Non-adrenergic Vasoconstriction Produced by Halothane and Cyclopropane Anesthesia

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Abstract
Vasoconstrictor responses produced by halothane (1.5%) and by cyclopropane (35%) in the perfused dog gracilis muscle persisted in the face of complete blockade of alpha-adrenergic receptors, indicating that the responses were not mediated by systemic or local release of catecholamines. Utilizing extracorporeal perfusion of the muscle, vasoconstriction produced by cyclopropane was the result of a direct stimulant action on vascular smooth muscle, the direct effect of halothane was one of depression. The vasoconstriction with halothane was mediated indirectly through liberation from the hypophysis of a substance which is probably antidiuretic hormone (vasopressin). The indirect vasoconstrictor effect of halothane, by opposing the direct vascular depressant action, makes an important contribution to the overall hemodynamic consequences of halothane anesthesia.