The mechanism of the peripheral vascular resistance change during exposure of dogs to bromotrifluoromethane

Abstract

Thirtytwo male beagle dogs were used in 16 cross-circulation experiments wherein arterial blood from one dog (donor) was perfused at constant flow rate through a hind limb (HL) of another dog (recipient). The HL innervation remained intact. Exposure of the donor to 67–70% CBrF 3 was accompanied by a reversible decrease in the donor's mean arterial blood pressure. The HL perfusion pressure (and therefore vascular resistance in HL) was unaltered. Exposure of the recipient to 67–70% CBrF 3 was accompanied by a reversible decrease in the recipient mean arterial blood pressure and HL perfusion pressure. The HL perfusion pressure change was greatly attenuated by pretreatment of the HL with phenoxybenzamine and abolished by pretreatment of the recipient with hexamethonium. Nictitating membrane tension and vagal inhibition of the heart in response to electrical stimulation of the corresponding cut ends of the vagosympathetic trunks were measured in 5 dogs before, during and after exposure to 80% CBrF 3. The CBrF 3 exposure was accompanied by a reversible decrease in both nictitating membrane tension and vagal inhibition of the heart. The mechanism of the decrease in mean arterial blood pressure during CBrF 3 exposure was concluded to be a decrease in vasomotor tone resulting from ganglionic blockade. No direct vascular smooth muscle effect of CBrF 3 was observed.