摘要
分别用细胞内微电极和Ｌａｎｇｅｎｄｏｒｆｆ心脏灌流技术在低氧复氧豚鼠心肌条和离体大鼠心脏上观察到：缺血多由折返机制产生以室性早搏（发生率为５／８）为主的心率失常；再灌注心律失常有触发机制参与，主要形成室颤（发生率为７／８）。高钾（１３ｍＭ／Ｌ）有类似低氧条件所致的电生理改变，且通过减少复氧早期钙离子内流而抑制后除极所致触发活动，并可阻断低氧心肌的折返通路而抑制再灌注心律失常。
By using intracellular microelectrode and Langendorff perfusing techniques, observations are given on hypoxic and reoxygenated guinea pig myocardiumstrips and isolated rat hearts. Results are as follows; ischemic arrythmias are mainlyventricle premature beats (VPB, incidence is 5/8) via reentry mechanisms , while reper-fusion arrythmias (RA) are chiefly resulted from triggered activity, form ventricle fib-rillation (VF incidence is 7/8) mostly. Hyperkalemia (13 mM/L) has almost the sameeffects on electrophysiological characteristics with hypoxic condition and can depressRA. Hyperkalemiareduce calcium influx of early period of reperfusion, depress trig-gered activity from afterdepolarization ,and interrupt reentry path in ischemic myocardium.
出处
《临床心电学杂志》
1996年第1期19-22,共4页
Journal of Clinical Electrocardiology
关键词
再灌注
心律失常
血钾过多
电生理学
reperfusion : arrhythmia
hyperkalemia
electrophysiology
