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Ann Thorac Surg 1994;58:1637-1644
© 1994 The Society of Thoracic Surgeons

Articles

Adenosine in blood cardioplegia prevents postischemic dysfunction in ischemically injured hearts

Dudley A. Hudspeth, MD, Katsuhiko Nakanishi, MD, Jakob Vinten-Johansen, PhD*, Zhi-Qing Zhao, MD, PhD, D.Scott McGee, BS, Mark W. Williams, BS, John W. Hammon, Jr, MD

Department of Cardiothoracic Surgery, The Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, North Carolina USA

Accepted for publication May 19, 1994.

* Address reprints requests to Dr Vinten-Johansen, Department of Cardiothoracic Surgery, The Bowman Gray School of Medicine, Medical Center Blvd, Winston-Salem, NC 27157-1096.

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) supplemented with ADO reduces postischemic left ventricular dysfunction in ischemically injured hearts. Twenty-one anesthetized dogs on total bypass were subjected to 30 minutes of normothermic global ischemia. Cold (4 °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 µmol/L ADO; and, in 7 dogs, ADO receptors were blocked with 8-p-sulfophenylthecohylline (30 mg/kg) given with 400 µmol/L ADO in BCP. Preischemic and postischemic left ventricular systolic function was assessed by the slope and volume axis intercept of the end-systolic pressure-volume (impedance catheter) relationship (ESPVR). In unsupplemented BCP, the postischemic slope of the ESPVR was significantly depressed by 42% versus the preischemic value (from 6.8 ± 1.2 mm Hg/mL to 3.9 ± 0.4 mm Hg/mL; p < 0.05 versus the preischemic value). In contrast, BCP supplemented with ADO was 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). This 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 preischemic value). Postischemic plasma creatinine kinase activity was elevated equally in all groups over the baseline values. We conclude that ADO in BCP attenuates postcardioplegia dysfunction in severely injured hearts through the operation of receptor-mediated mechanisms.




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