Thermoregulatory characteristics of neurogenic hyperthermia in the rat.

Abstract

SUMMARY1. The thermoregulatory characteristics of the neurogenic hyperthermia produced in rats by unilateral mechanical destruction of the rostral hypothalamic/preoptic region were studied.2. The investigational methods employed included (a) observing the thermoregulatory effector activities which were responsible for generation of hyperthermia, (b) observing the thermoregulatory reactions elicited by forcefully elevating or lowering core temperature during neurogenic hyperthermia and (c) observing the effect of ambient temperature on hyperthermia magnitude.3. At 26 0C, hyperthermia was effected by a transient increase in shivering thermogenesis and a concomitant minimization of heat loss through the tail.4. At 26 0C, perturbations of core temperature during the plateau phase of hyperthermia were induced by internal or external heating and cooling. The disturbances elicited compensatory changes in shivering activity and in tail vasomotor tonus, and core temperature was rapidly and precisely returned to its pre-perturbation level.5. The magnitudes of hyperthermias experienced by rats lesioned at 10, 15, 26 and 32 0C, as measured by the change in colonic temperature and by the area under the fever curve, were not significantly different. At 360C, rats were hyperthermic prior to lesioning, and the magnitude of the lesion-induced hyperthermia was significantly attenuated. 6. The results indicate that the neurogenic hyperthermia produced by unilateral hypothalamic puncture in the rat is generated by a coordinated modulation of thermogenic and heat retentive effectors and that the plateau level of hyperthermia is well regulated. These characteristics are compatible with the hypothesis that neurogenic hyperthermia is mediated by prostaglandins released from injured tissue and acting on surviving rostral hypothalamic tissue.

Interleukin-1 mediates endothelin-1-induced fever and prostaglandin production in the preoptic area of rats

“…As previously reported by others (1,8,62), the injection of vehicle into the POA of rats evoked by itself a rise in T c , which reached a maximum value of 0.7 Ϯ 0.25°C after 2.5 h. Microinjection of ET-1 (100 fmol) into the POA caused a slowly developing and long-lasting increase in T c , which was significantly higher compared with that induced by saline. ET-1-induced fever was significantly reduced when the rats were coinjected with IL-1ra (600 pmol).…”

“…*P Ͻ 0.05 vs. control. T c in rats (1,8,62), cats (11), guinea pigs (56), and rabbits (9). Different authors have related such increases to increased local production of inflammatory mediators by damaged tissue.…”

Antipyretic role of the NO-cGMP pathway in the anteroventral preoptic region of the rat brain

“…2A), but the magnitude of this response was small compared with previous studies that injected higher volumes (36,51). In fact, local injury due to microinjection procedures into the POA has been shown to increase T c in rats (1,14), cats (17), guinea pigs (40), and rabbits (13), a response that has been attributed to the production of inflammatory mediators by damaged tissue and, thus, has been shown to be attenuated by treatment with paracetamol (13) and indomethacin (40). Although in the present experiments a slight increase in T c was also observed after all microinjections, it should be emphasized that this effect was minimized by injecting a small volume (100 nl) over a relatively long period of time (1 min).…”

“…Therefore, we hypothesized that the thermoregulatory effect of NO in the AVPO is mediated by cGMP. To test this hypothesis, we first microinjected the inhibitors of sGC, 1H- [1,2,4]oxadiazolo[4,3,-a]quinoxaline-1-one (ODQ) and methylene blue, or their vehicles (1% DMSO in saline or saline alone, respectively) into the AVPO followed by administration of SNP. However, prior microinjections of the vehicles only abolished the thermoregulatory effect of SNP into the AVPO, a fact that precluded any further experiment using two consecutive intra-AVPO microinjections (data not shown).…”

Experimental Model of Small Deep Infarcts Involving the Hypothalamus in Rats

“…Second, in a parallel experiment with the use of the transorbital method for MCA occlusion (HTA and AChA are exempt from occlusion), neither proximal (nϭ4) nor distal (nϭ10) permanent occlusion of the MCA caused rectal temperature to increase significantly (our unpublished data). Finally, direct injury of the hypothalamus by acute mechanical puncture 19,20 or the electrolytic method 21 causes hyperthermia. Neurogenic hyperthermia induced by mechanical puncture is hypothesized to affect the pyrogenesis mechanism on the basis of a set point shift, mediated by prostaglandins released from injured tissue and acting on surviving hypothalamic tissue.…”