Participation of Oxygen in the Local Control of Skeletal Muscle Microvasculature
The control of the local supply of oxygen to a skeletal muscle vascular bed was analyzed by: (1) determining if a relative oxygen lack causes vascular dilation, (2) ascertaining the vascular elements responsible for the dilation, and (3) attempting to elucidate the mechanism of the dilation. When the concentration of oxygen in the inspiratory air was reduced from that in room air to 18% without increasing the carbon dioxide concentration or inducing a fall in systemic arterial blood pressure, a dilation significant at the 5% level was observed in the terminal arterioles, the metarterioles, and the distribution arterioles of the cremaster muscle of the rat; all of these vessels were oriented transversely to the skeletal muscle fibers and had diameters of less than 40µ. The magnitude of the dilation, expressed as a percent of the control diameter, was inversely related to the vessel's average control diameter. No significant dilation was noted in the precapillary sphincters or the major arterioles with control diameters greater than 40µ. Intra-arterial injections of sodium cyanide produced responses that paralleled in relative magnitude those observed in similar vessels during hypoxia. The microcirculatory adjustments to mild systemic hypoxia were not altered by pharmacological blockade of sympathetic ganglia or α, β, γ, or histaminergic receptors.
- Received January 15, 1973.
- Accepted October 15, 1973.
- © 1974 American Heart Association, Inc.