PERIPHERAL CIRCULATORY AND METABOLIC REACTIONS ASSOCIATED WITH ERGOTOXINE HYPER- AND HYPOTHERMIA IN ADULT ALBINO RATS

Abstract

Simultaneous recording of body and skin temps. and oxygen consumptions of Sprague-Dawley albino rats, with and without ergotoxine and under basal and cold-stress environmental conditions, indicated that ergotoxine hyper-thermia is due to a combination of peripheral vasoconstriction and increased metabolic activity. Peripheral vascular reactions were evaluated through the use of Burton''s "thermal circulation index." Both heat conservation and heat production mechanisms are believed to be activated through direct stimulation of hypo-thalamic centers by ergotoxine. Vasoconstriction, continued beyond the height of the hyperthermic reaction and associated with a rapid decrease in metabolism, as indicated by reduced oxygen consumption, is thought to be due to direct action of the drug upon the smooth musculature of peripheral vessels. Uninjected rats responded to cold stress by prompt and sustained peripheral vasoconstriction, while those given ergotoxine intraperit. exhibited marked vasodilatation, which was interpreted* as being due to epinephrine reversal. The peripheral vasodilatation of ergotoxine-injected rats, under cold stress, resulted in marked reduction in body temp.; this, in turn, appeared to decrease reaction rates of enzyme systems essential to heat production with consequent failure of such animals to use oxygen at as high rates as control animals subjected to the same environment.