ADENOSINE IN BLOOD CARDIOPLEGIA PREVENTS POSTISCHEMIC DYSFUNCTION IN ISCHEMICALLY INJURED HEARTS

Adenosine (ADO) is an endogenous cardioprotective autacoid that exerts receptor-mediated cardioprotection from ischemic-reperfusion injury. This study tested the hypothesis that blood cardioplegia (BCP) supplem ented with ADO reduces postischemic left ventricular dysfunction in is chemically injured hearts. Twenty-one anesthetized dogs on total bypas s were subjected to 30 minutes of normothermic global ischemia. Cold ( 4 degrees C) potassium BCP was then delivered every 20 minutes for 60 minutes of cardioplegic arrest. In 7 dogs, unsupplemented BCP was used ; in 7 dogs, BCP was supplemented with 400 mu mol/L ADO; and, in 7 dog s, ADO receptors were blocked with 8-p-sulfophenyltheophylline (30 mg/ kg) given with 400 mu mol/L ADO in BCP. Preischemic and postischemic l eft ventricular systolic function was assessed by the slope and volume axis intercept of the end-systolic pressure-volume (impedance cathete r) relationship (ESPVR). In unsupplemented BCF, the postischemic slope of the ESPVR was significantly depressed by 42% versus the preischemi c value (from 6.8 +/- 1.2 mm Hg/mL to 3.9 +/- 0.4 mm Hg/mL; p < 0.05 v ersus the preischemic value). In contrast, BCP supplemented with ADO w as found to restore the postischemic ESPVR slope to preischemic levels (7.7 +/- 1.0 mm Hg/mL versus 7.4 +/- 1.2 mm Hg/mL, respectively). Thi s cardioprotection was reversed by 8-p-sulfophenyltheophylline (9.9 +/ - 1.5 mm Hg/mL versus 4.5 +/- 0.7 mm Hg/mL; p < 0.05 versus the preisc hemic value). Postischemic plasma creatinine kinase activity was eleva ted equally in all groups over the baseline values. We conclude that A DO in BCP attenuates postcardioplegia dysfunction in severely injured hearts through the operation of receptor-mediated mechanisms.