摘要
目的 研究降钙素基因相关肽对正常和缺血心肌细胞动作电位的直接作用。方法 采用经典玻璃微电极细胞内记录技术 ,研究 1 0 - 8mol/LCGRP对家兔正常右房肌、左室肌和缺血左室肌跨膜动作电位的影响。结果 1 0 - 8mol/LCGRP可使家兔正常右房肌和左室肌细胞的APD95和APD50～95明显缩短 ,加速动作电位的后期复极 ;并能明显减小缺血左室肌AP异常复极程度。正常条件下 ,右房肌的APD95和APD50～ 95分别由用药前 (2 0 6± 8)ms和 (1 1 0± 8)ms缩短为 (1 96± 4)ms和 (99± 5)ms(P <0 0 5) ;左室肌的APD95和APD50～95分别由用药前 (2 67± 1 3)ms和 (54± 6)ms缩短为 (2 59± 1 2 )ms和 (45± 4)ms (P <0 0 5)。缺血条件下 ,1 0 - 8mol/LCGRP加入后 5min ,APD50 /APD95 由 (68 0± 4 5) %增大为 (75 0± 4 2 ) % (P <0 0 1 ) ;APD50～95由 (67± 8)ms缩短为 (45± 6)ms (P <0 0 1 )。结论 1 0 - 8mol/LCGRP可加速正常右房肌和左室肌细胞动作电位的后期复极 ;并能延缓缺血左室肌细胞AP复极的异常改变 。
Objective To investigate the effect of CGRP on myocardial action potential under normal and ischemic conditions.Methods Standard glass microelectrode technique was used to investigate the effects of 10 -8 mol/L CGRP on AP of the normal atrial,ventricular and ischemic ventricular myocardium.Results 10 -8 mol/L CGRP obviously decreased the APD 95 and APD 50～95 of normal right atrial and left ventricular myocardium,also decreased the abnormal repolarization degree of ischemic left ventricular myocardiums AP.Under normal condition,APD 95 and APD 50～95 of right atrium shortened respectively from (206±8)ms and (110±8)ms to (196±4)ms and (99±5)ms ( P <0 05); APD 95 and APD 50～95 of left ventricle shortened respectively from (267±13)ms and (54±6)ms to (259±12)ms and (45±4)ms ( P <0.05). Under ischemic condition,after CGRP used for 5 min,APD 50 /APD 95 increased from (68.0±4.5)% to (75.0±4.2)%;APD 50～95 decreased from (67±8)ms to (45±6)ms ( P <0.01).Conclusion 10 -8 mol/L CGRP obviously accelerates the latter repolarization of AP in normal right atrial and left ventricular myocardium,also prevents the further abnormal change of AP repolarization to improve the ischemic left ventricular myocardials physiological status.
出处
《西安医科大学学报》
CAS
CSCD
2000年第6期528-530,共3页
Journal of Xi'an Medical University(Chinese)
基金
国家自然科学基金资助项目!(No :396 70 32 3)
关键词
降钙素基因相关肽
心肌细胞电生理
心肌缺血
calcitonin gene related peptide
cellular electrophysiology
ischemia
myocardium
