摘要
为探讨家兔快速心房起搏所致的心房肌电重构的机制及粉防已碱对其影响 ,32只家兔随机分为三组 :正常对照组 (A组 ,n =8) ,快速心房起搏组 (B组 ,n =12 ) ,快速心房起搏 +粉防已碱组 (C组 ,n =12 )。经颈内静脉将电极置入右房 ,以 6 0 0次 /分行快速心房起搏 ,测定基础状态、给药后 0 .5h和起搏后 0 .5 ,1,2 ,4 ,6 ,8h ,S1S1为 2 0 0 ,15 0 ,130ms时的心房有效不应期 (AERP2 0 0 、AERP150 和AERP13 0 ) ,实验结束后取三组兔的右心耳组织 ,检测心肌细胞内Ca2 + 含量 ,观察心肌细胞超微结构。结果 :快速心房起搏后B组的AERP缩短 ,AERP的频率适应不良 ,心肌细胞内Ca2 + 含量增加 ,同基础状态比较差异有显著性 (P <0 .0 1) ,心房肌细胞损伤的超微结构变化明显 ,在C组粉防已碱抑制了快速起搏引起的心肌细胞Ca2 + 增加 ,AERP缩短和频率适应不良减轻。结论 :心房肌细胞内Ca2 + 水平的增高在快速起搏导致的心房肌电重构中起作用 ,粉防已碱能减轻快速心房起搏所致的电重构。
To investigate the mechanism of atrial electrical remodeling(ER) in rabbits and the effects of Tetrandrine on ER. 32 rabbits were randomely divided into 3 groups: normal group (A group, n =8), rapid pacing group(B group, n =12),rapid pacing+Tetrandrine group(C group, n =12), Atrial effective refractory period(AERP) was measured by programmed electrical stimulation before rapid atrial pacing and from 0 to 8 hours after the onset of the pacing. Ca 2+ content of atrial tissues was assessed by biochemical technique. The right atrial appendages were collected at 8 hours after rapid atrial pacing and were examined by electron microscopy.Results: The AERP shortened and the rate adapation of AERP was lost through the pacing process compared with before pacing( P <0.01).The ultrastructure of the atrial appendages was damaged, associated with the accumulation of intracellular Ca 2+ in B group.The shortenning AERP was attenuated in C group. The rate adapation was maintained. Conclusion: The ER of the atrium is at least in part mediated by an increased calcium influx in the atrial cells during prolonged rapid atrial pacing. Tetrandrine can prevent ER by inhibiting Ca 2+ influx.
出处
《中国心脏起搏与心电生理杂志》
2003年第5期386-388,共3页
Chinese Journal of Cardiac Pacing and Electrophysiology
关键词
粉防已碱
家兔
快速心房起搏
电重构
心房颤动
中药
Rapid pacing Electrical remodeling Ultrastructure Ca 2+ overload Tetrandrine Rabbit