Inhibitory effect of soman on stress induced hyperthermia in rats and the influence of central and peripheral cholinergic antagonists.
- Author:
Yong-Lu YANG
1
;
Yun-Li WANG
;
Yan LAI
;
Jin HUI
;
Xin LI
;
Xiao-Hua CHEN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Cholinergic Antagonists; pharmacology; Cholinesterases; blood; Female; Fever; drug therapy; Rats; Rats, Sprague-Dawley; Soman; antagonists & inhibitors; pharmacology; Stress, Physiological
- From: Chinese Journal of Applied Physiology 2008;24(1):19-23
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo determine the effect of soman on stress induced hyperthermia and the influence of central and peripheral cholinergic antagonists.
METHODSEffects of subcutaneous injection of soman, scopolamine, methylscopolamine and pyridostigmine on stress-induced hyperthermia were observed in rats by radio telemetry in an open-field environment. Plasma cholinesterase (ChE) activity was measured by a spectrophotometry.
RESULTS(1) Core temperature of the control group increased by 0.96 degrees C when exposed to open-field, whereas core temperature only increased by 0.55 degrees C in soman treated animals. Scopolamine, a central cholinergic antagonist, nearly abolished inhibitory effects of soman on core temperature when exposed to open-field. Methylscopolamine, a peripheral cholinergic antagonist, coadministered with soman reduced significantly the hyperthermic response to open-field exposure compared with rats dosed with soman. (2) Pyridostigmine, a peripheral anti-ChE agent that caused a 52% decrease in plasma ChE activity led to a significant enhancement of the hyperthermic response to open-field exposure. Methyl scopolamine nearly abolished the effects of pyridostigmine on stress-induced hyperthermia response.
CONCLUSIONInhibitory effect of soman on the open field hyperthermia suggested that soman treatment hampered the ability of the rat to develop a normal hyperthermic response when placed in the open-field environment. Its inhibitory effects were mediated primarily through a central muscarinic pathway. In addition, peripheral cholinergic nerve was involved in the control of stress hyperthermic response.