Chest
articlesEffect of Oxygen Concentration on Cellular Metabolism
Section snippets
Does Mitochondrial Oxidative Phosphorylation Act as a Sensor for Tissue Oxygen Concentration?
Many biochemical and physiologic parameters depend on tissue oxygen tension and, therefore, are potentially suitable for examining this question. One of the most dramatic is coronary flow. Over a wide range of cardiac work rates, coronary flow so precisely adjusts to oxygen utilization that the arterial-venous oxygen difference remains constant.1, 2, 3, 4 This phenomenon is observed in isolated perfused hearts, which indicates that it is due to local control, not to external neural or humoral
Summary
Mitochondrial oxidative phosphorylation is dependent on oxygen concentration in the physiologic range, expressed in alterations of the redox state of cytochrome c and [ATP]/[ADP]. In cells at oxygen concentrations greater than about 50 μM (≈30 mm Hg), [ATP]/[ADP][Pi] is usually greater than 1×104 M–1 and cytochrome c is approximately 15 percent reduced. When the oxygen concentration is lowered, the capacity of the mitochondria to synthesize ATP becomes limited, and the rate of ATP synthesis
Discussion
The discussion began with the locus of the possible energy sensor which regulated the coronary circulation. It was pointed out that in the heart the sensor for the energy levels regulating coronary flow is probably located in the myocardium rather than in the coronary arteries. The experiments to prove that coronary circulation is controlled by the energy potential in the myocardial cell and not the vessel wall would require separate biochemical analyses of myocardial cells and the vascular
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Supported by grant GM-21524 from the U.S. National Institutes of Health.