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Ann Thorac Surg 1989;47:809-815
© 1989 The Society of Thoracic Surgeons
Section of Thoracic Surgery, The University of Michigan Medical Center, Ann Arbor, Michigan USA
* Address reprint requests to Dr Bolling, The University of Michigan Hospital, 2120D Taubman Center, Box 0344, 1500 E Medical Center Dr, Ann Arbor, MI 48109.
This study was undertaken to investigate whether adenosine administered during cardioplegic arrest could enhance myocardial protection and improve recovery of function after ischemia. Isolated perfused rabbit hearts were subjected to 120 minutes of hypothermic (32 °C) multidose cardioplegia-induced ischemia. Control hearts (n = 23) received modified St. Thomas's cardioplegia, and the remaining hearts received cardioplegia with either 100 µM (n = 11), 200 µM (n = 11), or 400 µM (n = 11) adenosine. After ischemia and 45 minutes of reperfusion, left ventricular contractility was superior in all groups of adenosine-treated hearts compared with control hearts. Furthermore, there was a significant incremental increase in functional recovery with increasing dose of adenosine. Postischemic diastolic stiffness was significantly better in all adenosine groups compared with controls. No differences were noted in coronary flow or myocardial water content between adenosinetreated and control hearts. These data demonstrate that adenosine administered in these concentrations provides myocardial protection and improved recovery of both systolic and diastolic function after global ischemia, presumably metabolically by reducing depletion of adenosine triphosphate or enhancing repletion of adenosine triphosphate and enabling improved postischemic recovery.
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