PROTECTIVE EFFECTS OF ADENOSINE ON MYOCYTE CONTRACTILITY DURING CARDIOPLEGIC ARREST

Background. Adenosine delivery to the left ventricular myocardium has been demonstrated to provide protective effects in the setting of isch emia and reperfusion. However, whether adenosine has direct protective effects on isolated myocytes in the setting of cardioplegic arrest wa s unclear. Methods. Isolated porcine left ventricular myocytes were as signed to one of the following treatment groups: (1) cardioplegia: 24 mEq/L K+, 4 degrees C for 2 hours followed by rewarming (cell media, 3 7 degrees C; n = 29); (2) cardioplegia augmented with adenosine (1 to 200 mu mol/L) followed by rewarming (n = 98); and (3) normothermic con trol (cell media, 37 degrees C, 2 hours; n = 175). Myocyte contractili ty was measured by computer-aided videomicroscopy. Results. Cardiopleg ic arrest and rewarming reduced myocyte shortening velocity compared w ith normothermic control (25.3 +/- 2.5 mu m/s versus 50.9 +/- 1.4 mu m /s, p < 0.05). Adenosine-augmented cardioplegic arrest improved myocyt e contractility with rewarming in a concentration-dependent fashion. F or example, cardioplegia augmented with 10 mu mol/L adenosine improved myocyte shortening velocity by 33% (33.6 +/- 3.0 mu m/s versus 25.3 /- 2.5 mu m/s, p < 0.05), whereas 200 mu mol/L adenosine improved shor tening velocity by 97% (49.9 +/- 3.4 mu m/s vs 25.3 +/- 2.5 mu m/s, p < 0.05) compared with conventional cardioplegia. Conclusions. This stu dy demonstrated concentration-dependent protective effects of adenosin e-augmented cardioplegia on myocyte contractile function with subseque nt reperfusion and rewarming. These results suggest that stimulation o f putative myocyte adenosine receptors may provide enhanced protective effects on myocyte contractile processes during cardioplegic arrest. (C) 1997 by The Society of Thoracic Surgeons.