Protective effects of adenosine on myocyte contractility during cardioplegic arrest

Adenosine delivery to the left ventricular myocardium has been demonstrated to provide protective effects in the setting of ischemia and reperfusion. However, whether adenosine has direct protective effects on isolated myocytes in the setting of cardioplegic arrest was unclear.

Isolated porcine left ventricular myocytes were assigned to one of the following treatment groups: (1) cardioplegia: 24 mEq/L K+, 4 degrees C for 2 hours followed by rewarming (cell media, 37 degrees C; n = 29); (2) cardioplegia augmented with adenosine (1 to 200 micromol/L) followed by rewarming (n = 98); and (3) normothermic control (cell media, 37 degrees C, 2 hours; n = 175). Myocyte contractility was measured by computer-aided videomicroscopy.

Cardioplegic arrest and rewarming reduced myocyte shortening velocity compared with normothermic control (25.3 +/- 2.5 microm/s versus 50.9 +/- 1.4 microm/s, p < 0.05). Adenosine-augmented cardioplegic arrest improved myocyte contractility with rewarming in a concentration-dependent fashion. For example, cardioplegia augmented with 10 micromol/L adenosine improved myocyte shortening velocity by 33% (33.6 +/- 3.0 microm/s versus 25.3 +/- 2.5 microm/s, p < 0.05), whereas 200 micromol/L adenosine improved shortening velocity by 97% (49.9 +/- 3.4 microm/s vs 25.3 +/- 2.5 microm/s, p < 0.05) compared with conventional cardioplegia.

This study demonstrated concentration-dependent protective effects of adenosine-augmented cardioplegia on myocyte contractile function with subsequent reperfusion and rewarming. These results suggest that stimulation of putative myocyte adenosine receptors may provide enhanced protective effects on myocyte contractile processes during cardioplegic arrest.