CAJ | 학술논문

目的:探讨吡那地尔(pinacidil)建立的短QT间期综合征模型致室性心律失常的机制,并观察缝隙连接激动剂抗心律失常肽(AAP10)对该模型电生理参数的影响.方法:利用pinacidil灌注家兔楔形心肌块建立短QT间期综合征模型. 将20只新西兰长耳白兔随机分成pinacidil组和AAP10组,每组10只.pinacidil组灌流10 μmol/L的pinacidil,AAP10组灌流AAP10 500 nmol/l和pinacidil 10 μmol/L的混合液,同步记录灌流前后内外膜动作电位和容积心电图,观察灌流前后QT间期,跨室壁离散度(TDR),程序性刺激观察心肌组织不应期和室性心律失常的诱发情况.结果:灌流pinacidil后,QT间期从(291±19)ms缩到(232±19) ms (P<0.05),TDR从(44±12)ms减少到(22±7)ms(P<0.05),而不应期从(164±8)ms减少到(112±14)ms(P<0.05),室性心律失常发生率从0/10增加至8/10(P<0.05).AAP10 组和pinacidil组的TDR、QT间期、不应期及室性心律失常的诱发率无显著差别.结论:TDR减小和不应期的缩短可能是pinacidil建立的短QT间期模型致室性心律失常的基础,AAP10对pinacidil诱导的短QT间期综合征模型电不稳定性无明显影响.
목적:탐토필나지이(pinacidil)건립적단QT간기종합정모형치실성심률실상적궤제,병관찰봉극련접격동제항심률실상태(AAP10)대해모형전생리삼수적영향.방법:이용pinacidil관주가토설형심기괴건립단QT간기종합정모형. 장20지신서란장이백토수궤분성pinacidil조화AAP10조,매조10지.pinacidil조관류10 μmol/L적pinacidil,AAP10조관류AAP10 500 nmol/l화pinacidil 10 μmol/L적혼합액,동보기록관류전후내외막동작전위화용적심전도,관찰관류전후QT간기,과실벽리산도(TDR),정서성자격관찰심기조직불응기화실성심률실상적유발정황.결과:관류pinacidil후,QT간기종(291±19)ms축도(232±19) ms (P<0.05),TDR종(44±12)ms감소도(22±7)ms(P<0.05),이불응기종(164±8)ms감소도(112±14)ms(P<0.05),실성심률실상발생솔종0/10증가지8/10(P<0.05).AAP10 조화pinacidil조적TDR、QT간기、불응기급실성심률실상적유발솔무현저차별.결론:TDR감소화불응기적축단가능시pinacidil건립적단QT간기모형치실성심률실상적기출,AAP10대pinacidil유도적단QT간기종합정모형전불은정성무명현영향.
Objective:To study the mechanism of electrical instability of short QT syndrome modle induce by pinacid and the effect of gap junction agonist AAP 10 to the modle. Methods:To establish short QT syndrome modle by arterially perfuse pinacidil in rabbit left ventricular wedge preparations. 20 New-Zealand rabbits were fell into pinacidil group and AAP 10 group randomly , every group 10 rabbits, the pinacidil group perfused 10 μmol/L pinacidil and the AAP 10 group perfused pinacidil 10 μmol/L and AAP 10 500 nmol/L mised liquor. Transmural ECG as well as action potentials from both endocardium and epicardium were simultaneously recorded. To observe the change of TDR (transmural dispersion of repolarization),QT interval and refractory period ,and the induction of ventricular tachycardia (VT) or fibrillation (VF). Results:At a basic cycle length of 1 000 ms, pinacidil (10 mol/L) abbreviated the QT interval from (291±19) ms to (232±19)ms (P<0.05). The transmural dispersion of repolarization (TDR) decrease from (44±12) ms to (22±7) ms (P<0.05), refractory period decrease from (164±8) ms to (112±14)ms (P<0.05) and stimulation applied to the endocardium induced a polymorphic VT (pVT) in 8 of 10 wedge preparations (P<0.05).There are no signally different in QT interval , TDR refractory period and the induce of VT after addition of AAP 10.Conclusions:The decrease of TDR and refractory period possible is the ventricular arrhythmia mechanism of the short QT interval modle estabished by pinacidil .and there are no signally influence in short QT interval modle established by pinacidl caused by AAP 10.