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Catabolism of adenine nucleotides in the human heart before and after cardiac bypass surgery

Uric acid (UA) is a catabolite of the high‐energy purine phosphates and of purines in DNA and RNA. Thus, cardiac net release of UA could prevail in subjects with chronic myocardial ischemia and during coronary occlusion associated with cardiac artery bypass grafting surgery (CABG). However, in acute reperfusion, reactive oxygen species could cause chemical degradation of urate, perhaps even giving rise to a negative coronary arteriovenous difference. Blood was sampled simultaneously from the arterial and coronary venous system of 24 patients undergoing elective CABG. Blood was immediately deproteinated (0.4 M HClO4) in the presence of the glutathione‐scavenger N‐ethylmaleimide (60 mM), and the supernatant was analysed for UA, purines, and glutathione by high performance liquid chromatography. Before the operation, CABG patients revealed a small, but significant net production of UA in the heart (+28 μmol/liter whole blood; arterial level, 223±71 μM; mean± SD). There were no coronary differences for adenosine, inosine, or hypoxanthine. UA release was not elevated in early reperfusion after cardiac arrest and tended to decrease by 20–40 min of reperfusion (coronary sinus UA 10–18 μM above arterial level, not significant). Adenosine levels were <0.2 μM at all times in all blood samples. Coronary sinus (CS) inosine levels rose approximately 10‐fold during early reperfusion to 2 μM (not significant). However, CS hypoxanthine increased significantly from 8 (±3) to 35 (±14) μM at 1 min reperfusion, but after 5 min had returned to 15 μM. There was a net release of reduced glutathione from the hearts before intervention, and individual changes in coronary glutathione levels were approximately parallel to those of urate in early reperfusion. Surprisingly, urate release did not correlate to the duration of cardiac ischemia (crossclamp time). Thus, in human hearts with chronic ischemia, myocardial release of uric acid is approximately 10–30% higher than the arterial input, indicative of a pronounced catabolic state of the tissue. Metabolic recovery after CABG requires more than 1 h. Hypoxanthine (and not urate) is the better marker of acute myocardial nucleotide catabolism in early postischemic reperfusion. Adenosine underlies a tight homeostasis in the coronary system. The correlation of urate and glutathione release suggests that membrane perturbation may accompany and/or contribute to nucleotide catabolism. Drug Dev. Res. 45:159–165, 1998. © 1998 Wiley‐Liss, Inc.