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作 者:富冀枫[1] 胡优敏[1] 张照[1] 徐有秋[1]
机构地区:[1]上海第二医科大学基础医学院生理学教研室,上海200025
出 处:《上海第二医科大学学报》2005年第4期385-387,391,共4页Acta Universitatis Medicinalis Secondae Shanghai
摘 要:目的探讨缺血条件下不同浓度腺苷(Ad)和异丙肾上腺素(Iso)对绵羊浦肯野纤维起搏离子流(If)的影响。方法成年绵羊离体心室浦肯野纤维分为对照组、不同浓度腺苷组、缺血组、缺血+不同浓度腺苷组和缺血+不同浓度腺苷+Iso(1μmol/L)组,用双微电极电压钳制术,分别观察在膜电位-70~-120mV各指令电位的If幅值和激活时间。结果不同浓度腺苷组If幅值降低,呈一定的剂量依赖性,激活曲线向超极化方向移位,但激活时间无明显改变。缺血组If幅值降低,激活曲线向超极化方向移位,激活时间延长;缺血+不同浓度腺苷组If幅值进一步降低,腺苷的剂量有不同程度加剧缺血对If离子流的抑制作用;而缺血+不同浓度腺苷+Iso组If幅值与缺血组相比无显著性变化,但与对照组相比If幅值降低,且与腺苷剂量成正比。结论腺苷对正常自律活动有一定的剂量依赖性抑制作用,它能使缺血时已受抑的自律活动进一步受抑;局部即使存在大量Iso,只能部分改善缺血+腺苷的抑制效应,但不会使自律活动过度增强。Objective The purpose of this study was to observe the effects of isoproterenol(Iso) and adenosine(Ad), a main metabolite in acute ischemic myocardium, on pacemaker current I f in sheep cardiac Purkinje fibers. Methods By using two microelectrode voltage clamp technique, we observed the amplitude of I f current and activation time in sheep cardiac Purkinje fibers after perfusion with normal Tyrode solution Ad, ischemia added Ad,ischemia added Ad and Iso (1 μmol/L)at all membrane potential levels among -70^-120 mV. Results After perfusion with Ad in normal Tyrode solution, the amplitude of I f current was decreased and dependent on Ad concentration, with a result of shifting activation curve of I f to a more hyperpolarizing level but the activation time to a steady-state value was not changed. After perfusion with ischemia solution, the amplitude of I f current was decreased at all membrane potential levels, the activation time reaching a steady state value was prolongated, with a result of shifting activation curve of I f to a higher hyperpolarizing level. Ischemia added Ad, the amplitude of I f decreased significantly and was also dependent on Ad concentration. Ischemia added Ad and Iso, the amplitude of I f compared with that in the ischemia solution was not decreased significantly but in normal Tyrode solution was decreased significantly too. Conclusion This suggests that ischemia metabolite Ad may have an inhibitory effect on the normal pacemaker activity of the ventricle, which was aggravated on the condition of ischemia. Although there was accumulation of catecholamine to improve ischemia inhibition, normal automatic rhythmic activity couldn’t be abnormally strengthened and lead to ventricular tachyarrhythmia.
分 类 号:R33[医药卫生—人体生理学]
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