CAJ | 학술논문

目的：探讨钾离子通道开放剂（尼可地尔）在慢性缺氧诱导右心室肥厚及心房纤颤中的作用。方法预备120只健康 SD 大鼠（雌雄不限，250~300 g），并采用随机数字表法将其分为Ⅰ~Ⅵ共6组进行干预处理，每组20只。Ⅰ组为空白对照组，Ⅱ组为尼可地尔组，Ⅲ组为慢性缺氧组，Ⅳ组为慢性缺氧+尼可地尔组，Ⅴ组为慢性缺氧+尼可地尔+心房纤颤药物组，Ⅵ组为慢性缺氧+心房纤颤药物组。Ⅰ组不给予任何药物干预；Ⅲ~Ⅵ组均给予慢性缺氧处理10 d；Ⅳ组和Ⅴ组在每次缺氧处理前30 min 经大鼠尾静脉注射尼可地尔（0.8 mg/ kg），Ⅱ组同时给予尼可地尔（0.8 mg/ kg）；Ⅴ组和Ⅵ组均在第6天开始使用氯化钙10 mg/ ml 和乙酰胆碱66μg/ ml 混合液，连用4 d。记录最后一次给药后大鼠发生心房纤颤持续时间及右心室肥厚指数（RVHI）。结果6组大鼠 RVHI 比较，差异有统计学意义（P <0.05）。Ⅲ、Ⅳ、Ⅴ、Ⅵ组大鼠 RVHI 分别与Ⅰ组和Ⅱ组比较，差异有统计学意义（P <0.05）；Ⅰ组和Ⅱ组大鼠RVHI 比较，差异无统计学意义（P >0.05）；Ⅲ、Ⅳ、Ⅴ、Ⅵ组大鼠 RVHI 两两比较，差异无统计学意义（P >0.05）。Ⅰ组和Ⅱ组大鼠未发生心房纤颤，Ⅲ、IV 组有少部分大鼠发生心房纤颤，但发生时间和持续时间长短不一致。Ⅴ组和Ⅵ组大鼠经过慢性缺氧及心房纤颤药物诱导心律失常处理后，在实验进程第9天均出现心房纤颤。最后一次给药后，Ⅴ组大鼠心房纤颤持续时间短于Ⅵ组大鼠〔（18.63±1.70）s 与（20.18±2.10）s；t =2.57，P <0.05〕。结论尼可地尔可增强大鼠对慢性缺氧导致心房纤颤的耐受能力，降低心房纤颤持续时间；但短期内逆转心肌肥厚的作用不明显。
목적：탐토갑리자통도개방제（니가지이）재만성결양유도우심실비후급심방섬전중적작용。방법예비120지건강 SD 대서（자웅불한，250~300 g），병채용수궤수자표법장기분위Ⅰ~Ⅵ공6조진행간예처리，매조20지。Ⅰ조위공백대조조，Ⅱ조위니가지이조，Ⅲ조위만성결양조，Ⅳ조위만성결양+니가지이조，Ⅴ조위만성결양+니가지이+심방섬전약물조，Ⅵ조위만성결양+심방섬전약물조。Ⅰ조불급여임하약물간예；Ⅲ~Ⅵ조균급여만성결양처리10 d；Ⅳ조화Ⅴ조재매차결양처리전30 min 경대서미정맥주사니가지이（0.8 mg/ kg），Ⅱ조동시급여니가지이（0.8 mg/ kg）；Ⅴ조화Ⅵ조균재제6천개시사용록화개10 mg/ ml 화을선담감66μg/ ml 혼합액，련용4 d。기록최후일차급약후대서발생심방섬전지속시간급우심실비후지수（RVHI）。결과6조대서 RVHI 비교，차이유통계학의의（P <0.05）。Ⅲ、Ⅳ、Ⅴ、Ⅵ조대서 RVHI 분별여Ⅰ조화Ⅱ조비교，차이유통계학의의（P <0.05）；Ⅰ조화Ⅱ조대서RVHI 비교，차이무통계학의의（P >0.05）；Ⅲ、Ⅳ、Ⅴ、Ⅵ조대서 RVHI 량량비교，차이무통계학의의（P >0.05）。Ⅰ조화Ⅱ조대서미발생심방섬전，Ⅲ、IV 조유소부분대서발생심방섬전，단발생시간화지속시간장단불일치。Ⅴ조화Ⅵ조대서경과만성결양급심방섬전약물유도심률실상처리후，재실험진정제9천균출현심방섬전。최후일차급약후，Ⅴ조대서심방섬전지속시간단우Ⅵ조대서〔（18.63±1.70）s 여（20.18±2.10）s；t =2.57，P <0.05〕。결론니가지이가증강대서대만성결양도치심방섬전적내수능력，강저심방섬전지속시간；단단기내역전심기비후적작용불명현。
Objective To study the organizational structure changes of right ventricle with chronic hypoxia - induced and potassium channel openers - Nicorandil intervention on chronic hypoxia - induced atrial fibrillation. Methods 120 SD rats were randomly divided into six groups Ⅰ - Ⅳ of the intervention process. Ⅰ group was the control group,Ⅱ group is the Nic-orandil group,Ⅲ group is a group of chronic hypoxia,Ⅳ group is a chronic hypoxia and Nicorandil treatment group,Ⅴ group is a chronic hypoxia and Nicorandil and AF drug group,Ⅵ group is a group of chronic hypoxia and AF drugs. Ⅰ group,do not give any medical intervention;Ⅲ - Ⅵ group were given 10 days of chronic hypoxia,Ⅳ and Ⅴ groups in each group before hy-poxia 30 minutes were given tail intravenous injection of Nicorandil(0. 8 mg/ kg),Ⅱ group also given Nicorandil(0. 8 mg/ kg) in the same time;Ⅴ group and Ⅵ groups were given mixture in the sixth day of Calcium Chloride 10 mg/ ml and acetylcholine 66μg/ ml continuous administration of a mixture of four days,record rats AF duration and right ventricular hypertrophy index (RVHI)after the last dose. Results There was significant difference of RVHI in 6 groups(P < 0. 05). There was significant difference of RVHI in Ⅲ,Ⅳ,Ⅴ,Ⅵ groups compared with group Ⅰ and group Ⅱ(P < 0. 05). There was no significant difference of RVHI between groupⅠand Ⅱ( P > 0. 05). Comparison of Ⅳ,Ⅴ,Ⅵ,RVHI of the rats in group two,the difference was not significant(P > 0. 05). Group Ⅴ and Ⅵ rats after chronic hypoxia and atrial fibrillation drug induced ar-rhythmia after treatment,there were atrial fibrillation in the experimental process for ninth days. Group Ⅴ AF duration was shor-ter than group Ⅵ〔(18. 63 ± 1. 70)s vs. (20. 18 ± 2. 10)s;t = 2. 57,P < 0. 05〕. Conclusion Nicorandil enhanced rats tolerated the drug induced atrial fibrillation capacity,but for short - term reversal of cardiac hypertrophy is not obvious.