changes vascular ring tension was recorded and analyzed,concentration-response curve was made.Results:(1) Exogenous H2S induced significantly relaxation of mesenteric arterial rings preconstricted by KCL in a concentration-dependent manner.(2) Pretreatment with KATP channel blocker glibenclamide(Gli),calcium channels agonist Bay K8644,NOS inhibitor NG-nitro-L-arginine methyl ester(L-NAME),prostaglandin(PGI2) inhibitor indomethacin and removal of endothelium significantly inhibited NaHS-induced relaxation.The concentration-response curve shifted right obviously,but pretreatment with indomethacin and L-NAME did not change the maximum relaxation,neither.(3) Pretreatment with soluble guanylyl cyclase inhibitor 1H-oxadiazolo-quinoxalin-1-one(ODQ) had no significant influence on the effects of NaHS.Conclusion: Exogenous H2S induced concentration-dependent relaxation of rabbit mesenteric artery at the dosage of 50 ~ 800 μmol/L partly worked through opening of KATP channels and closing calcium channels.This effect is endothelium-dependent,NO and PGI2 produced a synergistic effect,while this process of H2S relaxation didn't involved activation of the cGMP pathway.