Excess purine degradation caused byanimbalance inthesupply ofadenosine triphosphate inpatients withcongestive heartfailure

To evaluatepurinedegradationin patients withcongestive heartfailure concentrations ofserum hypoxanthine, lactate,and noradrenalinewere measuredbeforeandaftersubmaximal treadmill exercise in 12 patientswith chroniccongestive heartfailure andnine healthyvolunteers. Infourpatients the concentration ofhypoxanthine was significantly higherthaninthecontrols or intheremaining eightpatients withcongestive heartfailure. Venouslactate and noradrenaline inthefourpatients with high concentrations of hypoxanthine werealsosignificantly higherthanthose intheeightpatients withnormalconcentrations of hypoxanthine. Patients whoresponded normally werealsomore likelyto have been treatedwith vasodilators andangiotensin converting enzymeinhibitors. Exercise inducedarrhythmiaswere more common in the patients withhighconcentrations of hypoxanthine. Theseresults suggestthattheexcess purinedegradation inpatients withcongestive heartfailure mightbetheresult ofa"relative" disturbance inthesupply ofadenosine triphosphate causedbythe shiftof cellularmetabolismfrom aerobic glycolysis toanaerobic glycolysis duringsubmaximalexercise and that hypoxanthine (asubstrate forxanthine oxidaseand a sourceoffreeradicals) wasincreased aftersubmaximalexercise insome patients withcongestive heart