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J Thorac Cardiovasc Surg 1995;110:63-74
© 1995 Mosby, Inc.
CARDIOPULMONARY BYPASS, |
Madison, Wis.
Supported by National Heart, Lung, and Blood Institute grant HL-34579-08.
Received for publication June 2, 1994. Accepted for publication Oct. 24, 1994. Address for reprints: Robert M. Mentzer, Jr., MD, Chairman, Division of Cardiothoracic Surgery, University of Wisconsin, Department of Surgery, Clinical Science Center, H4/358, 600 Highland Ave., Madison, WI 53792.
Abstract
Augmentation of endogenous adenosine levels is associated with decreased myocardial ischemic-reperfusion injury. The purpose of this study was to determine whether exogenous adenosine administered before ischemia could attenuate postischemic myocardial dysfunction. Regional myocardial stunning was induced by 15 minutes of coronary artery occlusion and 90 minutes of reperfusion in an open-chest canine preparation. Regional ventricular function was assessed by measurement of systolic wall thickening. Control untreated hearts were compared with two groups of hearts treated immediately before ischemia with intracoronary adenosine (5µg/kg per minute and 50µg/kg per minute). A fourth group of hearts was treated for the first 30 minutes of reperfusion with adenosine (50µg/kg per minute). Preischemic adenosine administration increased coronary flow sixfold to sevenfold without altering regional function, mean arterial pressure, or left ventricular end-diastolic pressure. Both adenosine pretreatments attenuated stunning compared with results in control animals (14.7%±5.1% and 21.6%±7.3% of preischemic systolic wall thickness versus -14.0%±10%). Adenosine treatment during reperfusion transiently increased function in parallel with increased coronary blood flow, but after termination of the infusion regional function was not different from that in control stunned hearts (-5.0%±13.1% of preischemic systemic wall thickness). These results indicate that adenosine pretreatment is associated with attenuation of stunning, an effect that can be produced at doses that do not alter systemic hemodynamics. (J THORAC CARDIOVASC SURG 1995;110:63-74)
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