ATP敏感性钾通道的活化改善心肌顿抑的作用  

Activation of ATPsensitive K^+ channels attenuates myocardial stunning

作　　者：李三潭[1] 王瑞英[1] 王虹[1] 任江华[1] 宋长杰[1] 

机构地区：[1]湖北医科大学附属第二医院心内科

出　　处：《中华心血管病杂志》1997年第6期460-463,共4页Chinese Journal of Cardiology

摘　　要：为了解ＡＴＰ敏感性钾通道（ＫＡＴＰ）的活性对心肌顿抑进程的影响。本实验结扎家兔左冠状动脉左室支１０分钟后，再灌注２小时造成短暂缺血－再灌注心肌顿抑模型，观察心电图、血流动力学、抗氧化酶、脂质过氧化物及细胞Ｋ＋、Ｎａ＋、Ｃａ２＋的变化。结果，与对照组比较，活化ＫＡＴＰ通道能显著降低心脏后负荷（８０±７ｖｓ．１０２±１０，Ｐ＜０．０５）和心肌耗氧量（２．２±０．０５ｖｓ．２．７５±０．０９，Ｐ＜０．０１），逆转缺血心肌细胞内钙超载（２．４９±０．２８ｖｓ．０．９９±０．０８，Ｐ＜０．０１），提高再灌注期ＬＶｄｐ／ｄｔｍａｘ（４１．５％ｖｓ．８９％，Ｐ＜０．０１），降低ＭＤＡ浓度及ＭＤＡ／ＳＯＤ值（３．６±０．４ｖｓ．７．６±０．５，Ｐ＜０．０１；０．０９２±０．００８ｖｓ．０．２７０±０．０３４，Ｐ＜０．０１）。表明活化ＫＡＴＰ通道能产生直接的心肌保护作用，逆转心肌顿抑。The objective of this study was to determine whether ATP senseitive K^+ channels (KATP) activation can attenuated myocardial stunning. 28 rabbits were subjected 10 minute left ventricular cornary artery occlusion followed by 2 hour reperfusion. Saline or nicorandil (KATP specific agonist) (0.1 mg/kg+40 ug/min) were infused intravenously 15 minutes befor and during occlusion with or without glybenclamide (KATP specific antagonist) (1 mg/kg). Hemodynamic variables, myocardial intracellular Na+, K+, Ca2+, Mg2+, area at risk and blood SOD and MDA were measured. The result showed there was no difference in area at risk between the groups. However compared with control group, activation of KATP by using nicorandil can (1) significantly reduce cardiac afterload (80±7 vs 102±10 mmHg,P<0.05) and myocardial oxygen consumption (2.2±0.05 vs 2.75±0.09, P<0.01); (2) depletes intracelluar calcium overoload in ischemic myocardium (2.49±0.28 vs 0.99±0.08, P<0.01); (3) increases LVdp/dt max in reperfusion phase (41.5% vs 89%, P<0.01); (4) significantly reduce MDA (3.6±0.4 vs 7.6±0.5, P<0.01) and MDA/SOD (0.092±0.08 vs 0.270±0.034, P<0.01). The results indicated that activation of KATP can attenuate myocardial stunning by direct cardioprotection.

关 键 词：腺苷三磷酸 钾通道 心肌顿抑 

分 类 号：R972[医药卫生—药品]