Cutaneous and skeletal muscle vascular responses to hypothermia

Vascular resistance and capacitance were studied in innervated or denervated canine forelimbs. Hypothermia (38-28 degrees C) was induced systemically, by external cooling of blood which returned to the right heart, or locally, by cooling blood perfusing the forelimb. Systemic cooling to 33 and then to 28 degrees C elicited significant decreases in limb weight with substantial increases in both skin and skeletal muscle vascular resistances. Acute denervation of the forelimbs attenuated both the fall in limb weight and increase in skin vascular resistance associated with cooling. These data support the contention that cutaneous vasoconstriction during systemic cooling is mediated primarily by sympathetic nerves, whereas skeletal muscle vasoconstriction is mediated primarily by circulating hormones. Local cooling elicited skin and skeletal muscle vascular dilation at 33 degrees C in both innervated and denervated forelimbs whereas either no change or a slight increase in skin and skeletal muscle vascular resistance resulted upon local cooling to 28 degrees C, perhaps due to the inhibition of Na+ - K+ - ATPase activity and/or a rise in blood viscosity. The locally induced vasodilation was found to override the powerful vasoconstrictor response caused by systemic cooling. The vasodilation is considered active rather than passive, because the increase in forelimb weight and decreases in forelimb vascular resistances occurred in the denervated as well as innervated limbs.