【摘要】 目的 :研究氯离子通道阻滞剂的抗缺血再灌注后的心律失常作用 ,并探讨其机制 .方法 :利用豚鼠离体自搏Langendorff心脏 ,制作缺氧复氧模型 ,并使用氯离子通道阻滞剂SITS和NFA(niflumicacid)进行干预 ,观察SITS ,NFA对心脏缺氧复氧后的心律、单相动作电位时程 (MAPD)的影响 .结果 :使用SITS和NFA后 ,缺氧复氧后心律失常发生率明显减少 ,心率恢复幅度较对照组高 [SITS :(194± 2 0 )min-1vs (113± 2 1)min-1,P <0 .0 1;NFA :(192± 2 1)min-1vs(113± 2 1)min-1,P <0 .0 1];加入SITS和NFA能对抗缺氧心肌MAP复极至 90 %的时程 (MAPD90 )的缩短 (缺氧后MAPD90 与缺氧前MAPD90 的比值分别为 0 .79± 0 .0 4和 0 .77± 0 .0 3,和对照组 0 .6 0± 0 .0 4相比P <0 .0 5 ) .结论 :氯离子通道阻滞剂能延长缺氧心肌细胞的MAPD90 ,缩短可兴奋间隙 ,具有抗心律失常作用更多还原

【Abstract】 AIM: To investigate the antiarrhythmia effects and the mechanism of chloride channel blockers during the course of anoxia/reoxygenation. METHODS: An ischemic/reperfusion model was made on the Langendorff guinea pig hearts with simulated ischemia and simulated reperfusion solution. The protocol was repeated after 500 μmol·L -1 SITS and 1 mmol·L -1 niflumic acid were added to the mimic ischemia solution respectively. The cardiac electric activity such as the heart rate and 90 percent of monophasic action potential duration (MAPD90) was detected at the same time. RESULTS: The incidence of arrhythmias after reoxygenation decreased and the recovery of heart rate was more significant in SITS and niflumic acid groups compared with that in normal controls (SITS:194±20 bpm vs 113±21 bpm, P <0.01;NFA: 192±21 bpm vs 113±21 bpm, P <0.01). The MAPD was shortened in anoxia myocardium, which could be counteracted by SITS and NFA(relative changes of MAPD90 in SITS: 0.79±0.04 vs 0.60±0.04, P <0.05; NFA: 0.77±0.03 vs 0.60±0.04, P <0.05). CONCLUSION: Chloride channel blockers exert an antiarrhythmia effects on anoxia/reoxygenation guinea pig hearts by extending the MAPD90 and shortening the excitable intervals.更多还原