生理学报Acta Physiologica Sinica, June 25, 2003, 55(3)
研究论文
牵张所致心室不应性变化的频率依赖现象及其机制
王兴祥1,*, 程龙献2, 陈君柱1, 周利龙2, 朱建华1, 郭晓纲1, 尚云鹏1
1浙江大学医学院第一附属医院心内科暨心血管病研究所, 杭州 310003;
2华中科技大学同济医学院心血管病研究所, 武汉 430022
摘要: 本文旨在探讨牵张所致麻醉兔心室不应性变化的频率依赖现象及其机制。采用部分夹闭兔主动脉根部以增加左室后负荷的在体心脏模型, 观察不同起搏周长时左室后负荷增加后心室有效不应期(effective refractory period, ERP)的变化及链霉素对此的影响。结果显示, 当起搏周长为1000和500 ms时, 左室收缩期内压增加后的心室ERP较主动脉夹闭前略有缩短(1000 ms, 3±2 ms, 1.5%; 500 ms, 7±3 ms, 4.0%. P>0.05), 而起搏周长300和200 ms时则明显缩短(300 ms, 21±5 ms, 17.0%; 200 ms, 19±3 ms, 18.8%. P<0.01); (2)链霉素可有效消除基本驱动周长300和200 ms时左心室后负荷增加对ERP的影响(P>0.05, 组内比较)。结果提示牵张所致心室ERP变化具有快频率依赖性, 且链霉素通过抑制牵张激活性离子通道的活化而消除这种电生理效应。
关键词: 不应期; 链霉素; 机-电反馈; 兔
中图分类号: Q463
Dependence of
ventricular wallstress-induced refractoriness changes on pacing cycle lengths
and its mechanism
WANG Xing-Xiang1,， CHENG Long-Xian2, CHEN Jun-Zhu1, ZHOU Li-Long2, ZHUO Jian-Hua1,
GUO Xiao-Gang1, SHANG Yun-Peng1
1Cardiovascular Disease Department, First Hospital Affiliated to Medical College of Zhejiang University,
Hangzhou 310003; 2Cardiovascular Disease Department, Union Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022
Abstract: The aim of this article was to investigate the dependence of ventricular wallstress-induced refractoriness changes on pacing cycle lengths and its mechanism in anaesthetized rabbits. The rabbit heart preparation was used. The left ventricular afterload was increased by partially clipping the root of the ascending aorta. The changes in effective refractory periods (ERP) induced by the left ventricular afterload rising were examined at different pacing cycle lengths (1000, 500, 300 and 200 ms). In addition, the effect of streptomycin on these changes was also observed. The results are as follows: (1) The rising of left ventricular afterload led to marked changes in ERP at rapidly pacing cycle lengths (300 ms, 21±5 ms, 17.0%; 200 ms, 19±3 ms, 18.8%. P<0.01) than at slow ones (1000 ms, 3±2 ms, 1.5%; 500 ms, 7±3 ms, 4.0%. P>0.05); (2) Streptomycin inhibited the changes caused by the left ventricular afterload rising at pacing cycle lengths 300 ms and 200 ms (P>0.05). It is suggested that ventricular wallstress-induced refractoriness changes are pacing cycle length-dependent, and the effect of streptomycin appears to be consistent with the inhibition of stretch-activated ion channels.
Key words: repfractory period; streptomycin; mechano-electric feedback; rabbit