A fluorometric study of oxidative metabolism in the in vivo canine heart during acute ischemia and hypoxia.

Optical techniques for monitoring the fluorescence of intramitochondrial nicotinamide adenine dinucleotide (NADH) were employed to allow an on-line, non-invasive study of the metabolic state of healthy and ischemic cardiac tissue in the intact dog. Acute interruption of blood flow to the area of myocardium studied resulted in an immediate rise in NADH, indicating impairment of oxidative metabolism due to limitation of oxygen availability. Release of the coronary artery occlusion resulted in an oxidation of NADH to preocclusion baseline and signaled repayment of incurred O2 debt. Collateral flow produced a spontaneous fall in NADH levels towards preocclusion baseline. Hypoxic tissue was recognized by an oxidation of NADH on ventilation with 100 per cent O2, while in normal hearts no oxidation indicated the O2 was not rate limiting. Ischemic NADH increases preceded the onset of epicardial EKG changes, suggesting that an inability to rephosphorylate ADP to ATP is the primary cause of the EKG changes. Fluorometry of the in vivo heart provides a sensitive, continuous technique of monitoring cardiac cellular mitochondrial NAD;NADH redox levels and, therefore, the adequacy of high energy phosphate production and allows localization of cardiac tissue with marginal oxygen supply.