Abstract

The effects of hypoxia and ischemia on the firing rate of fibrillation potentials in denervated rat muscle were examined. We recorded electromyograms from the denervated left extensor digitorum longus muscle. Hypoxia was induced by low-oxygen ventilation. Ischemia was established by ligating the abdominal aorta and inferior vena cava, with or without extracorporeal hindlimb perfusion. The fibrillation potential firing rate correlated with the PaO2 (P < 0.0001) and temperature (P = 0.0001). Fibrillation potentials disappeared after the initiation of ischemia and reappeared after restitution of blood flow; they disappeared during ischemia with extracorporeal perfusion. The attenuation curves for the firing rate of fibrillation potentials during ischemia were well-described by exponential curves, but there was no significant difference in the attenuation constants for circulatory arrest and perfusion with a physiologic salt solution. We conclude that the fibrillation potential firing rate is proportional to oxygen supply, presumably because of the rate of aerobic metabolism.

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