Key result
Transient anoxia and elevation of heart rate in open-chest dogs caused rapid elevation in intramitochondrial NADH levels, indicating changes in myocardial oxygen balance despite autoregulation.
This experimental model demonstrates that autoregulation of coronary blood flow during increased heart rate may not fully compensate for myocardial oxygen demand, as evidenced by persistently elevated NADH levels.
Suggests coronary autoregulation may incompletely compensate for myocardial oxygen demand during stress; hypothesis-generating for human ischemia and requires clinical validation.
Quantitative evaluation of myocardial oxygen balance can be accomplished by measurement of oxygen supply, demand, and intracellular oxygen concentration. Experimentally, these parameters are often related to coronary blood flow, cardiac contractility, and mitochondrial NADH redox level, respectively. Methods were developed to measure these three parameters in a local region on the myocardial surface in open-chest dogs. Local coronary blood supply was measured with the aid of a small surface thermistor, and cardiac work with a miniature strain gauge arch. NADH oxidation--reduction state was recorded using surface fluorometry through a fibre optic light guide. Transient anoxia produced by nitrogen breathing caused a rapid but reversible elevation in NADH levels, which was not always accompanied by a concomitant change in contractile force. Elevation of heart rate resulted in a rise in intramitochondrial NADH followed by an increase in coronary flow. In spite of the increased flow, NADH levels remained elevated, indicating a change in the O2 balance; this may indicate that autoregulation does not necessarily result in total compensation.
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Kedem et al. (1981) studied Myocardial oxygen balance. Transient anoxia and elevation of heart rate vs. Baseline was evaluated on NADH levels, contractile force, and coronary flow. Transient anoxia and elevation of heart rate in open-chest dogs caused rapid elevation in intramitochondrial NADH levels, indicating changes in myocardial oxygen balance despite autoregulation.
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