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(Circulation. 1999;100:II-376.)
© 1999 American Heart Association, Inc.

Myocardial Protection and Vascular Biology

Adenosine-Supplemented Blood Cardioplegia Attenuates Postischemic Dysfunction After Severe Regional Ischemia

Vinod H. Thourani, MD; Russell S. Ronson, MD; David G.L. Van Wylen, PhD; Steven T. Shearer, BS; Sara L. Katzmark, BS; Zhi-Qing Zhao, PhD; David C. Han, MD; Robert A. Guyton, MD; Jakob Vinten-Johansen, PhD

From the Division of Cardiothoracic Surgery, Department of Surgery, Carlyle Fraser Heart Center-Cardiothoracic Research Laboratory, Crawford Long Hospital of Emory University School of Medicine, Atlanta, Ga.

Correspondence to Jakob Vinten-Johansen, PhD, Cardiothoracic Research Laboratory, Crawford Long Hospital, 550 Peachtree Street, NE, Atlanta, GA 30365-2225. E-mail jvinten{at}emory.edu

Background—Various studies have reported that the administration of adenosine (ADO) in cardioplegia reduces myocardial ischemic injury, but this timing may not utilize ADO’s potential against myocardial reperfusion injury. This study tested the hypothesis that ADO-supplemented blood cardioplegia (BCP) or ADO administered during reperfusion reduces postischemic dysfunction after severe regional ischemia.

Methods and Results—After 75 minutes of left anterior descending coronary artery occlusion, total cardiopulmonary bypass was initiated; cold (4°C) antegrade BCP (8:1 blood:crystalloid) was delivered every 20 minutes for the first 3 doses, and 27°C BCP was delivered for the terminal infusion. Dogs (n=6 per group) received unsupplemented BCP, ADO (100 µmol/L/L) supplemented in all infusions of BCP (ADO-CP), or ADO (100 µmol · L^-1 · L^-1) supplemented only in the terminal infusion of BCP followed by intravenous ADO (140 µg · kg^-1 · min^-1) infusion for the first 30 minutes of reperfusion (ADO-R). Postischemic regional systolic shortening was significantly greater in the ADO-R group (5±2.0%) than in the BCP group (-3±1.0%), but not in the ADO-CP group (2±0.2%). Postischemic regional diastolic stiffness in the area at risk during end reperfusion was lower with ADO-R (1.8±0.3%) than with ADO-CP (2.7±0.3%) or BCP (4.4±0.5%). Infarct size was reduced in the ADO-CP (29±2%) and ADO-R (21±2%) groups compared with the BCP group (42±4%). Edema in the myocardial area at risk was decreased in the ADO-CP (82±0.2%) and ADO-R (80±0.4%) groups compared with the BCP group (86±0.7%). Adherence of fluorescently labeled neutrophils (PMNs) to postischemic coronary artery endothelium was attenuated by ADO-R (55±2 PMNs/mm²), but not by ADO-CP (114±5 PMNs/mm²), compared with BCP (118±3 PMNs/mm²).

Conclusions—The results show that BCP supplemented with ADO reduces infarct size, preserves postischemic systolic and diastolic regional function but does not attenuate coronary artery endothelial dysfunction unless administered during reperfusion.

Key Words: adenosine • cardioplegia • myocardial protection