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1 Faculdade de Odontologia de Ribeirão Preto, Universidade de São Paulo, 14040-904, Ribeirão Preto, São Paulo, Brasil; 2 Department of Biological Sciences, Kent State University, Kent 44242; and 3 Research Foundation, Summa Health System, Akron, Ohio 44304
The concept that hypoxia elicits a drop in body temperature (Tb) in a wide variety of animals is not new, but the mechanisms remain unclear. We tested the hypothesis that adenosine mediates hypoxia-induced hypothermia in toads. Measurements of selected Tb were performed using a thermal gradient. Animals were injected (into the lymph sac or intracerebroventricularly) with aminophylline (an adenosine receptor antagonist) followed by an 11-h period of hypoxia (7% O2) or normoxia exposure. Control animals received saline injections. Hypoxia elicited a drop in Tb from 24.8 ± 0.3 to 19.5 ± 1.1°C (P < 0.05). Systemically applied aminophylline (25 mg/kg) did not change Tb during normoxia, indicating that adenosine does not alter normal thermoregulatory function. However, aminophylline (25 mg/kg) significantly blunted hypoxia-induced hypothermia (P < 0.05). To assess the role of central thermoregulatory mechanisms, a smaller dose of aminophylline (0.25 mg/kg), which did not alter hypoxia-induced hypothermia systemically, was injected into the fourth cerebral ventricle. Intracerebroventricular injection of aminophylline (0.25 mg/kg) caused no significant change in Tb under normoxia, but it abolished hypoxia-induced hypothermia. The present data indicate that adenosine is a central and possibly peripheral mediator of hypoxia-induced hypothermia.
thermoregulation; aminophylline; body temperature; behavior; anapyrexia
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