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Ann Thorac Surg 1999;67:1732-1737
© 1999 The Society of Thoracic Surgeons
a Division of Cardiothoracic Surgery, Department of Surgery, Carlyle Fraser Heart Center-Cardiothoracic Research Laboratory, Emory University School of Medicine, Atlanta, Georgia, USA
Accepted for publication January 4, 1999.
Address reprint requests to Dr Vinten-Johansen, Cardiothoracic Research Laboratory, Crawford Long Hospital, 550 Peachtree NE, Atlanta, GA 30365-2225
e-mail: jvinten{at}emory.edu
Background. The cardioprotective effects of the adenosine A3 receptor in a cardioplegia model have not been described. We tested the hypothesis that infusion of the A3 receptor agonist, Cl-IB-MECA (100 nM), as a pretreatment (PTx) and/or as a cardioplegic (CP) additive reduces postischemic myocardial injury.
Methods. Isolated perfused rat hearts underwent 30 minutes of normothermic ischemia, 60 minutes of intermittent hypothermic cardioplegia (10°C), followed by 2 hours of reperfusion. Hearts were divided into four groups: (1) no pretreatment (PTx) and unsupplemented cardioplegia (CP) (control), (2) Cl-IB-MECA PTx and unsupplemented CP (A3-PTx), (3) no PTx and Cl-IB-MECA CP (A3-CP), or (4) Cl-IB-MECA PTx and Cl-IB-MECA CP (A3-[PTx+CP]).
Results. Coronary flow was not increased after A3 pretreatment when compared to baseline values. After 2 hours of reperfusion, left ventricular developed pressure in control and A3-CP groups was depressed to 43% ± 3% and 47% ± 2% of baseline; while A3-PTx and A3-[PTx+CP] significantly increased left ventricular developed pressure (65% ± 3% and 61% ± 5%) from baseline relative to control and A3-CP. Effluent creatine kinase activity was significantly decreased by A3-PTx (1520 ± 32 IU/L), A3-[PTx+CP] (1481 ± 41 IU/L) from control (1734 ± 54 IU/L) and A3-CP (1750 ± 43 IU/L). Myocardial edema (% tissue water) was significantly less in A3-PTx (78 ± 0.6%) and A3-[PTx+CP] (76% ± 2%) compared with control (85% ± 0.4%) and A3-CP (83% ± 2%).
Conclusions. Adenosine A3 receptor stimulation as a pretreatment attenuates postischemic cardiodynamic dysfunction and creatine kinase release but has no cardioprotection as an adjunct to cold cardioplegia.
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