Abstract
Thermoregulatory characteristics of neurogenic hyperthermia produced in rats by unilateral mechanical destruction of the rostral hypothalamic/preoptic region were studied. Investigational methods employed included observing thermoregulatory effector activities which were responsible for generation of hyperthermia, observing thermoregulatory reactions elicited by forcefully elevating or lowering core temperature during neurogenic hyperthermia, and observing the effect of ambient temperature on hyperthermia magnitude. At 26.degree. C, hyperthermia was effected by a transient increase in shivering thermogenesis and a concomitant minimization of heat loss through the tail. At 26.degree. C, perturbations of core temperature during plateau phase of hyperthermia were induced by internal or external heating and cooling. Disturbances elicited compensatory changes in shivering activity and tail vasomotor tonus, and core temperature was rapidly and precisely returned to its pre-perturbation level. Magnitudes of hyperthermias experienced by rats lesioned at 10, 15, 26 and 32.degree. C, as measured by change in colonic temperature and by area under fever curve, were not significantly different. At 36.degree. C, rats were hyperthermic prior to lesioning and the magnitude of lesion-induced hyperthermia was significantly attenuated. Neurogenic hyperthermia produced by unilateral hypothalamic puncture in the rat was generated by a coordinated modulation of thermogenic and heat retentive effectors. Plateau level of hyperthermia was well regulated. These characteristics are compatible with the hypothesis that neurogenic hyperthermia was mediated by prostaglandins released from injured tissue and acting on surviving rostral hypothalamic tissue.