Detection of intracellular anoxia and its relationship to onset of hemodynamic dysfunction and ST-segment elevation in the intact dog heart.

Abstract

The temporal relationships among onset of cellular anoxia after coronary artery occlusion, contractile dysfunction, and electrocardiographic ischemia were studied in dogs with an intact circulation. Nicotinamide adenine dinucleotide (NADH) fluorescence was used to detect intracellular anoxia, using a fiber-optic method. Paired NADH concentrations from ischemic (394 +/- 10 mumol/g) and normoxic (285 +/- 11 mumol/g) regions of the heart were obtained, and the differences (delta[NADH]) were correlated with compensated fluorescence (r = 0.76, P less than 0.01). Onset of fluorescence occurred 1 to 2 sec after coronary artery occlusion, followed by hemodynamic (5 sec) and electrocardiographic (13 sec) changes. These data indicate that intracellular anoxia, with alterations in redox potential, is not synchronous with the onset of contractile failure and provide indirect support for intracellular acidosis as the likely mediator of contractile failure.