Oxidative Phosphorylation in Hypoxic Airway Smooth Muscle

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Abstract
The impairment of mechanical function that we have previously reported in tracheal smooth muscle under conditions of hypoxia and substrate depletion may be due to a defect in the utilization of the energy produced, to a decrease in energy production in the muscle after the hypoxic inhibition of mitochondria, or to a combination of these. To test the second hypothesis mitochondria were isolated from the trachealis smooth muscle of dogs whose had been maintained at 30 mm Hg ± 7 (S.E.), for 1 h before death. Studies of oxidative phosphorylation revealed no significant differences in ADP/O ratios in these mitochondria as compared with normal nor was there any significant difference in rate of O2 uptake as long as ADP was available (state 3 respiration). However, there was a significant difference in respiratory control ratios (R.C.R.), generally regarded as the most sensitive biochemical index of the function integrity of mitochondria, as well as a significant difference between control and experimental conditions in the rate of O2 uptake when ADP was not available (state 4 respiration). These findings suggested loose coupling between electron transport and oxidative phosphorylation.

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