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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 ,改善缺血对心肌细胞的影响
Objective To study the direct effect of calcitonin gene-related peptide on the action potentials of normal and ischemic cardiomyocytes. Methods The classical glass microelectrode intracellular recording technique was used to study the effect of 1 0 - 8 mol / L LCGR on the transmembrane action potentials of normal right atrium, left ventricle and left ventricular muscle in rabbits. Results 1 0 - 8 mol / L LCGRP could significantly shorten APD95 and APD50 ~ 95 in normal right atrium and left ventricular myocytes of rabbits and accelerate the postpulmonary repolarization of action potentials, and significantly reduce the abnormal AP of ischemic left ventricular muscle Extreme degree. Under normal conditions, the APD95 and APD50 ~ 95 of the right atrium were shortened to (1 96 ± 4) ms and (99 ± 5) ms respectively before (206 ± 8) ms and (110 ± 8) ms (P <0.05). The APD95 and APD50 ~ 95 of left ventricular muscle decreased from (2 67 ± 1 3) ms and (54 ± 6) ms to (2 59 ± 1 2) ms and (45 ± 4) ms (P <0 0 5). Under ischemic condition, APD50 / APD95 increased from (68 0 ± 4 5)% to (75 0 ± 4 2)% (P 0 01) at 5 min after addition of 1 0-8 mol / (67 ± 8) ms to (45 ± 6) ms (P <0.01). Conclusion 1 0 - 8mol / L LCGRP can accelerate the repolarization of the action potentials of normal right atrium and left ventricular myocytes and delay the abnormal changes of AP repolarization in ischemic left ventricular myocytes and the effect of ischemia on cardiomyocytes