The onset of global myocardial ischemia was related to mechanical function (intraventricular pressure), cellular redox state (NADH fluorophotography), and high energy phosphate profile (phosphorous-31 nuclear magnetic resonance). Ten rabbit hearts were excised and perfused on a modified Langendorff apparatus (37°C; pO2 480 Torr). Developed pressure and positive and negative dp/dt were determined at control, 1-10, 15, 30, 45, and 60 sec of acute global ischemia. NADH fluorophotographs were taken at control, 1-10, 15, 20, 30, 60 sec, and 5, 10, and 30 min. P-31 NMR spectra in 14 guinea pig hearts under identical conditions were obtained at control, 1, 5, 10, 20, 40, and 60 min of acute global ischemia. LV contractility diminished within 1 sec (P < 0.01) of ischemia and dropped to less than 35% of control by 1 min. Reduction of mitochondria was detected by epicardial NADH fluorophotography at 2 sec of ischemia. Cellular pH diminished 0.3 pH units by 5 min. Adenosine triphosphate (ATP) concentration remained at control levels while phosphocreatine (PCr) dropped to 63 ± 8.5% of control by 1 min of ischemia. Conclusions: After the onset of global ischemia (1) mitochondrial electron transport ceases by 2 sec; (2) acidosis develops immediately; (3) LV contractility diminishes by 1 sec; (4) ATP concentration appears to be buffered by PCr, and is dissociated from myocardial function.
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