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J Appl Physiol 82: 1406-1410, 1997;
8750-7587/97 $5.00
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Journal of Applied Physiology
Vol. 82, No. 5, pp. 1406-1410, May 1997
CONTROL OF BREATHING, CIRCULATION, AND TEMPERATURE

Pregnancy alters body-core temperature response to a simulated open field in rats

James E. Fewell and Patricia A. Tang

Department of Physiology and Biophysics, University of Calgary Health Sciences Center, Calgary, Alberta, Canada T2N 4N1

ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
FOOTNOTES
REFERENCES

ABSTRACT

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.

stress-induced hyperthermia; thermoregulation

INTRODUCTION

NUMEROUS PHYSIOLOGICAL changes occur during the maternal adaptation to pregnancy. In rats, these changes include reversible alterations in thermoregulatory control. For example, baseline 24-h body-core temperature (Tbc) in rats decreases as gestation advances and then increases around the time of parturition (13). Furthermore, there are different thermoregulatory responses to cold (15) and to pyrogens such as bacterial endotoxin (20), interleukin (IL)-1beta (IL-1beta ; Ref. 28), and prostaglandin (PG) E1 (PGE1; Ref. 30) in near-term pregnant rats compared with those observed in nonpregnant rats.

Exposure of a rat to a novel environment induces a transient increase in Tbc of ~1.5°C (7). This response is often called stress-induced hyperthermia. Several laboratories have provided evidence that stress-induced hyperthermia results from a regulated thermoregulatory response and shares some common mechanisms with fever in response to bacterial pyrogens (5, 29). Considering this and the aforementioned information on pregnancy and fever in response to pyrogens, the present experiments have been carried out to test the hypothesis that pregnancy would alter the Tbc response to a simulated open field in rats.

METHODS

Experiments were carried out on 8 nonpregnant and 16 pregnant Sprague-Dawley rats (aged 8-11 wk) undergoing their first pregnancy (Charles River Breeding Laboratories, St. Constant, Quebec, Canada). The rats were housed individually in Plexiglas cages at 22 ± 1°C in a 12:12-h light-dark cycle, with lights on from 0700 to 1900. To familiarize the animal with the investigator, rats were handled at least three times before an experiment. All animals had continuous access to food (Lab Diet 5001) and tap water.

Surgical preparation. No sooner than 3 days before an experiment, each rat was anesthetized by inhalation of halothane (4.0% for induction and 1.5-2.0% for maintenance) in oxygen. A paramedian laparotomy was done, and a free-floating battery-operated biotelemetry device (VM-FH; Mini-Mitter) was inserted into the peritoneal cavity for later measurement of Tbc. The skin was sutured to close the wound.

All surgical and experimental procedures were carried out in accordance with the "Guide to the Care and Use of Experimental Animals" provided by the Canadian Council on Animal Care and with the approval of the Animal Care Committee of the University of Calgary.

Conditions of observations. Our laboratory contains two environmental chambers: a home environmental chamber in which the animals are housed on a day-to-day basis and an experimental environmental chamber that houses a simulated open field. The simulated open field consists of a 30-in. (wide) × 60-in. (length) × 24-in. (high) white acrylic finish box that is illuminated by two hanging fluorescent lights.

Each rat underwent three experiments on consecutive days: a home-cage experiment, a sham experiment, and an open-field experiment. The home-cage, sham, and open-field experiments were carried out in a random order with each animal in each of four groups of rats. The nonpregnant rats were studied on three consecutive days (group 1). The pregnant rats were studied on days 9, 10, and 11 (group 2); days 14, 15, and 16 (group 3); or days 19, 20, and 21 (group 4) of gestation (term = ~22 days). All experiments were carried out between 0800 and 1200 to avoid any possible circadian effects on the response.

During a home-cage experiment, each rat was left in her cage in the home environmental chamber. For a sham experiment, each rat was carried in her cage from the home environmental chamber to the experimental environmental chamber, her cage was placed on the floor, and she was picked up out of her cage for ~10 s. She was then returned to her cage, and the cage was carried back to the home environmental chamber. For an open-field experiment, each rat was carried in her cage from the home environmental chamber to the experimental environmental chamber. Her cage was placed on the floor, and she was picked up out of her cage and placed in the center of our simulated open field.

During measurement of Tbc, both the animal cage in the home environmental chamber as well as the simulated open field in the experimental environmental chamber were placed on platform antennas (RLA1020 Receiver, Data Sciences International) that received the output frequency (Hz) from the biotelemetry device. The received output was then fed into a peripheral processor connected to an IBM computer for determination of Tbc.

Experimental protocol. Tbc was measured at 2-min intervals during a control period and at 10-min intervals for 3 h after the home-cage, sham, or open-field manipulation. A suitable control period was defined as one in which five consecutive measurements of Tbc did not vary by >0.1°C.

Statistical analysis. Statistical analysis was carried out using a three-factor multivariant analysis of variance (MANOVA) for repeated measures followed by a Newman-Keuls multiple-comparison test to determine whether time (control; 10-, 20-, 30-min, etc.), experiment type (home cage, sham, or open field), or gestation (nonpregnant, days 9-11, 14-16, or 19-21 of gestation) affected Tbc. In addition, a two-factor MANOVA for repeated measures, followed by a Newman-Keuls multiple-comparison test, was used to determine whether experiment or gestation affected the Tbc index, which was expressed as area under the Tbc curve in degrees, centigrade per hour after the home cage, sham, or open field manipulation. All results are presented as means ± one SD. P < 0.05 was considered to be of statistical significance.

RESULTS

Tbc index increased significantly after exposure to a simulated open field in nonpregnant and gestation day-10 rats but was not different from that observed during a home-cage experiment on days 15 and 20 of gestation (Fig. 1). On being placed into the center of the simulated open field, all rats moved to a wall of the box, circled the perimeter once or twice, and then settled in a corner where they usually stayed for the duration of the experiment. There was no effect of pregnancy on this behavior.

Fig. 1. Body-core temperature index during home-cage (open bars), sham (hatched bars), and open-field (solid bars) experiments in nonpregnant (NP, n = 8), gestation day 10 (d10, n = 6), gestation day 15 (d15, n = 5), and gestation day 20 (d20, n = 5) rats. Data are means ± SD. * P < 0.05 vs. home-cage experiment; # P < 0.05 vs. sham experiment at given gestation by multivariant analysis of variance (MANOVA) and Newman-Keuls test.
[View Larger Version of this Image (14K GIF file)]

In nonpregnant animals, exposure to a simulated open field produced a rapid increase in Tbc of ~0.9°C that peaked at 20 min. Tbc was significantly increased above control level at 10 min after exposure to a simulated open field and continued to be elevated for ~80 min (Fig. 2). In day 10 gestation rats, exposure to a simulated open field produced a more gradual increase in Tbc of ~0.7°C that peaked at 60 min. Tbc was increased by 10 min but remained elevated for the duration of our recordings (i.e., ~180 min). On day 15 of gestation, Tbc was elevated only at 40 min after exposure to a simulated open field; and on day 20 of gestation, Tbc did not change after exposure to a simulated open field. During a sham experiment, Tbc was elevated only in nonpregnant rats (Fig. 3). The magnitude of the response as well as the duration of the response, however, were attenuated compared with that observed during an open field experiment. No changes in Tbc occurred during a home-cage experiment in any of the groups (Fig. 4).

Fig. 2. Body-core temperatures during an open-field experiment in nonpregnant (A), gestation day 10 (B), gestation day 15 (C), and gestation day 20 rats (D). Data are means ± SD. * P < 0.05 vs. C (control) by MANOVA and Newman-Keuls test.
[View Larger Version of this Image (34K GIF file)]

Fig. 3. Body-core temperatures during sham experiment in nonpregnant (A), gestation day 10 (B), gestation day 15 (C), and gestation day 20 (D) rats. Data are means ± SD. * P < 0.05 vs. C (control) by MANOVA and Newman-Keuls test.
[View Larger Version of this Image (50K GIF file)]

Fig. 4. Body-core temperatures during home-cage experiment in nonpregnant (A), gestation day 10 (B), gestation day 15 (C), and gestation day 20 (D) rats. Data are means ± SD.
[View Larger Version of this Image (36K GIF file)]

DISCUSSION

Our experiments provide new and important information about the maternal adaptation to pregnancy in rats. A novel finding in our study was that pregnancy altered the Tbc response of rats after exposure to a simulated open field; this response was gestation dependent.

Exposure of a rat to a novel stimulus (whether it be restraint, handling, a loud noise, or a novel environment) causes a rise in Tbc (see Ref. 22 for recent review). After exposure to a novel environment, an increase in Tbc occurs, which is often called stress-induced hyperthermia. This increase is thought to result from a regulated thermoregulatory response because it occurs when the animals are studied in a cold environment as well as when they are studied in a warm environment (4, 6, 19), and it is accompanied by activation of heat-producing (27) and heat-conserving mechanisms (5, 6). Although the mechanisms that initiate stress-induced hyperthermia are not clear, prostaglandins (5, 29) and endogenous opioids (3, 25) appear to play important roles in mediating the Tbc response, and glucocorticoids appear to play an important role in modulating (21, 23) the Tbc response. Circulating interleukin-1 (IL-1) does not appear to be involved in mediating stress-induced hyperthermia, as Long et al. (18) and Watkins et al. (32) have shown that neither an intraperitoneal injection of antiserum against IL-1alpha - nor a subcutaneous injection of recombinant human IL-1beta -receptor antagonist alters the Tbc response of rats after exposure to a novel environment. Interestingly, Watkins et al. have recently shown that subdiaphragmatic vagotomy blocks stress-induced hyperthermia in rats after their exposure to a novel environment.

Although our experiments were not designed to investigate the mechanism of the attenuated stress-induced hyperthermic response near term of pregnancy in rats after their exposure to a simulated open field, there are a number of possibilities. Corticosterone, which appears to modulate stress-induced hyperthermia after exposure to a novel environment (21, 23), is elevated from day 18 of gestation through to parturition in the rat (12). Glucocorticoids (e.g., corticosterone) are antipyretic (10, 11) and are known to stimulate the production of lipocortin-1, a calcium-dependent phospholipid-binding protein, which inhibits phospholipase A2, a key enzyme involved in the synthesis of PG (14).

Alternatively, a pregnancy-related activation of an endogenous antipyretic system may have regulated the attenuated Tbc response on exposure to a simulated open field near the term of pregnancy. Arginine vasopressin, which functions as an endogenous antipyretic substance in the central nervous system (16), is elevated in plasma (17) and in a number of hypothalamic nuclei in rats near term of pregnancy (9, 17). Ruwe et al. (26) have shown that administration of arginine vasopressin into the ventral septal area of the rat reduces the increase in Tbc evoked by the intracerebroventricular (icv) injection PGE2. Furthermore, we have recently shown that the Tbc response to icv administration of PGE1 is attenuated in near-term pregnant rats compared with nonpregnant rats (30). Thus it is possible that a pregnancy-related activation of this endogenous antipyretic system may have regulated the Tbc response on exposure to a simulated open field in our experiments.

Finally, Shibata and Nagasaka (27) have shown that nonshivering thermogenesis in brown adipose tissue serves as an important thermoregulatory effector organ for heat generation during stress-induced hyperthermia in rats. A number of investigations, however, have demonstrated that the thermogenic capacity and activity of brown adipose tissue are decreased late in gestation as well as throughout lactation in rodents (2, 31). Thus it is possible that an altered brown adipose tissue response may have forced the attenuated stress-induced hyperthermic response on exposure to a simulated open field near term of pregnancy in our rats. These possible mechanisms require further investigation.

Regardless of the mechanism of the altered stress-induced hyperthermic response on exposure to a simulated open field near term of pregnancy in rats, what are the possible consequences for the fetus? From the standpoint of oxygen supply and demand, it may be of advantage to the fetus for the mother not to develop stress-induced hyperthermia for several reasons. One reason is that stress-induced hyperthermia may cause circulatory adjustments such that blood flow from internal body organs, including the uterus and placenta, shifts toward thermogenic organs (e.g., brown adipose tissue). Under conditions of maximal stimulation, brown adipose tissue, which usually represents <1% of body weight, can receive up to 60% of the cardiac output (24). A decrease in uteroplacental blood flow can compromise placental gas exchange, with a resulting decrease in fetal oxygen supply. Another reason is that during stress-induced hyperthermia, fetal Tbc, which is normally 0.4-0.8°C higher than maternal Tbc (1), would most likely increase in parallel with the rise in maternal Tbc with a resulting increase in oxygen demand secondary to the temperature coefficient of metabolism (i.e., Q10). A moderate increase in Tbc during the latter part of gestation may be detrimental to the fetus not only by increasing oxygen demand but also by causing a rightward shift of the oxyhemoglobin dissociation curve, thereby decreasing oxygen affinity and hemoglobin oxygen saturation. Furthermore, in conditions in which fetal oxygen availability is severely limited (e.g., asphyxia during birth), an increase in Tbc may exacerbate neuronal injury (8) and increase perinatal morbidity and mortality.

ACKNOWLEDGEMENTS

The authors thank Dr. Francine G. Smith for critical review of this manuscript.

FOOTNOTES

   This study was supported by the Medical Research Council of Canada. This work was done during J. E. Fewell's tenure as a Senior Medical Scholar of the Alberta Heritage Foundation for Medical Research. P. A. Tang was supported by a studentship from the Alberta Heritage Foundation for Medical Research.

Address for reprint requests: J. E. Fewell, Heritage Medical Research Bldg., Univ. of Calgary, 3330 Hospital Dr., NW, Calgary, Alberta, Canada T2N 4N1 (E-mail: fewell{at}acs.ucalgary.ca).

Received 16 August 1996; accepted in final form 19 December 1996.

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0161-7567/97 $5.00 Copyright © 1997 the American Physiological Society


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