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Experimental Biology 1997 Symposium on Neurobiology of Thennoregulation: Role of Stress: POISONS AND FEVER
Author(s) -
Gordon Christopher J.,
Rowsey Pamela J.
Publication year - 1998
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1998.tb02194.x
Subject(s) - hyperthermia , neurochemical , sodium salicylate , organophosphate , pharmacology , toxicity , chemistry , medicine , immunology , biology , endocrinology , pesticide , agronomy
SUMMARY 1. Dysfunction of the thermoregulatory system is one of many pathologies documented in experimental animals and humans exposed to toxic chemicals. The mechanism of action responsible for many types of poison‐induced fevers is not understood. Some elevations in body temperature are attributed to the peripheral actions of some poisons that stimulate metabolic rate and cause a forced hyperthermia. Exposure to organophosphate (OP) pesticides and certain metal fumes appears to cause a prolonged, regulated elevation in body temperature (Tb). 2. Activation of cyclo‐oxygenase (COX) and the production of prostaglandin (PG)E 2 in central nervous system (CNS) thermoregulatory centres is required to elicit a fever. Activating the COX‐PGE 2 pathway by a poison may occur by one of three mechanisms: (i) induction of cell‐mediated immune responses and the subsequent release of cytokines; (ii) induction of lipid peroxidation in the CNS; and (iii) direct neurochemical activation. 3. Radiotelemetric monitoring of core temperature in unstressed rodents has led to an experimental animal model of poison‐induced fever. Rats administered the OP agents chlorpyrifos and diisopropyl fluorophosphate display an initial hypothermic response lasting approximately 24 h, followed by an elevation in diurnal core temperature for 24–72 h after exposure. The hyperthermia is apparently a result of the activation of the COX‐PGE 2 pathway because it is blocked by the anti‐pyretic sodium salicylate. Overall, the delayed hyperthermia resulting from OP exposure involves activation of thermoregulatory pathways that may be similar to infectionmediated fever.