S-nitroso human serum albumin improves oxygen metabolism during reperfusion after severe myocardial ischemia

被引:20
作者
Dworschak, M
Franz, M
Hallström, S
Semsroth, S
Gasser, H
Haisjackl, M
Podesser, BK
Malinski, T
机构
[1] Univ Hosp Vienna, Div Cardiothorac Anesthesia & Intens Care, A-1090 Vienna, Austria
[2] Ludwig Boltzmann Inst Cardiosurg Res, Vienna, Austria
[3] Birkmayer Labs, Dept Res & Dev, Vienna, Austria
[4] Ohio Univ, Dept Chem & Biochem, Athens, OH 45701 USA
关键词
heart preservation; ischemia/reperfusion; controlled reperfusion; myocardial blood flow; myocardial oxygen metabolism; nitric oxide; postischemic contractile function;
D O I
10.1159/000079139
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Nitric oxide ( NO) supplementation may modify myocardial oxygen consumption and vascular function after ischemia. We investigated the effects of the NO donor, S-nitroso human serum albumin (S-NO-HSA), on cardiac oxygen metabolism during controlled reperfusion on normothermic cardiopulmonary bypass after severe myocardial ischemia. Pigs randomly received either S-NO-HSA or human serum albumin prior to and throughout global myocardial ischemia. Myocardial oxygen utilization is impaired at the onset of reperfusion, which is not amenable to S-NO-HSA. However, NO supplementation during ongoing supply dependency of oxygen consumption eventually leads to greater myocardial oxygen delivery and consumption. In conjunction with a better washout of lactate, this indicates an improved capillary perfusion in the S-NO-HSA group during reperfusion, which results in a better contractile function post bypass. Copyright (C) 2004 S. Karger AG, Basel.
引用
收藏
页码:106 / 112
页数:7
相关论文
共 19 条
[1]  
AMRANI M, 1992, J THORAC CARDIOV SUR, V104, P1375
[2]   Endothelial dysfunction in chronic myocardial infarction despite increased vascular endothelial nitric oxide synthase and soluble guanylate cyclase expression -: Role of enhanced vascular superoxide production [J].
Bauersachs, J ;
Bouloumié, A ;
Fraccarollo, D ;
Hu, K ;
Busse, R ;
Ertl, G .
CIRCULATION, 1999, 100 (03) :292-298
[3]   EFFECT OF INCREASING DEGREES OF ISCHEMIC-INJURY ON MYOCARDIAL OXIDATIVE-METABOLISM EARLY AFTER REPERFUSION IN ISOLATED RAT HEARTS [J].
GORGE, G ;
CHATELAIN, P ;
SCHAPER, J ;
LERCH, R .
CIRCULATION RESEARCH, 1991, 68 (06) :1681-1692
[4]   S-nitroso human serum albumin treatment reduces ischemia/reperfusion injury in skeletal muscle via nitric oxide release [J].
Hallström, S ;
Gasser, H ;
Neumayer, C ;
Fügl, A ;
Nanobashvili, J ;
Jakubowski, A ;
Huk, H ;
Schlag, G ;
Malinski, T .
CIRCULATION, 2002, 105 (25) :3032-3038
[5]   Prostaglandin E1 reduces ischemia/reperfusion injury by normalizing nitric oxide and superoxide release [J].
Huk, I ;
Brovkovych, V ;
Nanobashvili, J ;
Neumayer, C ;
Polterauer, P ;
Prager, M ;
Patton, S ;
Malinski, T .
SHOCK, 2000, 14 (02) :234-242
[6]  
Huk I, 1997, CIRCULATION, V96, P667
[7]   ACE-inhibition prevents postischemic coronary leukocyte adhesion and leukocyte-dependent reperfusion injury [J].
Kupatt, C ;
Habazettl, H ;
Zahler, S ;
Weber, C ;
Becker, BF ;
Messmer, K ;
Gerlach, E .
CARDIOVASCULAR RESEARCH, 1997, 36 (03) :386-395
[8]   Nitric oxide mitigates leukocyte adhesion and vascular leak after myocardial ischemia [J].
Kupatt, C ;
Zahler, S ;
Seligmann, C ;
Massoudy, P ;
Becker, BF ;
Gerlach, E .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1996, 28 (03) :643-654
[9]   Peroxynitrite inhibits leukocyte-endothelial cell interactions and protects against ischemia-reperfusion injury in rats [J].
Lefer, DJ ;
Scalia, R ;
Campbell, B ;
Nossuli, T ;
Hayward, R ;
Salamon, M ;
Grayson, J ;
Lefer, AM .
JOURNAL OF CLINICAL INVESTIGATION, 1997, 99 (04) :684-691
[10]   FK409 ameliorates ischemia-reperfusion injury in heart transplantation following 12-hour cold preservation [J].
Mohara, J ;
Oshima, K ;
Tsutsumi, H ;
Takeyoshi, I ;
Matsumoto, K ;
Morishita, Y .
JOURNAL OF HEART AND LUNG TRANSPLANTATION, 2000, 19 (07) :694-700