CAJ | 학술논문

目的：探讨长期口服血管紧张素 II的1型受体拮抗剂缬沙坦对兔心肌梗死后室性心律失常发生的影响及其可能机制。方法：24只新西兰大白兔随机分为假手术对照组（n＝8）、心肌梗死组（n＝8）和缬沙坦组（n＝8）。假手术对照组只开胸不结扎左冠状动脉前降支，心肌梗死组和缬沙坦组分别结扎左冠状动脉前降支。缬沙坦组术后第二天用缬沙坦（10 mg·kg-1·d-1）灌胃，三组共喂养12周。三组分别在心肌梗死前、梗死12周后记录左心室内、中、外层心室肌细胞单相动作电位（MAP），并记录心肌梗死12周后诱发的恶性心律失常次数。结果：1.心肌梗死12周后，缬沙坦组室速/室颤（VT/VF）的发生次数较心肌梗死组显著减少[（3.1±0.8）次比（12.7±1.5）次，P＜0.05]；2.心肌梗死组左室三层心肌细胞从MAP起始到复极完成90%的时间（APD90）较心肌梗死前明显延长[（259.2±22.1）ms，（288.0±25.8）ms，（244.6±22.6）ms 比（230.1±23.2）ms，（244.2±23.4）ms，（229.0±21.7）ms，P＜0.05或＜0.01]；缬沙坦组左室三层心肌细胞APD90与心肌梗死前相比没有明显差异（P 均＞0.05）；且心肌梗死组跨壁复极离散度（TDR）较假手术对照组、缬沙坦组明显延长[（37.2±10.2）比（18.8±6.2）比（23.9±7.7），P＜0.05或＜0.01]；缬沙坦组与假手术对照组之间 TDR比较无显著性差异（P＞0.05）。结论：长期口服缬沙坦明显降低兔心肌梗死后恶性室性心律失常的发生次数，这可能与改善兔心肌梗死后跨壁复极离散度有关。
목적：탐토장기구복혈관긴장소 II적1형수체길항제힐사탄대토심기경사후실성심률실상발생적영향급기가능궤제。방법：24지신서란대백토수궤분위가수술대조조（n＝8）、심기경사조（n＝8）화힐사탄조（n＝8）。가수술대조조지개흉불결찰좌관상동맥전강지，심기경사조화힐사탄조분별결찰좌관상동맥전강지。힐사탄조술후제이천용힐사탄（10 mg·kg-1·d-1）관위，삼조공위양12주。삼조분별재심기경사전、경사12주후기록좌심실내、중、외층심실기세포단상동작전위（MAP），병기록심기경사12주후유발적악성심률실상차수。결과：1.심기경사12주후，힐사탄조실속/실전（VT/VF）적발생차수교심기경사조현저감소[（3.1±0.8）차비（12.7±1.5）차，P＜0.05]；2.심기경사조좌실삼층심기세포종MAP기시도복겁완성90%적시간（APD90）교심기경사전명현연장[（259.2±22.1）ms，（288.0±25.8）ms，（244.6±22.6）ms 비（230.1±23.2）ms，（244.2±23.4）ms，（229.0±21.7）ms，P＜0.05혹＜0.01]；힐사탄조좌실삼층심기세포APD90여심기경사전상비몰유명현차이（P 균＞0.05）；차심기경사조과벽복겁리산도（TDR）교가수술대조조、힐사탄조명현연장[（37.2±10.2）비（18.8±6.2）비（23.9±7.7），P＜0.05혹＜0.01]；힐사탄조여가수술대조조지간 TDR비교무현저성차이（P＞0.05）。결론：장기구복힐사탄명현강저토심기경사후악성실성심률실상적발생차수，저가능여개선토심기경사후과벽복겁리산도유관。
Objective:To explore influence of long-term oral valsartan-angiotensin II type 1 receptor blocker on ventricular arrhythmia after myocardial infarction (MI)in rabbits and its possible mechanism.Methods:A total of 24 NeW Zealand rabbits Were randomly divided into sham operation group (n=8),MI group (n=8)and valsartan group (n=8)according to number table.Sham operation group only received thoracotomy Without ligation of ante-rior descending branch of left coronary artery (LAD),While MI group and valsartan group received ligation of ante-rior descending branch of LAD.Valsartan group received valsartan gavage (10 mg·kg-1 ·d-1 )since the second day after operation,three groups all Were fed for 1 2 Weeks.Mono active potential (MAP)of left ventricular myo-cardial cells of subendocardial myocardium (inner layer myocardium),subepicardial myocardium (outer layer myo-cardium) and middle layer myocardium Were recorded before MI and 1 2 Weeks after MI,and times of provocative malignant arrhythmias Were recorded on 1 2 Weeks after MI in three groups.Results:1. Ventricular tachycardia or fibrillation (VT/VF)episodes Were markedly decreased in VAL group than that in MI group on 1 2 Weeks after MI [(3.1±0.8)vs.(12.7±1.5),P<0.05];2. After MI 12 W,the action potential duration to 90% repolarization (APD90)of three-layer ventricular myocytes in MI group Was prolonged than that before MI [(259.2±22.1)ms, (288.0±25.8)ms,(244.6±22.6)ms vs.(230.1±23.2)ms,(244.2±23.4)ms,(229.0±21.7)ms,P<0.05 or <0.01];but there Were no significant difference in APD90 of three layers ventricular myocytes betWeen before and af-ter MI in valsartan group (P>0.05 all);Compared With sham operation group and valsartan group,there Was sig-nificant prolonged in transmural dispersion of repolarization (TDR)[(18.8±6.2)vs.(23.9±7.7)vs.(37.2± 10.2),P<0.05 or <0.01]in MI group;There Was no significant difference in TDR betWeen valsartan group and sham operation group (P>0.05).Conclusion:Long-term oral valsartan can significantly reduce malignant ventricu-lar arrhythmia incidence in rabbits after MI,Which may be related to improving TDR in rabbits after MI.