Abstract
The purpose of this study was to examine whether oxygen supply is critical to the generation of fibrillation potentials in the denervated rat muscle. Twenty-eight male Wistar rats each weighing between 200 and 352 grams were used. All procedures were performed under general anesthesia with thiopental sodium (80mg/kg). Denervated muscle was prepared by resection of the left sciatic nerve in the upper thigh region. A needle electromyogram was recorded in the left extensor digitorum longus muscle one week after resection of the nerve. Fibrillation potentials were observed in all rats. The effects of arrested circulation and hypoxia induced by controlled ventilation on fibrillation potentials were examined. Fibrillation potentials first transiently increased, then decreased exponentially and disappeared after the circulation had been arrested by ligating the abdominal aorta and inferior vena cava. Fibrillation potentials recovered rapidly after renewal of circulation. In other experiments in which blood flow was replaced by infusion of a physiologic solution via the abdominal aorta, fibrillation potentials transiently increased, then decreased exponentially, and finally disappeared during irrigation. The interval between circulatory arrest and disappearance of the fibrillation potentials was 406±171sec (mean±standard deviation, n=14), and it showed no statistically significant difference from the interval (454±270sec) between the start of irrigation and disappearance of the fibrillation potentials. Secondly, the fibrillation potential firing rate always decreased in hypoxia due to low-oxygen ventilation (n=14). The firing rate during hypoxia (partial pressure of arterial blood oxygen: Pao2=39.0±10.1torr) averaged 40.1% of the firing rate during room-air ventilation (Pao2=88.6±5.7torr). According to these results, it can be concluded that the generation of fibrillation potentials depends on oxygen supply.
