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作 者:郑旭[1,2] 潘孝仁[1,2] A.Muelsch R.Busse E.Bassenge
机构地区:[1]中日友好医院 [2]德国弗莱堡大学应用生理研究所
出 处:《中华心血管病杂志》1997年第3期212-214,共3页Chinese Journal of Cardiology
摘 要:本研究用离体兔心灌注模型探讨硝基类扩血管剂(NVD)及内皮源性舒张因子(EDRF)样物质对冠状动脉微循环的作用机制。将硝酸甘油(NTG,3~1000nmol/L)、硝普钠(SNP,1~1000nmol/L)、3-morpholinosydnonimin(SIN-1,3~10000nmol/L)、S-亚硝基-L-半胱氨酸(CYS-NO,1~1000pmol/L)、双亚硝基-亚铁复合物(DNIC,3~3000nmol/L)和一氧化氮(NO,0.1~30nmol/L)依次注入主动脉内,呈现一系列瞬时的剂量依赖性的冠状动脉灌注压(CPP)降低,EDRF样物质的有效半量或有效半量比值明显低于NVD,而其曲线斜率A值高于NVD。另在持续输入谷胱甘肽-S-转换酶(GST)抑制剂溴酚酞磺酸钠(SBP,30umol/L)前后分别给予NTG(3,30,300nmol/L),后者所引起的CPP下降百分数及扩张持续时间均明显被抑制。上述结果提示:(1)冠状动脉微血管内缺乏NVD生物转化所需的巯基供体,这是冠状动脉阻力血管对EDRF类物质的反应性显著高于NVD的原因;(2)GST参与NTG的生物代谢。By using the model of isolated rabbit heart perfusion, the mechanism of nitrovasodilators (NVD) and EDRF mimetics on coronary microcirculation was investigated. Nitroglycerin (NTG, 3 1000 nmol/L), sodium nitroprusside (SNP, 1 1000 pmol/L), 3 morpholinosydnonimin (SIN 1, 3 10000 nmol/L), S nitroso L cysteine (CYS NO, 1 1000 pmol/L), dinitrosyI iron(II) complex (DNIC, 3 3000 pmol/L) and nitric oxide (NO, 0.1 30mmol/L) were orderly injected into isolated rabbit heart by bolus and then NTG (3,30,300 nmol/L) were injected by bolus before and after perfusion of sulfobromophthalein (SBP, 30 umol/L), a potent inhibitor of GST, respectively. Injection of the above agents elicited a series of transient and dose dependent decreases in coronary perfusion pressure (CPP); ED 50 /ED 50 ratio of EDRF species (CYS NO, DNIC and NO) was much lower than that of NVD (NTG, SNP and SIN 1); the dilatation by NTG was significantly blocked by SBP. Conclusion: (1) rabbit coronary resistance vessels are more sensitive to the vasodilating action of EDRF species than that of NVD due to lack of the sulfhydryl groups required for bioconversion of NVD in the coronary resistance bed; (2) GST participates in the metabolism of NTG in rabbit heart.
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