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Department of Physiology and Biophysics, Health Sciences Centre, University of Calgary, Calgary, Alberta, Canada T2N 4N1
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
FOOTNOTES
REFERENCES
ABSTRACT 
Eliason, Heather L., and James E. Fewell. Influence of
pregnancy on the febrile response to ICV administration of
PGE1 in rats studied in a
thermocline. J. Appl. Physiol. 82(5):
1453-1458, 1997.
Rats near term of pregnancy have an attenuated
febrile response to intracerebroventricular (ICV) injection of
prostaglandin E1 (PGE1) when they are studied at
an ambient temperature below their thermoneutral zone. Given that
nonshivering thermogenesis in brown adipose tissue is impaired in
rodents near term of pregnancy, it is possible that the attenuated
febrile response is forced by impairment of this component of the
autonomic thermoregulatory response. If this were the case, then
near-term pregnant rats should develop a "normal" fever after
PGE1 administration if they were
studied in a thermocline where they could utilize behavioral as well as
autonomic thermoregulatory effectors to increase their body core
temperature (Tbc). Experiments
were, therefore, carried out on 13 nonpregnant and 14 pregnant
chronically instrumented rats in a thermocline (temperature gradient
10-40°C) to investigate their
Tbc responses to ICV injection of
PGE1. ICV injection of 0.2 µg
PGE1 produced significant
increases in Tbc and fever index in both nonpregnant and pregnant animals (day
19 of gestation); the increases, however, were
significantly attenuated in the pregnant compared with the nonpregnant
rats. Behavioral (e.g., selected ambient temperature) and autonomic
(e.g., oxygen consumption) thermoregulatory effectors were activated to
increase Tbc after ICV
PGE1 in both groups of animals,
but the duration of activation was shortened in pregnant compared with
nonpregnant rats. The abbreviated thermoregulatory effector responses
and the resulting attenuated febrile response to
PGE1 in the pregnant rats may have resulted from a pregnancy-related activation of an endogenous antipyretic system.
autonomic thermoregulation; behavioral thermoregulation; endogenous
pyrogen; exogenous pyrogen; fever; prostaglandin; intracerebroventricular
INTRODUCTION NUMEROUS PHYSIOLOGICAL CHANGES occur during the
maternal adaptation to pregnancy. In rats, these changes include
reversible alterations in thermoregulatory control. For example,
baseline body core temperature
(Tbc) decreases as gestation
advances and then increases around the time of parturition (12, 19).
Furthermore, there are different thermoregulatory responses to cold
(17) and to pyrogens such as bacterial endotoxin (25), interleukin-1 Previous experiments in our laboratory designed to investigate the
influence of pregnancy on the thermoregulatory response to
PGE1 (39) were carried out at an
ambient temperature of 22 ± 1°C, which is several degrees below
the thermoneutral zone of nonpregnant rats (14). In these experiments,
an intracerebroventricular (ICV) injection of 0.2 µg of
PGE1 produced significant
increases in Tbc in both
nonpregnant and near-term pregnant animals. The increase in
Tbc was, however, significantly
attenuated in near-term pregnant compared with nonpregnant rats.
Nonshivering thermogenesis in brown adipose tissue, which is an
important autonomic thermoregulatory effector for heat production
during the development of fever in rats studied at an ambient
temperature below their thermoneutral zone (13), is impaired in rodents
near term of pregnancy (2, 41). Thus it is possible that the attenuated
febrile response observed in near-term pregnant rats was forced by an
impairment of this component of the autonomic thermoregulatory response
such that Tbc did not increase to
reach the new central nervous system thermoregulatory set point after
PGE1 administration. If this were
the case, then we would expect near-term pregnant rats to develop a
"normal" fever after PGE1
administration if they were placed in a thermocline where they could
utilize behavioral as well as autonomic thermoregulatory effectors to
increase their Tbc (5,
24). Therefore, our present experiments were carried out
to test the hypothesis that nonpregnant and near-term pregnant rats
would develop similar fevers after ICV administration of PGE1 when they are studied in a
thermocline.
METHODS Experiments were carried out on 13 nonpregnant and 14 pregnant
Sprague-Dawley rats (weighing 224 ± 15 and 226 ± 11 g,
respectively, at the time of surgery and 243 ± 21 and 313 ± 17 g at the time of experiment) undergoing their first
pregnancy (Charles River Laboratories). The rats were housed in
individual cages at 22 ± 1°C in a light-dark cycle with lights
on from 0700 to 1900 and were handled every alternate day to
familiarize the animal with the investigator. All animals had
continuous access to food (Lab Diet 5001) and tap water.
(35), and prostaglandin E1
(PGE1) (39) in near-term
pregnant rats compared with those observed in nonpregnant rats. The
mechanism(s) of these pregnancy-induced changes is presently unknown.
0.6 mm anteroposterior and 2.0 mm lateral in relation to the
bregma and 2.0 mm below the surface of the brain (31).
Jeweler's screws and dental acrylic were used to fix the guide cannula
to the skull; the skin was then sutured to close the incision. A
25-gauge stainless steel stylet was placed in the guide cannula between
surgery and an experiment.
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.
The experiments were carried out with the animals in a thermocline,
which consisted of a platform containing a 200-cm sealed perspex
cylinder with an internal diameter of 11.5 cm. A linear temperature gradient of 10-40°C was produced in the
thermocline by circulating hot and cold water into copper coils wrapped
around the cylinder (Endocal Refrigerated Circulating Bath RTE-8DD,
Neslab). Selected ambient temperature was determined by monitoring the position of the animal in the thermocline and recording the
corresponding ambient temperature. For measurement of
Tbc, the thermocline was placed
over a series of platform antennas (PhysioTel CTR 86, Mini-Mitter), which received the output frequency (Hz) from the biotelemetry device;
these were interfaced with a peripheral processor (Dataquest III, Data
Sciences), which was connected to an IBM computer. Oxygen consumption
was calculated from the difference in oxygen concentrations between the
inflow and outflow gases (Ametek-Applied Electrochemistry S-3A/I
O2 analyzer) and the flow rate
(2.00 l/min).
Experimental protocol.
The rats were divided into two groups, with each animal being studied
only once. The rats were given an ICV injection of either PGE1 [0.2 µg in 10 µl of
artificial cerebrospinal fluid (CSF) or vehicle (10 µl artificial
CSF)]. Within each of these experimental groups, both nonpregnant
rats and near-term pregnant rats (day 19 or 20 of gestation)
were studied. On the day of an experiment, the animal was brought into
the laboratory in the morning, removed from its cage, and placed in the
thermocline. After at least 1 h had passed, control measurements were
made at 2-min intervals. A suitable control period was defined as one
in which Tbc was stable (i.e.,
±0.2°C) for five consecutive measurements. After the 10-min
control period, the rat was removed from the thermocline and given an
ICV injection of either PGE1 or
vehicle. For each ICV injection, a 25-gauge injection cannula was
placed into the guide cannula, and the solution of choice was allowed
to flow via gravity into the lateral ventricle over 30 s. After an
injection, the animal was placed back into the thermocline, and
Tbc, selected ambient temperature,
and oxygen consumption were measured at 10-min intervals for 2 h. Fever
index was expressed as area under the Tbc curve in degrees celcius per
hour.
After an experiment, each rat was anesthetized, and the injection
cannula was reinserted into the previously used guide cannula. Ten
microliters of black ink were then injected via gravity flow. The chest
was opened, and the cerebral vascular system was perfused through the
heart with 10% buffered Formalin to firm up the brain tissue. The
brain was then removed and sectioned. Correct placement of the
injection cannula was verified by the presence of ink in the
cerebroventricular system.
Prostaglandin.
PGE1 was purchased as
Prostin (ampule of 500 µg/ml in absolute ethanol, Upjohn) and divided
into 25-µl portions and stored in sterile plastic vials at
70°C. Artificial CSF [128 mM
Na+, 2.5 mM
K+, 1.3 mM
Ca2+, 1.0 mM
Mg2+, and 135 mM
Cl
(22)] was added to
the vial to make a working solution of 50 µg/ml immediately before
the injection. The choice of dose (50% effective dose) was based on
previous ICV PGE1
dose-Tbc response experiments in
nonpregnant rats reported by Marques et al. (24). Marques
et al. and Stitt (38) have shown that this ICV dose of
PGE1 produces an increase in
Tbc between 1.6 and 1.8°C. We have previously found that the concentration of ethanol in the injectate does not cause changes in
Tbc in either nonpregnant or
pregnant rats when mixed with artificial CSF alone (unpublished observations).
Statistical analysis.
Statistical analysis was carried out by using a three-factor
multivariate analysis of variance for repeated measures, followed by a
Newman-Keuls multiple-comparison test to determine whether state
(pregnant or nonpregnant), injectate (vehicle or
PGE1), or time influenced the
measured or calculated variables. A two-factor multivariate analysis of variance followed by a Newman-Keuls
multiple-comparison test was used to determine whether drug or state
influenced the fever index and whether state or time influenced the
change in Tbc from control after
ICV administration of PGE1. All
results are presented as means ± SD, with the exception of selected
ambient temperature, which is presented as the mode;
P < 0.05 was considered to be of
statistical significance unless otherwise indicated.
RESULTS
ICV injection of 0.2 µg PGE1
produced a significant increase in
Tbc in both nonpregnant and
pregnant animals (Fig. 1). The increase,
however, was significantly greater at 30 min in the nonpregnant rats
compared with the pregnant rats (Fig. 2).
In addition, the fever index was significantly greater in nonpregnant (0.45 ± 0.19°C/h) than in pregnant (0.26 ± 0.13°C/h)
animals after ICV administration of
PGE1. In the nonpregnant rats,
Tbc increased by 10 min, peaked at
30 min, and remained elevated for 40 min. In the pregnant rats,
Tbc increased by 10 min, peaked at
20 min, and remained elevated for 50 min. Artificial CSF did not
significantly affect Tbc in either
group of animals.
Tbc) after
intracerebroventricular administration of prostaglandin
E1 in nonpregnant (open bars) and
pregnant rats (solid bars). Values are means ± SD.
* P < 0.05 nonpregnant vs.
pregnant at a given time.
Pregnant and nonpregnant rats selected warmer ambient temperatures of
similar magnitude after ICV injection of
PGE1 (Fig. 3). In the nonpregnant rats, selected
ambient temperature increased by 10 min and remained elevated for 20 min. In the pregnant rats, selected ambient temperature increased by 10 min and remained elevated for 10 min. In both groups of animals,
selected ambient temperature decreased transiently during febrilysis.
Interestingly, after ICV injection of vehicle, selected ambient
temperature decreased in both groups of animals, the duration of which
was increased in the nonpregnant rats compared with the pregnant rats.
Pregnant and nonpregnant rats increased their oxygen consumption by
similar amounts after ICV injection of
PGE1 (Fig.
4). In the nonpregnant rats, oxygen
consumption increased by 10 min and remained elevated for 20 min. In
the pregnant rats, oxygen consumption increased by 10 min and remained
elevated for 10 min. After ICV injection of vehicle, oxygen consumption
increased in both groups of animals, the duration of which was
increased in the nonpregnant rats compared with the pregnant rats.
DISCUSSION
Our experiments provide new and important information about pregnancy and fever in rats. Novel findings in our study were the following: 1) ICV injection of 0.2 µg PGE1 produced a significant increase in Tbc in both nonpregnant and pregnant animals studied in a thermocline; the increase, however, was significantly greater in nonpregnant compared with pregnant rats and 2) both nonpregnant and pregnant rats activated behavioral (i.e., they selected a warmer ambient temperature) and autonomic (i.e., they increased their total body oxygen consumption) thermoregulatory effectors during febrigenesis; the duration of their activation, however, was shortened in pregnant compared with nonpregnant rats. Since in the absence of shivering, the increase in total body oxygen consumption after ICV administration of PGE1 provides an indirect estimate of heat production by nonshivering thermogenesis, our data do not support the hypothesis that an impairment of this component of the autonomic thermoregulatory response mediates the attenuated febrile response in rats near term of pregnancy .
Considerable evidence has accumulated that prostaglandins of the E
series play a role in mediating the febrile response to exogenous and
endogenous pyrogens (37). More than 20 years ago, Milton and Wendlandt
(26) showed that ICV administration of prostaglandin E produced a
dose-dependent increase in deep body temperature in cats.
Similar observations have been made in other species, including rabbits
(27) and rats (24, 33), and numerous studies have shown that
prostaglandins are released into the CSF during pyrogen-induced fevers
(3, 11, 32). Furthermore, Komaki et al. (20) have shown that an
intravenous injection of interleukin-1 causes release of
prostaglanin E2
(PGE2) into the interstitial
fluid of the organum vasculosum of the lamina terminalis and the medial
preoptic area of the hypothalamus in rats. Although it is
generally acknowledged that PGE2
is likely to be the "natural" prostaglandin mediator of fever,
there is no evidence that PGE1, as
used in our experiments, acts in any way differently from
PGE2 (28).
Fever, which is defined as a regulated increase in Tbc (36), is achieved by activation of heat-conserving and heat-producing mechanisms, the relative contributions of which depend on the pyrogen dose and type, the ambient temperature, and the age and size of the host (4, 6, 30, 40). Previous experiments in our laboratory have shown that the febrile response to ICV administration of PGE1 (39) is attenuated in pregnant rats compared with nonpregnant rats when they were studied at an ambient temperature below their thermoneutral zone. Given that nonshivering thermogenesis in brown adipose tissue, which is an important autonomic thermoregulatory effector for heat production during the development of fever in rats studied at an ambient temperature below their thermoneutral zone (13), is impaired in rodents near term of pregnancy (2, 41), it is possible that the attenuated febrile response was forced by an impairment of this component of the autonomic thermoregulatory response such that Tbc did not increase to reach the new central nervous system thermoregulatory set point after PGE1 administration. If this were indeed the case, then we would expect near-term pregnant rats to develop a normal fever after PGE1 administration if they were placed in a thermocline where they could utilize behavioral as well as autonomic thermoregulatory effectors to increase their Tbc (5, 24). This did not occur despite activation of both behavioral and autonomic thermoregulatory effectors after ICV injection of PGE1. Although we observed an activation of both behavioral and autonomic thermoregulatory effectors after ICV injection of PGE1, the duration of their activation was abbreviated in pregnant compared with nonpregnant rats. The nonpregnant rats selected a warmer ambient temperature and increased their total body oxygen consumption for 30 min after ICV administration of PGE1, whereas the pregnant rats selected a warmer ambient temperature for only 20 min and increased their total body oxygen consumption for only 10 min. During activation, however, the magnitudes of the behavioral and autonomic thermoregulatory effector responses were similar in nonpregnant and pregnant animals. The shortened thermoregulatory effector response in pregnant rats appeared to limit the magnitude of the febrile response after ICV injection of PGE1.
It is possible that the abbreviated thermoregulatory effector response observed in rats near term of pregnancy resulted from the activation of an endogenous antipyretic system. Arginine vasopressin, which functions as an endogenous antipyretic substance in the central nervous system (18), is elevated in plasma (22) and in a number of hypothalamic nuclei in rats near term of pregnancy (9, 22). Furthermore, Ruwe et al. (34) have shown that administration of arginine vasopressin into the ventral septal area of the rat limits the increase in Tbc evoked by the ICV injection of PGE2. Thus it is possible that a pregnancy-related activation of arginine vasopressin as an endogenous antipyretic substance may have limited the febrile response to ICV PGE1 in our experiments. This requires further investigation.
Perspectives. Regardless of the mechanism of the altered febrile response to pyrogen in rats near term of pregnancy, what are the possible consequences for the fetus? From the standpoint of oxygen supply and demand, it may be advantageous to the fetus for the mother not to develop fever for several reasons. One reason is that fever may cause circulatory adjustments such that blood flow from internal body organs, including the uterus and placenta (7), 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 (29). An ensuing decrease in uteroplacental blood flow could compromise placental gas exchange, with a resulting decrease in fetal oxygen supply (10). Another reason is that during fever, fetal body temperature, which is normally 0.4-0.8°C higher than maternal body temperature (1), increases in parallel (1, 15), or exceeds (21) the rise in maternal body temperature, with a resulting increase in oxygen demand secondary to the temperature coefficient of metabolism (i.e., Q10). If the Q10 in humans is ~2.3 (16), then metabolic rate increases ~10% for each 1°C increase in body temperature. A moderate increase in body temperature 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 oxygen saturation. Furthermore, in conditions where fetal oxygen availability is severely limited (e.g., asphyxia during birth), an increase in body temperature may exacerbate neuronal injury (8, 23) and increase perinatal morbidity and mortality.ACKNOWLEDGEMENTS
We thank Dr. Francine G. Smith for critical review of this manuscript.
FOOTNOTES
Address for reprint requests: J. E. Fewell, Heritage Medical Research Bldg., Univ. of Calgary, 206, 3330 Hospital Dr., N.W., Calgary, AB, Canada T2N 4N1 (E-mail: fewell{at}acs.ucalgary.ca).
Received 20 May 1996; accepted in final form 18 December 1996.
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A. I. Ivanov, A. A. Romanovsky, K. Matsumura, A. Mouihate, M. S. Clerget-Froidevaux, J. L. Wallace, and Q. J. Pittman Near-term suppression of fever: inhibited synthesis or accelerated catabolism of prostaglandin E2? Am J Physiol Regulatory Integrative Comp Physiol, March 1, 2003; 284(3): R860 - R865. [Full Text] [PDF]
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K. Imai-Matsumura, K. Matsumura, A. Terao, and Y. Watanabe Attenuated fever in pregnant rats is associated with blunted syntheses of brain cyclooxygenase-2 and PGE2 Am J Physiol Regulatory Integrative Comp Physiol, December 1, 2002; 283(6): R1346 - R1353. [Abstract] [Full Text] [PDF]
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 J. E. Fewell, H. L. Eliason, and R. N. Auer Peri-OVLT E-series prostaglandins and core temperature do not increase after intravenous IL-1beta in pregnant rats J Appl Physiol, August 1, 2002; 93(2): 531 - 536. [Abstract] [Full Text] [PDF]
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P. A. Tang, J. E. Fewell, and H. L. Eliason Role of AVP in mediating the altered core temperature response to a simulated open field in pregnant rats J Appl Physiol, July 1, 1999; 87(1): 170 - 174. [Abstract] [Full Text] [PDF]
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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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H. L. Eliason and J. E. Fewell Thermoregulatory control during pregnancy and lactation in rats J Appl Physiol, September 1, 1997; 83(3): 837 - 844. [Abstract] [Full Text] [PDF]
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