Superior myocardial protection with nicorandil cardioplegia

被引:14
作者
Steensrud, T [1 ]
Nordhaug, D [1 ]
Elvenes, OP [1 ]
Korvald, C [1 ]
Sorlie, DG [1 ]
机构
[1] Univ Hosp N Norway, Dept Cardiothorac & Vasc Surg, N-9038 Tromso, Norway
关键词
cardioplegia; energetics; myocardial protection; nicorandil;
D O I
10.1016/S1010-7940(03)00070-8
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objective: The ATP-sensitive potassium channel (K-ATP) activator nicorandil used as cardioplegic agent may protect the left ventricle during cardiac arrest. Nicorandil in cold blood was compared with standard hyperkalemic blood and crystalloid cardioplegia. Methods: Twenty-one pigs were randomly assigned to three groups: (1) cold hyperkalemic crystalloid (n = 7); (2) cold hyperkalemic blood (n = 7); and (3) nicorandil as cardioplegia in cold blood (n = 7). Left ventricular mechanical performance, pressure-volume area (PVA) and myocardial oxygen consumption (MVO2) were measured before and at I and at 2 It after 60 min of cold global ischemia on cardiopulmonary bypass using intraventricular pressure-volume conductance catheters, coronary flow probes and O-2-content difference. Results: The slope (M,) of the stroke work end-diastolic volume relationship, the preload recriutable stroke work relationship, was unchanged after ischemia in the nicorandil group, but was reduced to averaged 62.5% (standard deviation 14) of baseline values in both hyperkalemic perfusions (P < 0.05). The slope of the MVO2-PVA relationship was unchanged after nicorandil cardioplegia while the slope after hyperkalemic blood and crystalloid cardioplegia increased with 33% (P < 0.02) and 52% (P < 0.02) of baseline values, respectively. Conclusions: Nicorandil as sole cardioplegic agent in cold blood given intermittently preserves left ventricular contractility and myocardial energetics significantly better than traditional forms of cardioplegia after cardiac arrest. (C) 2003 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:670 / 677
页数:8
相关论文
共 27 条
[1]   CONTINUOUS MEASUREMENT OF LEFT-VENTRICULAR VOLUME IN ANIMALS AND HUMANS BY CONDUCTANCE CATHETER [J].
BAAN, J ;
VANDERVELDE, ET ;
DEBRUIN, HG ;
SMEENK, GJ ;
KOOPS, J ;
VANDIJK, AD ;
TEMMERMAN, D ;
SENDEN, J ;
BUIS, B .
CIRCULATION, 1984, 70 (05) :812-823
[2]   Mechanisms by which opening the mitochondrial ATP-sensitive K+ channel protects the ischemic heart [J].
Dos Santos, P ;
Kowaltowski, AJ ;
Laclau, MN ;
Seetharaman, S ;
Paucek, P ;
Boudina, S ;
Thambo, JB ;
Tariosse, L ;
Garlid, KD .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2002, 283 (01) :H284-H295
[3]   Myocardial metabolism and efficiency after warm continuous blood cardioplegia [J].
Elvenes, OP ;
Korvald, C ;
Ytrebo, LM ;
Irtun, O ;
Myrmel, T ;
Larsen, TS ;
Sorlie, D .
ANNALS OF THORACIC SURGERY, 2000, 69 (06) :1799-1805
[4]   Opening mitochondrial KATP in the heart -: what happens, and what does not happen [J].
Garlid, KD .
BASIC RESEARCH IN CARDIOLOGY, 2000, 95 (04) :275-279
[5]  
Garlid KD, 1997, CIRC RES, V81, P1072
[6]   Sarcolemmal versus mitochondrial ATP-sensitive K+ channels and myocardial preconditioning [J].
Gross, GJ ;
Fryer, RM .
CIRCULATION RESEARCH, 1999, 84 (09) :973-979
[7]   ATP-sensitive potassium channels: A review of their cardioprotective pharmacology [J].
Grover, GJ ;
Garlid, KD .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 2000, 32 (04) :677-695
[8]   Mitochondrial ATP-sensitive K+ channels modulate cardiac mitochondrial function [J].
Holmuhamedov, EL ;
Jovanovic, S ;
Dzeja, PP ;
Jovanovic, A ;
Terzic, A .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 1998, 275 (05) :H1567-H1576
[9]   Opening of mitochondrial KATP channels attenuates the ouabain-induced calcium overload in mitochondria [J].
Ishida, H ;
Hirota, Y ;
Genka, C ;
Nakazawa, H ;
Nakaya, H ;
Sato, T .
CIRCULATION RESEARCH, 2001, 89 (10) :856-858
[10]  
Jayawant AM, 1997, CIRCULATION, V96, P240