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AJP - Regulatory, Integrative and Comparative Physiology, Vol 243, Issue 1 104-R111, Copyright © 1982 by American Physiological Society
ARTICLES |
A. H. Rezvani, C. J. Gordon and J. E. Heath
Male New Zealand White rabbits, Oryctolagus cuniculus, were stereotaxically implanted with a guide tube above the preoptic/anterior hypothalamus area (PO/AH) for the injection of the opioid peptide, beta-endorphin (beta-E), naloxone, sodium salicylate, or physiological saline. PO/AH and ear temperature, oxygen consumption, and evaporative heat loss (EHL) were recorded in free-moving rabbits before and after injection of saline followed with beta-E, naloxone, or sodium salicylate at ambient temperatures (Ta) of 2-31 degrees C. A 5-micrograms injection of beta-E promoted a rapid reduction in ear temperature followed by a prolonged rise in PO/AH (body) temperature. Preinjection with an isovolumetric amount of the opiate antagonist, naloxone, inhibited the thermoregulatory effects of beta-E. The beta-E-induced rise in body temperature was directly correlated with Ta. beta-E had no effect on oxygen consumption at Ta's of 5 and 27 degrees C. When measured 30 min after injection, beta-E demonstrated a significant inhibition of EHL at Ta's of 27 and 31 but not 5 degrees C. The beta-E-induced rise in body temperature was not antagonized with preinjections of sodium salicylate in the PO/AH. These data indicate that beta-E promotes a regulated increase in body temperature. The mechanism of activation appears to be distinct from that of an infectious fever.
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