Role of oxotremorine in arginine vasopressin-induced hypothermia and its effects on behavioral thermoregulatory response in rats / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To investigate the role of oxotremorine in arginine vasopressin (AVP)-induced hypothermia and its effects on the behavioral thermoregulatory response.</p><p><b>METHODS</b>Core temperature (Tc), brown adipose tissue (BAT) temperature and motor activities were monitored in undisturbed female SD rats using radiotelemetry. The behavioral thermoregulatory response was monitored in rats using radiotelemetric temperature gradient apparatus. Effect of AVP (10 microg/kg) and oxotremorine (0.25 mg/kg) on Tc, motor activities, BAT temperature (T(BAT)), grooming activities and the behavioral thermoregulatory response were observed in rats.</p><p><b>RESULTS</b>Administration of AVP and oxotremorine caused a significant drop in Tc, T(BAT), and an increases in grooming activities, respectively. The hypothermic responses were accompanied with a preference for cooler ambient temperature. Oxotremorine augmented the reduction of Tc, T(BAT), and the elevation of grooming activities resulting from AVP, and lasting a longer time. Administration of oxotremorine followed immediately by AVP injection in rats was also shown to induce a preference for cooler ambient temperature, but there was no significant difference compared with AVP.</p><p><b>CONCLUSION</b>AVP-induced hypothermia was related with the set point temperature reduction, inhibiton of BAT thermogenesis and an increases in grooming activities. Oxotremorine could participate in peripheral AVP-induced hypothermia by affecting BAT thermogenesis and behavioral thermoregulation.</p>

Simultaneous telemetric analyzing of the temporal relationship for the changes of the circadian rhythms of brown adipose tissue thermogenesis and core temperature in the rat / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To measure simultaneously the time course for the circadian rhythm of brown adipose tissue(BAT) thermogenesis and core temperature, and analyzing their temporal relationship.</p><p><b>METHODS</b>The circadian rhythm of core temperature (Tc), BAT temperature (T(BAT)), axillary temperature (Tax) and motor activity were simultaneously measured by telemetry in adult male Sprague-Dawley rats at an ambient temperature of 22 degrees C during a 12-h light:12-h dark photoperiod (lights on at 06:00 h and lights off at 18:00 h).</p><p><b>RESULTS</b>(1) T(BAT) was 0.67 degrees C lower than Tc group under the light phase, but it was similar to that Tc during the dark phase. The rate of increase in T(BAT) was higher than corresponding increases in Tc at the start of transition from the light to dark phase, and increase in T(BAT) commenced approximately 8 min before Tc increases. Whereas at the start of transition from the dark to light phase, decrease in T(BAT) commenced approximately 4 min before Tc decreases. (2) The amplitude of the circadian Tax rhythm was similar to that of Tc. During either the light phase or dark phase, Tax was lower than simultaneous measurement of Tc. (3) Increases in behavioral activity commenced before increases in T(BAT) and Tc at the start of transition from the light to dark phase.</p><p><b>CONCLUSION</b>BAT thermogenesis contributes to increase in core temperature during the dark phase, indicating that circadian changes of BAT thermogenesis does indeed play significant role in the overall maintenance of the circadian rhythm of core temperature.</p>

Inhibitory effect of soman on stress induced hyperthermia in rats and the influence of central and peripheral cholinergic antagonists / 中国应用生理学杂志

<p><b>AIM</b>To determine the effect of soman on stress induced hyperthermia and the influence of central and peripheral cholinergic antagonists.</p><p><b>METHODS</b>Effects 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.</p><p><b>RESULTS</b>(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.</p><p><b>CONCLUSION</b>Inhibitory 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.</p>

Effects of central and peripheral administration of a nitric oxide synthase inhibitor on AVP-induced hypothermia in rats / 中国应用生理学杂志

<p><b>AIM</b>To explore the role of nitric oxide (NO) in arginine vasopressin (AVP)-induced hypothermia.</p><p><b>METHODS</b>Colonic temperature was measured at 30 min intervals with a digital thermometer. Effects of central and peripheral administration of nitric oxide synthase (NOS) inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) on AVP-induced hypothermia were observed in rats.</p><p><b>RESULTS</b>(1) Intravenous injection (i.v.) of AVP (4 microg x kg(-1)) and L-NAME (30 mg x kg(-1)) produced a significant drop in body temperature, respectively. Coadministration of L-NAME i.v. with AVP i.v. did not significantly influence the magnitude of AVP-induced hypothermia. (2) Intracerebroventricular (i.c.v.) injection of L-NAME (1 mg x kg(-1)) caused a significant increase in body temperature, but when the treatments with AVP and L-NAME were combined, i.c.v. injection of L-NAME markedly blocked the hypothermic effect of AVP intravenous injection.</p><p><b>CONCLUSION</b>Endogenous NO in the central nervous system plays a major role in AVP-induced hypothermia. In addition, central NO seems to play a tonic thermoregulatory role by reducing normal body temperature because an increase in body temperature was observed after treatment with NOS inhibitor L-NAME.</p>