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1 Department of Pharmacology, College of Medicine, University of Iowa, Iowa City, Iowa
The vasoconstrictor action of halothane in skeletal muscle was shown previously to be mediated indirectly by liberation of vasopressin. In the present experiments it was demonstrated that during halothane (1%) inhalation vascular resistance in skin is decreased at the time when muscle vascular resistance increases. An attempt was made to determine why halothane administration fails to increase vascular resistance in skin vessels, which are presumably exposed to the same concentration of vasopressin. Responses to norepinephrine, angiotensin, vasopressin and sympathetic nerve stimulation were measured in isolated and separately perfused skin and muscle vessels. Halothane administration produced a parallel reduction in respouses of skin and muscle vessels to norepinephrine, angiotensin and sympathetic nerve stimulation. However, the response to vasopressin in skin was depressed significantly more than in muscle. It was concluded that halothane administration produces a general depression of vasoconstrictor responses but specifically depresses the response to vasopressin in skin, thus preventing an increase in skin vascular resistance.
Submitted on January 13, 1969