Influence of nicotine on the core temperature response to a novel environment in pregnant rats

1997 ◽  
Vol 83 (5) ◽  
pp. 1612-1616 ◽  
Author(s):  
James E. Fewell ◽  
Patricia A. Tang

Fewell, James E., and Patricia A. Tang. Influence of nicotine on the core temperature response to a novel environment in pregnant rats. J. Appl. Physiol.83(5): 1612–1616, 1997.—Exposure of a male or nonpregnant female rat to a novel environment, such as a simulated open field, induces a transient increase in core temperature, which is often called stress-induced hyperthermia. Pregnancy alters this response such that the core temperature index increases significantly during exposure to a simulated open field on day 10 but not on days 15 and 20 of gestation in rats. The present experiments were carried to investigate the effect of chronic administration of nicotine (0, 1, 2, 4, or 8 mg ⋅ kg−1 ⋅ 24 h−1 for 13–15 days) on the core temperature response to a simulated open field in chronically instrumented pregnant ( day 20 or 21 of gestation) and nonpregnant Sprague-Dawley rats. In nonpregnant rats, the core temperature index increased more during exposure to a simulated open field after chronic administration of nicotine at all doses than after chronic administration of vehicle; the core temperature response was not dependent on the dose of nicotine. In pregnant rats, significant increases in core temperature as well as in the core temperature index occurred only during exposure to a simulated open field after chronic administration of nicotine in doses of 2, 4, or 8 mg ⋅ kg−1 ⋅ 24 h−1; the core temperature response was dependent on the dose of nicotine. Our data provide evidence that chronic exposure to nicotine enhances the core temperature response to a simulated open field in nonpregnant rats and unmasks a maternal thermogenic response that is not seen to the same stimulus near term of pregnancy. The possible physiological consequences for the fetus are presently unknown and require investigation.

1999 ◽  
Vol 87 (1) ◽  
pp. 170-174
Author(s):  
Patricia A. Tang ◽  
James E. Fewell ◽  
Heather L. Eliason

Near the term of pregnancy, rats have an attenuated core temperature response on exposure to a novel environment (e.g., a simulated open field) compared with that observed early in pregnancy or in nonpregnant rats. The present experiments were carried out on 26 nonpregnant and 26 pregnant rats to test the hypothesis that arginine vasopressin, functioning as an endogenous antipyretic substance in the central nervous system, mediates this attenuated core temperature response. Exposure to a simulated open field after intracerebroventricular (ICV) vehicle produced a significant increase in core temperature in both nonpregnant and pregnant animals, the magnitude and duration of which were greater in the nonpregnant rats. In nonpregnant rats, exposure to a simulated open field after ICV vasopressin V1-receptor antagonist altered the pattern of the core temperature response but not the core temperature index compared with that observed on exposure to a simulated open field after ICV vehicle. In pregnant animals, ICV vasopressin V1-receptor antagonist did not alter the core temperature response to a simulated open field compared with that observed after ICV vehicle. Thus our data do not support the hypothesis that a pregnancy-related activation of arginine vasopressin attenuates the core temperature response to a simulated open field in rats near the term of pregnancy.


1998 ◽  
Vol 274 (4) ◽  
pp. R1158-R1161
Author(s):  
Evvi-Lynn M. Rollins ◽  
James E. Fewell

In newborns and adults of a number of species including humans, exposure to acute hypoxemia produces a “regulated” decease in core temperature, the mechanism of which is unknown. Considering that various cortical areas participate in autonomic regulation including thermoregulation, the present experiments were carried out to test the hypothesis that the cerebral cortex plays a role in modulating the regulated decrease in core temperature during acute hypoxemia. This hypothesis was tested by determining the core temperature response to acute hypoxemia in chronically instrumented adult Sprague-Dawley rats before and after cortical spreading depression (i.e., functional decortication) was produced by the local application of potassium chloride to the dura overlying the cerebral hemispheres. There was no effect of cortical spreading depression on baseline core temperature. Core temperature decreased during acute hypoxemia in a similar fashion when the cerebral cortex was intact as well as during functional decortication. Thus our data do not support the hypothesis that the cerebral cortex modulates the regulated decrease in core temperature that occurs in adult rats during acute hypoxemia.


1997 ◽  
Vol 82 (5) ◽  
pp. 1406-1410 ◽  
Author(s):  
James E. Fewell ◽  
Patricia A. Tang

Fewell, James E., and Patricia A. Tang. Pregnancy alters body-core temperature response to a simulated open field in rats. J. Appl. Physiol. 82(4): 1406–1410, 1997.—Exposure of a rat to a novel environment (e.g., a simulated open field) induces a transient increase in body-core temperature, which is often called stress-induced hyperthermia. Although pregnancy is known to influence thermoregulatory control, its effect on stress-induced hyperthermia is unknown. Therefore, 24 Sprague-Dawley rats (8 nonpregnant and 16 pregnant) were studied to test the hypothesis that pregnancy would alter the development of stress-induced hyperthermia after exposure to a simulated open field. Body-core temperature index increased significantly after exposure to a simulated open field in nonpregnant and gestation day-10 rats but not in gestation day-15 and day-20 rats. Thus our data provide evidence that pregnancy influences the body-core temperature response of rats exposed to a simulated open field in a gestation-dependent fashion. The functional consequences as well as the mechanisms involved remain to be determined.


1995 ◽  
Vol 269 (5) ◽  
pp. R1179-R1182 ◽  
Author(s):  
R. L. Simrose ◽  
J. E. Fewell

Rats have an attenuated or absent febrile response to exogenous pyrogen (e.g., bacterial endotoxin) near term of pregnancy. With the aim of providing insight into possible mechanism(s) of the altered febrile response to exogenous pyrogen, experiments have been carried out on 67 time-bred Sprague-Dawley rats to investigate the febrile response to endogenous pyrogen [i.e., interleukin-1 beta (IL-1 beta)]. On day 13 of gestation, intravenous injection of IL-1 beta produced a significant increase in body temperature with a latency of approximately 30 min and a duration of approximately 120 min. In contrast, on days 17 and 21 of gestation as well as on the day of delivery, intravenous injection of IL-1 beta produced significant decreases in body temperature. Thus rats do not develop fever in response to endogenous pyrogen near term of pregnancy but rather become hypothermic. The mechanism of the altered body temperature response to exogenous pyrogen as pregnancy proceeds remains unknown. We speculate, however, that it most likely lies downstream from the formation of endogenous pyrogen.


2002 ◽  
Vol 93 (2) ◽  
pp. 531-536 ◽  
Author(s):  
James E. Fewell ◽  
Heather L. Eliason ◽  
Roland N. Auer

Rats have an attenuated febrile response to endogenous pyrogen near the term of pregnancy. Given the fundamental role of E-series prostaglandins (PGEs) in mediating the febrile response to blood-borne endogenous pyrogen, the present experiments were carried out to determine whether PGEs increase in the area surrounding the organum vasculosum laminae terminalis (peri-OVLT) of near-term pregnant (P) rats as in nonpregnant (NP) rats after intravenous (iv) administration of recombinant rat interleukin-1β (rrIL-1β). Core temperature was measured by telemetry and peri-OVLT interstitial fluid was sampled in 12 NP and 12 P chronically instrumented, Sprague-Dawley rats by microdialysis for determination of total PGEs by radioimmunoassay. Basal core temperatures were higher in NP compared with P rats (NP 37.9°C ± 0.5, P 36.9°C ± 0.4; P < 0.05), but basal peri-OVLT PGEs were similar in both groups (NP 260 ± 153 pg/ml, P 278 ± 177 pg/ml; P =not significant). Intravenous administration of rrIL-1β to NP rats produced a significant increase in core temperature with a latency, magnitude, and duration of 10 min, 0.87°C, and at least 170 min, respectively; peri-OVLT PGEs were increased significantly by 30 min and averaged 270% above basal levels throughout the experiment. In P rats, however, neither core temperature nor peri-OVLT PGEs increased significantly after iv administration of rrIL-1β. Intravenous administration of vehicle did not significantly alter core temperature or peri-OVLT PGEs in either group of rats. Thus peri-OVLT PGEs do not increase in P rats as they do in NP rats after iv administration of rrIL-1β. The mechanism of this interesting component of the maternal adaptation to pregnancy, which likely plays a major role in mediating the attenuated febrile response to endogenous pyrogen near the term of pregnancy, warrants further investigation.


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