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Department of Physiology and Biophysics, The University of Calgary, Health Sciences Centre, Calgary, Alberta T2N 4N1, Canada
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
FOOTNOTES
REFERENCES
ABSTRACT 
Eliason, Heather L., and James E. Fewell.
Thermoregulatory control during pregnancy and lactation in rats.
J. Appl. Physiol. 83(3): 837-844, 1997.
Although the mechanisms remain unknown, maternal core
temperature (Tc) decreases near
term of pregnancy and is increased throughout lactation in rats. The
purpose of our present experiments was to determine whether pregnancy and lactation shift the thermoneutral zone of rats and to investigate whether the changes in maternal Tc
during pregnancy and lactation result from "forced" or
"regulated" thermoregulatory responses. Conscious, chronically
instrumented nonpregnant and pregnant and lactating rats were studied
both in a thermocline (a chamber with a linear temperature gradient
from 12 to 36°C) and in a metabolic chamber to determine the
influence of pregnancy and lactation on selected ambient temperature as
well as the thermoregulatory response to changes in ambient
temperature. We found that selected ambient temperature, oxygen
consumption, and thermal conductance did not change in rats studied in
a thermocline as Tc decreased near
term of pregnancy. There was, however, a downward shift in the
thermoneutral zone of rats studied in a metabolic chamber near term of
pregnancy. During lactation, selected ambient temperature decreased in
rats studied in a thermocline as oxygen consumption and
Tc increased. The thermoneutral
zone of lactating rats was not different from that of nonpregnant
animals. Thus our data provide evidence that the decrease in
Tc near term of pregnancy in rats
results from a regulated thermoregulatory response,
whereas the increase in Tc during
lactation results from a forced thermoregulatory response.
autonomic thermoregulation; behavioral
thermoregulation
INTRODUCTION NUMEROUS PHYSIOLOGICAL CHANGES occur during the
maternal adaptation to pregnancy and lactation. In rats, these changes
include reversible alterations in thermoregulatory control. For
example, baseline core temperature
(Tc) decreases as gestation
advances in rats and then rises sharply within 4 h after the onset of
parturition (11). Throughout lactation,
Tc remains at a level ~0.5°C
above baseline levels of nonpregnant rats (11). Furthermore, there are
different thermoregulatory responses to cold (20) and to pyrogens such
as bacterial endotoxin (24), interleukin-1 The aforementioned experiments on baseline
Tc regulation during pregnancy
were carried out at ambient temperatures of 22-25°C, which are
several degrees below the thermoneutral zone of nonpregnant rats (16).
Given that nonshivering thermogenesis in brown adipose tissue, which is
an important autonomic thermoregulatory effector organ for heat
production in rats (12), is impaired near term of pregnancy (36), it is
possible that the decrease in Tc
is "forced" such that this thermoregulatory effector is
overwhelmed and Tc falls below the
central nervous system set-point temperature [i.e., forced
hypothermia (15)]. Alternatively, it is possible that the
decrease in Tc near term of
pregnancy is "regulated" such that
Tc follows a decrease in the
central nervous system set-point temperature [i.e., regulated
hypothermia (15)].
During lactation, the thermogenic capacity of the brown adipose tissue
remains suppressed (36). Other sources of heat production, however,
become increasingly activated during this period. Metabolic heat
production is increased because of greater food intake and milk
production, which is a highly exothermic process (1). These factors,
combined with a decreased ability to dissipate heat and a greater heat
load from the nest (1), could contribute to a chronic elevation of
Tc. Altered levels of hormone,
including progesterone and corticosterone, may also contribute to
increased heat production (1). Because of this increase in heat
production during lactation, the higher
Tc during lactation may be due to a forced thermoregulatory response, whereby the capability
of the thermoregulatory effectors to dissipate heat is overwhelmed and
Tc rises above the central nervous
system set point temperature [i.e., forced hyperthermia
(15)]. It is also possible that the increased
Tc during lactation is a
regulated hyperthermic response, by which the central
nervous system set point temperature is elevated, thereby stimulating
the activity of the heat-producing and heat-conserving effectors and
resulting in a subsequent rise in
Tc.
The purpose of our present experiments was to determine whether
pregnancy and lactation shift the thermoneutral zone of rats and to
investigate whether the changes in maternal
Tc during pregnancy and lactation
result from forced or regulated thermoregulatory responses.
METHODS Experiments were carried out in 11 nonpregnant and 8 pregnant
Sprague-Dawley rats (aged 8-11 wk) undergoing their first
pregnancy (Charles River Breeding Laboratories). Term of pregnancy in
this strain of rats is 21-22 days. Except during surgery and
experiments, the rats were housed singly in Plexiglas cages containing
Aspen-Chip Laboratory Bedding (Northeastern Products) at 22 ± 1°C in a 12:12-h light-dark cycle, with lights on from 0700 to
1900. All animals had continuous access to food (Lab Diet 5001) and tap
water.
Surgical Preparation
(33), and prostaglandin
E1
(PGE1) (35) in near-term
pregnant rats compared with those observed in nonpregnant rats.
Similarly, lactating rats demonstrate an altered ability to
thermoregulate in both hot (1) and cold (2) environments. The
mechanism(s) of these changes, however, is presently unknown.
Experimental Protocol
Experiment I: Thermocline. On the day of an experiment, each rat was brought to the laboratory and placed first in a thermocline for a period of 2 h. The measured and calculated variables were determined at 6-min intervals during the second hour. The pregnant animals were studied on days 10 or 11, 15 or 16, and 20 or 21 of gestation, and the lactating animals were studied on postpartum days 4 or 5 and 19 or 20. Experiment II: Metabolic chamber. Each rat was removed from the thermocline and placed immediately in the metabolic chamber for a period of 6 h. The measured and calculated variables were determined during the last 5 min of 30-min periods as the ambient temperature was increased in 2-°C increments from 14° to 36°C.Experimental Apparatus
Experiment I: Thermocline. The thermocline used in our experiments consisted of a sealed Plexiglas cylinder (200 cm long; internal diameter 11.5 cm) with a plastic grid along the bottom into which flowed room air at 2.0 l/min. A linear temperature gradient from 12 to 36°C was produced by circulating hot and cold water (Endocal Refrigerated Circulating Bath RTE-8DD, Neslab) into two copper coils wrapped around the cylinder. Experiment II: Metabolic chamber. The metabolic chamber consisted of a double-walled Plexiglas cylinder (60 cm long; internal diameter 10 cm) with a plastic grid along the bottom into which flowed room air at 1.4 l/min. Chamber ambient temperature was controlled by circulating water from a temperature-controlled bath through the space between the walls.Experimental Measurements and Calculations
Selected ambient temperature was determined in experiment I by observing the position of the rat in the thermocline. For measurement of Tc, platform antennas (PhysioTel CTR 86; Data Sciences International), which received the output frequency (Hz) from the previously implanted biotelemetry device, were placed under the thermocline and metabolic chamber. The received output was then fed into a peripheral processor (Dataquest III, Data Sciences International) connected to an IBM computer. Oxygen consumption was calculated by knowing the oxygen concentration (Ametek-Applied Electrochemistry S-3A/I O2 Analyzer) of the inflow and outflow gas as well as the flow rate. Thermal conductance, which is a measure of the ease of heat transfer from the body to the environment by radiation, conduction, convection, and evaporation (3), was calculated as oxygen consumption divided by the difference between Tc and ambient temperature. The lower critical temperature was estimated as the ambient temperature below which oxygen consumption (i.e., an indirect measure of metabolic heat production) increased to maintain thermal balance (21).Statistical Analysis
In experiment I, average values for the measured and calculated variables were determined for each experiment. These values were used for statistical analysis that was carried out by using a one-factor analysis of variance followed by a Newman-Keuls multiple-comparison test to determine whether pregnancy or lactation influenced the measured or calculated variables. In experiment II, average values for the measured and calculated variables were determined at each ambient temperature for each experiment. These values were used for statistical analysis that was carried out using a twofactor analysis of variance for repeated measures followed by a Newman-Keuls multiple-comparison test to determine whether day of pregnancy/lactation or ambient temperature influenced the measured or calculated variables. All results are presented as means ± SD; P < 0.05 was considered to be of statistical significance.RESULTS
Experiment I: Thermocline
As we have previously observed in pregnant rats housed and studied at an ambient temperature below their thermoneutral zone (11), Tc decreased ~1°C during the second half of gestation when pregnant rats were studied in a thermocline (Fig. 1A). This decrease in Tc was not accompanied by changes in selected ambient temperature, oxygen consumption, or thermal conductance (Fig. 1, B-D). During lactation, Tc increased to ~0.5°C above baseline. This increase was accompanied by a significant drop in selected ambient temperature and a rise in oxygen consumption. Thermal conductance was unchanged throughout lactation.
Experiment II: Metabolic Chamber
Tc was significantly influenced in an overall fashion by gestation and ambient temperature (Fig. 2). Furthermore, an interaction between gestation and ambient temperature on Tc occurred such that Tc decreased more in the late gestation rats than in nonpregnant, midgestation, or lactating rats at low ambient temperatures.
The minimal rate of oxygen consumption occurred at ambient temperatures of 28-30°C as the ambient temperature was varied from 14 to 36°C (Fig. 3). Oxygen consumption was not significantly affected in an overall fashion by gestation or lactation but varied significantly with ambient temperature. The lower critical temperature decreased from ~26°C in the nonpregnant and midgestation rats to ~22°C in the late-gestation pregnant rats and returned to ~24-26°C during lactation.
Thermal conductance was not significantly affected in an overall fashion by gestation or lactation but varied significantly with ambient temperature (Fig. 4). The threshold for an increase in thermal conductance decreased from ~30°C in the nonpregnant and early-gestation and midgestation pregnant rats to ~28°C in the late-gestation pregnant rats and returned to ~30°C during lactation.
DISCUSSION
Our experiments provide new information about thermoregulatory control during pregnancy and lactation in rats. Novel findings in our study were 1) that selected ambient temperature, oxygen consumption, and thermal conductance did not change in rats studied in a thermocline as Tc decreased near term of pregnancy, 2) that there was a downward shift in the thermoneutral zone of rats studied in a metabolic chamber near term of pregnancy, 3) that selected ambient temperature decreased in rats studied in a thermocline as oxygen consumption and Tc increased during lactation, and 4) that the thermoneutral zone of lactating rats was not different from that of nonpregnant animals. Thus our data provide evidence that the decrease in Tc near term of pregnancy in rats results from a regulated thermoregulatory response, whereas the increase in Tc during lactation results from a forced thermoregulatory response.
The interpretation of our data collected from rats studied in a thermocline was on the basis of the fact that rats employ their somatomotor nervous system (e.g., voluntary movement system-behavioral thermogenesis) as well as the sympathetic portion of the autonomic nervous system (e.g., nonshivering thermogenesis in brown adipose tissue) as effector mechanisms for thermoregulation. We reasoned that if the thermoregulatory response was forced near term of pregnancy such that nonshivering thermogenesis in brown adipose tissue was impaired and Tc decreased below the central nervous system set-point temperature [i.e., forced hypothermia (15)], as previously suggested by Naccarato and Hunter (27), then the animal would rely increasingly on behavioral thermogenesis and would move to a warmer region of the thermocline in an attempt to restore Tc to the central nervous system set-point temperature. Alternatively, if the thermoregulatory response was regulated such that the decrease in Tc followed a decrease in the central nervous system set point temperature [i.e., regulated hypothermia (15)], then the animal would either not move or would move to a cooler region in the thermocline. Similarly, if the hyperthermia was forced during lactation, the animal would be expected to move to a cooler ambient temperature, whereas it would select either an unchanged or warmer ambient temperature if the increase in Tc was regulated. This strategy has previously been used by others in investigations of the neuropharmacology of temperature regulation (17).
There is little information in the literature with which to compare and contrast the results of our experiments on pregnant or lactating rats in the thermocline. Selected ambient temperatures for a number of species, both in males and nonpregnant females, have been determined and recently reviewed by Gordon (17). In general, most species select an ambient temperature that coincides with the middle of their thermoneutral zone. Adult guinea pigs and rats are unusual in that they select ambient temperatures that are at the upper and lower end, respectively, of their thermoneutral zones. We also found that nonpregnant rats in the thermocline selected an ambient temperature that was just below or at the lower end of their thermoneutral zone determined from the metabolic chamber. Gelineo and Gelineo (14) have shown that when pregnant rats are placed in a Herter apparatus with six compartments of varying temperatures (i.e., 50-42.4; 42.4-30.6; 30.6-23.2; 23.2-19.8; 19.8-17.8; and 17.8-12.9°C), they select temperatures at or near thermoneutral temperatures (i.e., 30.6-23.2°C) but build their nest and give birth in a cooler thermal environment (i.e., 17.8-12.9°C). Our results on selected ambient temperature during pregnancy and lactation confirm and extend their findings.
Late in gestation, changes in maternal anatomy and physiology occur that effect the regulated hypothermia. These include a reduced insulation on the ventral body surface, a decreased Tc threshold for salivation and grooming, and an increased motivation to keep cool during heat stress. In humans, a reduction in regulatory thermogenesis (i.e., heat production after a meal) may decrease the heat load with which the mother has to cope with near term of pregnancy (9). In the present experiments, we found that the lower critical temperature as well as the threshold for an increase in thermal conductance decreased in rats near term of pregnancy compared with nonpregnant and midgestation pregnant rats (Figs. 3 and 4). If one uses the threshold of thermal conductance to estimate the upper critical temperature, then these changes produced a downward shift as well as a widening of the thermoneutral zone near term of pregnancy, which returned to nonpregnant values by day 5 of lactation. This may have possible consequences for the fetus in that it would allow the mother to be exposed to a lower ambient temperature before she initiates oxygen-requiring thermogenic mechanisms (e.g., nonshivering thermogenesis) to maintain Tc. Activation of nonshivering thermogenesis may cause circulatory adjustments such that blood flow from internal body organs, including the uterus and placenta (5), 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 25% of the cardiac output (29). An ensuing decrease in uteroplacental blood flow could compromise placental gas exchange, with a resulting decrease in fetal oxygen supply (8).
Our results confirm and extend those of Imai-Matsumura et al. (20), whose investigations focused on ambient temperatures below the thermoneutral zone, and of Wilson and Stricker (37), whose investigations focused on ambient temperatures above the thermoneutral zone. During lactation, rats experience an increased heat load, both because of the highly exothermic process of milk production and contact with the pups in the nest. The present experiments, however, suggest that the increased heat load experienced by the mother because of contact with the pups in the nest is not the primary cause of the rise in Tc during lactation because Tc remained elevated while the animal was separated from her nest. Although the lactating rats in our experiments did not return their Tc to nonpregnant levels by using behavioral means, it is possible that they would have if they had been placed in a thermocline that allowed them to select an ambient temperature cooler than 10°C. This requires further investigation.
Even though decreases in Tc near the term of pregnancy have been reported to occur in a number of species including rabbits (27), sheep (22), and rats (11, 20), information regarding mechanisms is lacking. Although our experiments were not designed to investigate the mechanism(s) of the regulated change in Tc near term of pregnancy, or the forced change during lactation, there are a number of possible explanations. The regulated decrease in Tc near term of pregnancy may have resulted from hormonal changes that occur at this time of gestation in rats. These include an increase in serum luteinizing hormone (25), prolactin (25), and estradiol levels (32) and a decrease in serum progesterone levels (31). Progesterone has long been known to have thermogenic effects (13, 30) and recently has been shown to influence firing patterns of preoptic thermosensitive neurons (28). Progesterone levels decrease dramatically from day 19 to term of gestation in rats and is therefore a likely candidate influencing Tc (25). This premise requires further investigation. Glucocorticoids, including corticosterone, are known to influence Tc by chronically increasing tissue metabolism (23). During lactation, maternal corticosterone levels are elevated; therefore, it is possible that this hormone plays a role in the increase in Tc during lactation (34).
Previous experiments from our laboratory as well as from
others have shown that the febrile response to pyrogens such as
bacterial endotoxin (24), interleukin-1 (33), and
PGE1 (10, 35) is attenuated in
near-term pregnant rats compared with that observed in early gestation
and nonpregnant rats. Is it possible that the attenuated febrile
response to pyrogens near the term of pregnancy and the regulated
decrease in Tc share common
mechanisms? Although possible, it seems unlikely because recent
experiments in our laboratory have shown that the
intracerebroventricular administration of an arginine vasopressin
V1-receptor antagonist restores
the febrile response to intracerebroventricular administration of PGE1 near the term of pregnancy in
rats but does not alter basal Tc
(unpublished observations). Thus it appears that arginine vasopressin, functioning as an endogenous antipyretic substance in the central nervous system, mediates the attenuated febrile response to pyrogens near the term of pregnancy in rats but does not mediate the regulated decrease in Tc as observed in our
present experiments.
Regardless of the mechanism of a lower maternal Tc near term of pregnancy in rats, what are the possible consequences for the fetus? One is that a lower maternal Tc and thus lower fetal Tc during the latter part of gestation may decrease fetal oxygen requirements. If the temperature coefficient of metabolism (i.e., Q10) in humans is ~2.3 (18), then metabolic rate changes ~10% for each 1°C change in Tc. A moderate decrease in Tc during the latter part of gestation may be beneficial not only by decreasing oxygen demand but also by causing a leftward shift of the oxyhemoglobin dissociation curve, thereby increasing oxygen affinity and oxygen saturation. In conditions under which fetal oxygen availability is severely limited (e.g., asphyxia during birth), a decrease in Tc may reduce neuronal injury (6) and decrease perinatal morbidity and mortality. Maternal hyperthermia produced during gestation by an elevated ambient temperature has been shown to retard fetal growth and increase neonatal mortality in rats (4, 38). It is also possible that the lower maternal Tc and thus lower fetal Tc during the latter part of gestation may influence central nervous system thermoregulatory "imprinting" for the newborn. Hull et al. (19) have provided evidence that newborn rabbits select ambient temperatures that mimic their intrauterine experience and regulate their Tc to a level of ~0.8°C above the maternal body Tc on the day before delivery (i.e., at a level similar to that which they experienced late in fetal life).
In summary, our data do not support the view that the decrease in Tc near term of pregnancy in rats results from a failure of homeostasis (7). Rather, the regulated hypothermia provides an example of rheostasis (26) or regulation around a shifted set point, perhaps to optimize oxygen supply and oxygen demand in an attempt to ensure growth and survival during the perinatal period. Conversely, the increase in Tc during lactation appears to involve a failure of homeostasis in which the animal's heat load is increased to an extent where it is unable to dissipate the excess heat produced and its Tc rises to a higher than normal level.
ACKNOWLEDGEMENTS
This work was done during the tenure of J. E. Fewell as a Scientist of the Medical Research Council of Canada and a Medical Scholar of the Alberta Heritage Foundation for Medical Research.
FOOTNOTES
Address for reprint requests: J. E. Fewell, Heritage Medical Research Bldg., 206, The Univ. of Calgary, 3330 Hospital Drive, NW, Calgary, Alberta T2N 4N1, Canada (E-mail fewell{at}acs.ucalgary.ca).
Received 6 December 1996; accepted in final form 22 April 1997.
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 H. L. Eliason and J. E. Fewell Arginine vasopressin does not mediate the attenuated febrile response to intravenous IL-1beta in pregnant rats Am J Physiol Regulatory Integrative Comp Physiol, February 1, 1999; 276(2): R450 - R454. [Abstract] [Full Text] [PDF]
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H. L. Eliason and J. E. Fewell AVP mediates the attenuated febrile response to administration of PGE1 in rats near term of pregnancy Am J Physiol Regulatory Integrative Comp Physiol, September 1, 1998; 275(3): R691 - R696. [Abstract] [Full Text] [PDF]
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