离体兔肺静脉肌袖心肌细胞电生理特性

摘要

目的 应用常规玻璃微电极细胞内记录技术,研究家兔肺静脉肌袖(PVC)电生理特性,观察PVC与左心房心肌细胞(LAC)之间的电传导现象,探讨肺静脉起源的阵发性房颤的发生机制.方法 50只健康成年家兔,获取肺静脉及相连左房心肌组织,应用常规微电极细胞内技术:记录PVC与LAC动作电位(AP),并进行各项参数比较(APD20,APD50,APD90);分别于PVC端和LAC端予不同频率脉冲刺激,观察另一端AP的产生情况;改用加有钾离子通道阻滞剂2mmol/L氯化铯(CsCl)的台式液,观察二者早后除极(EAD)发生的可能性.结果 PVC的APD20,APD50,APD90均较LAC长(APD20 (23.09±5.44)ms vs (19.50±1.66)ms,APD50 (52.40±7.93)ms vs (28.90±4.36)ms,APD90 (123.35±8.26)ms vs (69.65±9.44)ms),均有显著性差异(P均<0.05);在一定的刺激频率范围内,肺静脉的刺激均能传导至左心房,而后者较少能逆传至肺静脉(100% vs 10%,P<0.05);加用药物灌流后,PVC更易发生EAD(90% vs 15%,P<0.05).结论 PVC和LAC之间的电兴奋传导是不均一的,这可能是形成折返的基础.CsCl作为一种K+通道阻滞剂能延长复极过程,为后除极的发生创造条件,PVC的长AP时程特性,具备发生EAD的倾向性,并且兴奋易于传入左心房,这可能是促进房性心律失常的发生基础.%Objective It is to study the electrophysiological characteristics of cardiocyte from pulmonary vein cardiac muscle ( PVC ) of rabbit applying intracellular recording technique of routine glass microelectrode, to observe the electrical conduction between PVC and left atrium cardiocyte ( LAC ) and to approach the mechanism of paroxysmal atrial fibrillation originated from pulmonary vein. Methods Multiple cardiocytes preparations from pulmonary vein and left atrium of 50 healthy adult rabbits were obtained. The routine intracellular microelectrode technique was applied to record action potential ( AP ) of PVC and LAC , and a comparison of action potential duration ( APD20 , APD50 , APD90 ) between them was made. Different frequency of pulse stimulation was given at PVC terminal and LAC terminal respectively and the generated information of AP at the other terminal was observed. Two mmol/L Caesium chloride ( CsCl ) was added into the superfusate, and the occurred probability of early after depolarization ( EAD ) in the two parts was observed. Results APD20 , APD50 , APD90 of PVC were all longer than those of LAC ( APD20 23.09 ±5.44 vs 19.50 ±1.66, APD50 52.40 ±7. 93 vs28.90 ±4.36, APD90 123.35 ± 8. 26 vs 69. 65 ± 9. 44 ) and the difference was significant ( all P < 0. 05 ). At determinate extent of stimulation frequency , the AP signals from PVC could be conducted freely to LAC. On the contrary, the conduction signals from LAC could seldom reach PVC ( 100% vs 10% , P <0. 05 ). EAD was more easily induced in PVC after drug perfusion added ( 90% vs 15% , P < 0. 05 ). Conclusion The conduction of AP between PVC and LAC was unequal, which may be the basis of reentry formation. CsCl, as a K + channel blockers, can lengthen repolarization process and create the condition of the occurrence of after depolarization. The long APD characteristics of PVC have the proneness of early after depolarization occurred and the excitation is easy conduct into left atrium, which maybe promote the occurred basis of the atrial arrhythmia.