Circulatory Responses to Chemical Stimulation of Oxygen Uptake in Canine Hindlimb

Abstract

The increase in blood flow that occurs with stimulation of oxygen uptake in skeletal muscle is caused by at least three potential vasodilatory inputs to the area, according to Honig (1979). One of these, active sympathetic vasodilation, is dependent on extrinsic innervation and is usually seen as a transient response in anticipation of exercise. That would hardly apply in an anesthetized dog. The early increase in blood flow to contracting muscle in such a case can be attributed to the action of intrinsic nerves with neuronal cell bodies in the wall of small arteries and arterioles. The blood flow response would then be reinforced and sustained by metabolic vasodilation, which has a slower onset, in the unifying hypothesis of exercise vasodilation proposed by Honig. I thought that a rather neat test to this hypothesis could be made by chemically stimulating oxygen uptake in the hindlimb of an anesthetized dog by local injection of 2,4-dinitrophenol (DNP), an uncoupler of oxidative phosphorylation. This would avoid stimulation of intrinsic nerves while still supplying metabolic stimulation and would thus allow separation of the two potential vasodilator influences.

Supported by Research Grants HL 14693 and HL 26927, National Heart, Lung, and Blood Institute.