Effect of Nitric Oxide on Oxygen Consumption of Skeletal Muscle

Mammalian cells require a continuous and sufficient supply of oxygen to carry out their functions. The oxygen pathway has an overall direction taking O2 from the air to the mitochondria, which is a result of the mitochondrial O2 consumption (VO2) NO various effects on the mitochondria: at low concentrations for short periods NO specifically and irreversibly inhibits cytochrome c and reversibly inhibits cytochrome c oxidase, to decrease VO2. Thus, NO can modulate VO2 of skeletal muscle. The purpose of the present study was to measure VO2 of the rat spinotrapezius muscle under conditions of altered NO. The methods used provide a direct way to measure PO2 in the interstitium (PISFO2) and use it as indicator of local metabolic changes. Intravital microscopy and phosphorescence quenching were used to record PISFO2 in resting muscle for 120 s before, 60 s during, and 420 s after a period of tissue compression that abruptly halted perfusion. Control VO2 measurements were made, followed by those in which the spinotrapezius muscle had been treated by topical application of agents known to alter NO levels (L-NAME, C-PTIO, Sperm/NO). The compression was achieved by rapid inflation of a Saran film air bag, attached to a X20 objective lens, which pressed the muscle against the animal platform. The rapid pressure onset (0-120 mmHg in ISFO2, which started immediately after the airbag inflation, was used to calculate VO2 and was based on the assumption that the amount of blood in the tissue after compression was small. Control VO2 was 5.91 ± 0.2 ml O2 · kg-1 · min-1. Since the presence of RBCs sequestered in capillaries cannot be ruled out during compression, this value can be considered a lower limit for VO2 by resting muscle. Comparison of baseline and treatment measurements of VO2 showed no significant differences between them. This was unexpected based on in vitro studies and may reflect an impaired ability of the agents used to alter NO at the mitochondrial level