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.