PERFUSION DELAY CAUSES UNINTENTIONAL ISCHEMIC PRECONDITIONING IN ISOLATED HEART PREPARATION

This study sought to show that unintentional preconditioning can be in duced in the isolated perfused heart during the preparation procedure. The following four groups were compared: hearts were placed in ice co ld saline and cooled for 5s and then mounted to the Langendorff appara tus (n = 5; cool immediate group); hearts were cooled for 60 s and mou nted (n = 5; cool delay group); hearts were mounted directly to the ap paratus within 15 s after the isolation without cooling (n = 5; non co ol immediate group); hearts were mounted without cooling, but the moun ting was delayed for 60 s after the isolation (n = 5; noncool delay gr oup). All hearts were paced at a fixed rate of 300 bpm, and an occlusi on of left coronary (LCA) for 60 min was performed, which was followed by reperfusion for another 60 min. Coronary flow (CBF)? left ventricu lar developed pressure (LVDP), and creatine phosphokinase (CPK) releas e did not change among the four groups during ischemia. At the end of reperfusion the LVDP values were 70 +/- 1%, 66 +/- 2%, 62 +/- 3%, and 73 +/- 2% of preischemic values in cool immediate, cool delay, noncool immediate and noncool delay groups, respectively. CPK values were 116 +/- 4, 121 +/- 7, 138 +/- 6, and 29 +/- 1 x 10(3) U/g myocardium, and percentage necrosis/risk areas were 24 +/- 1.0%, 21 +/- 1.7%, 38 +/- 2.6%, and 13 +/- 0.5% in cool immediate, cool delay, noncool immediate , and noncool delay groups, respectively. The noncool delay group demo nstrated high LVDP, least amount of CPK release, and smallest size of necrosis. These results indicate that an unintentional preconditioning effect can be induced when the cooling procedure is not applied and p erfusion is delayed.