Influence of sympathetic nerves on oxygen uptake or resting mammalian skeletal muscle,.
Gracilis muscles of anesthetized dogs were isolated and perfused with blood at constant flow. Oxygen uptake (Vo2) was measured by spectrophotometry of paired arterial and venous samples and monitored by continuous recording of HbO2 saturation. The sympathetic chain, connected to the isolated muscles, was stimulated electrically with supramaximal pulses. High frequencies (8-16/s) increased vascular resistance (R, ratio to control 1.86 +/- 0.6 SEM) and decreased Vo2 (0.61 +/- 0.02). Both effects could be maintained 10 min or longer. After stimulation there was an increase in Vo2, which could be less than equal to, or greater than the O2 deficit, depending on the stimulation frequency, the period of stimulation, and the blood flow. Low frequencies (0.5-4/s) increased R (1.39 +/- 0.04) and increased Vo2 during (1,18 +/- 0.03) and after stimulation. In several experiments there was an initial decrease in Vo2 which changed to an increase during the stimulation period while R remained elevated. These observations indicate that the decrease in Vo2 is due to closure of precapillary sphincters, whereas the increase is a direct effect on cell metabolism.
D000818:Animals; D001285:Atropine / Q000494:pharmacology; D004285:Dogs; D004558:Electric Stimulation; D005260:Female; D005703:Gallamine Triethiodide / Q000494:pharmacology; D008297:Male; D009132:Muscles / Q000098:blood supply / Q000294:innervation / Q000378:metabolism*; D010101:Oxygen Consumption / Q000187:drug effects; D012018:Reflex; D012039:Regional Blood Flow; D013564:Sympathetic Nervous System / Q000502:physiology*; D014655:Vascular Resistance; D014666:Vasomotor System / Q000502:physiology
D001285:Atropine; D005703:Gallamine Triethiodide