Hemodynamic effects of aerosol propellants. III. Vascular resistance in the canine hind limb

The question as to whether or not the hypotension observed as part of the effect of tricholorofluoromethane (FC11), dichlorofluoromethane (FC 12), dichlorotetrafluoroethane (FC 114) and methyl chloroform was due to a vasodepressor component of action, in addition to the previously documented depression in myocardial contractile force, was answered by testing these agents in an anesthetized dog preparation in which one hind limb was perfused at constant flow through the femoral artery. 5% FC 11, 20% FC 12 and 20% FC 114 decreased vascular resistance of the perfused limb, as reflected by decrease in mean femoral arterial perfusion pressure, in vagotomized but not in intact preparations. Methyl chloroform decreased vascular resistance even in intact preparations. Spontaneous blood flow in the intact femoral artery decreased following FC 11 and methyl chloroform administration in vagotomized preparations and was associated with marked decrease in mean aortic pressure. Blockade of alpha and beta adrenergic receptors with phentolamine and propranolol in the vagotomized preparation had no modifying influence of the effect of FC 11 and methyl chloroform. It may be concluded from this study that FC 11, FC 12 and FC 114 exhibit a vasodepressor activity on skeletal muscle vascular bed which is readily overcome by the hypotension-induced activation of the sympathetic system but which becomes evident when reflex activity is prevented by vagotomy. Methly choloroform exhibits a vasodepressor effect even in intact preparations probably because of concomitant depression of reflex activity through its general anesthetic action. A decrease in spontaneous femoral blood flow following FC 11 and methyl chloroform administration is referable to the accompanying severe hypotension notwithstanding concomitant vascular relaxation. Neither FC 11 nor methly chloroform directly liberate catecholamines from their sites of storage.