【摘要】 目的:研究牛磺酸与河豚毒素对氯化铯诱发的家兔心脏早后去极化（EAD）及室性早搏（VP）的作用.方法:气管切开维持人工呼吸,经右颈外静脉向右心室插入Franzy导管记录单相动作电位（MAP）,股静脉插管给药.结果:注射氯化铯(1 mmol L^-1)后,MAP幅度减少,MAPD₅₀和MAPD₉₀延长,30秒内发生EAD,并由此触发VP.牛磺酸(100 mg kg^-1)或河豚毒素(10 μg kg^-1)能减少EAD的幅度,EAD的持续时间缩短,VP的程度和发生率减轻.结论:牛磺酸和河豚毒素对氯化铯诱发的EAD和VP的抑制效应涉及增加外向电流或减少内向电流.更多还原

【Abstract】 AIM:To study the effects of taurine (Tau) and tetrodotoxin (Tet) on cesium chloride (CsCl)-induced triggered activity and arrhythmia in anesthetized rabbits. METHODS: With a cuffed endotracheal tube, the rabbit ventilation was maintained by a respirator. A Franzy’s contact electrode catheter was advanced into the right ventricle through the right external jugular vein and positioned against the anteroapical endocardial surface to record the monophasic action potential (MAP). A catheter was placed into femoral vein for systemic drug administration. RESULTS: CsCl (1 mmol L-1 iv) produced a decrease in the amplitude of MAP from 42. 2 ±2. 1 to 37. 0±3.8 mV (P<0. 01), a prolongation of MAPD50(156±22 to 209 ± 26 ms, P <0. 01) or MAPD90(205±25 to 250 ± 20 ms, P < 0. 01 ) and an early afterdepolarization (EAD) developed within 30 s after CsCl injection. The ventricular premature (VP) resulted from EAD triggered by CsCl. In the Tau (100 mg kg-1)-or Tet (10 ug kg~1)-pretreat-ed group, not only was the amplitude of EAD decreased (Tau, 4-2 ± 2.7; or Tet, 5.2 ± 2.6, respectively vs 16.1± 8.6mv, P < 0. 01 ), but also the duration of EAD was shortened (Tau, 695 ± 164; or Tet, 492 ± 172, respectively, vs 1068±166 ms, P< 0.01). The severity of triggered arrhythmia (TA) was alleviated and the incidence of TA was lowered within 30 min after iv CsCl by either Tau or Tet. CONCLUSION: Thedepressant effects of Tau and Tet on EAD and VP induced by CsCl were involved in an increase of outward current or a decrease of an inward current.更多还原