PubMed1987
To investigate the mechanism(s) involved in chlordecone (CLD)-induced hypothermia, we examined colonic (Tcol) and tail skin (Tsk) temperatures, preferred ambient temperature (Ta), evaporative water loss, and metabolic rate following CLD exposure in the rat. Single ip dosages (0, 50, and 75 mg/kg) in corn oil were administered to Fischer-344 rats. At a Ta of 22.5 degrees C, Tcol was reduced by 50 and 75 mg/kg as early as 0.5 hr, and this effect persisted for 4 hr after dosing. Tcol was increased 24 hr after both CLD dosages. Tsk was elevated 2, 3, 4, and 6 hr after 75 mg/kg and 2 hr after 50 mg/kg. At Ta of 30.5 degrees C, Tcol was decreased at early exposure times after both dosages and was increased 3, 4, and 6 hr after 75 mg/kg. At 10.0 degrees C, an enhanced hypothermia was observed 1-6 hr following 50 and 75 mg/kg CLD. The preferred Ta was significantly decreased by approximately equal to 2.8 degrees C following CLD exposure while activity within the temperature gradient was unchanged. At 25.0 degrees C, evaporative water loss was decreased while metabolic rate was not affected by CLD administration. To study the enhanced hypothermia at 10.0 degrees C, metabolic rate was measured continuously for 2 hr following 75 mg/kg CLD and found to be significantly different from controls. The intensified hypothermia in the cold may be due to the inability of the CLD-treated rat to stimulate metabolic thermogenesis in response to cold in addition to the loss of body heat following cutaneous vasodilation. These data suggest that CLD-induced hypothermia at a neutral Ta is associated with cutaneous vasodilation and not with a decreased metabolic rate or increased evaporative water loss.