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1 Department of Physiology, School of Allied Health Sciences, Osaka University Faculty of Medicine, Yamadaoka 1 - 7, Suita, Osaka, 565-0871, and 2 Department of Human Behavior Science, Nara Women's University, Kitauoyahigashimachi, Nara, 630-8506, Japan
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Effects of estrogen on thermoregulatory vasomotion and heat-escape behavior were investigated in ovariectomized female rats supplemented with estrogen (replaced estrogen rats) or control saline (low estrogen rats). First, we measured tail temperature of freely moving rats at ambient temperatures (Ta) between 13 and 31°C. Tail temperature of the low estrogen rats was higher than that of the replaced estrogen rats at Ta between 19 and 25°C, indicating that the low estrogen rats exhibit more skin vasodilation than the replaced estrogen rats. There was no significant difference in oxygen consumption and core temperature between the two groups. Second, we analyzed heat-escape behaviors in a hot chamber where rats could obtain cold air by moving in and out of a reward area. The low estrogen rats kept Ta at a lower level than did the replaced estrogen rats. These results imply that the lack of estrogen facilitates heat dissipation both by skin vasodilation and by heat-escape behavior. Ovariectomized rats may mimic climacteric hot flushes not only for autonomic skin vasomotor activity but also for thermoregulatory behavior.
autonomic thermoregulation; behavioral thermoregulation; hot flush
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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ESTROGEN, ONE
OF THE MOST physiologically potent substances, affects many
homeostatic functions. For thermoregulation, estrogen seems to have no
(4, 11, 14) or a slight hyperthermic effect (16). Oxygen consumption
(
O2) is not influenced by estrogen (14, 25). It is, however, a common observation in rats
that estrogen causes skin vasoconstriction (11, 12, 19).
Although the above-mentioned measurements of
O2 were done in unrestrained animals,
all the experiments involving vasomotion were done under restraint,
which is known to have a major effect on thermoregulatory responses
(3, 7). Thus it is still an open question as to whether
estrogen influences skin vasomotor activity under unstressed conditions.
Recently, the effect of estrogen on peripheral vasomotor activity has been suggested as a possible model to investigate the etiology of human menopausal hot flushes (11, 19). The hot flush is a sudden hot feeling accompanied by skin vasodilation (13). Hyperthermic stimuli such as a high ambient temperature (Ta), wearing excessive clothing, and drinking hot beverages accelerate hot flushes (6, 13). Therefore hot flushes have been considered to be a malfunction of thermoregulatory heat dissipation mechanisms. Because the administration of estrogen to climacteric women reduces the incidence of menopausal hot flushes (22), it is generally accepted that estrogen is closely related to the etiology of hot flushes. Although tail vasodilation of ovariectomized rats has been suggested as a model of human hot flushes (11, 19), the supporting data were drawn from experiments on restrained animals. Also, Ta was not carefully documented. During hot flushes, climacteric women seek to lower Ta by air conditioning and undressing (13), which are normally thermoregulatory responses appropriate under conditions of "hyperthermia." Therefore the modulation of behavioral thermoregulation may be also related to the etiology of hot flushes, but this as yet has not been closely examined.
The aim of this study is to investigate the effects of estrogen on tail vasomotion and heat-escape behavior in freely moving ovariectomized rats and to examine the validity of these responses as a model of hot flushes. First, we investigated tail vasomotor responses in freely moving rats with or without estrogen administration in a wide range of Ta with the method we recently developed (10). Second, we examined the effect of estrogen on operant heat-escape behavior in an apparatus that was also recently developed (5). Preliminary results of the experiments of vasomotion previously appeared in abstract form (9).
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Animal preparation. We used 56 9-wk-old virgin female crj-Wistar rats (220-270 g) in this series of experiments. Rats were housed under a 12:12-h lighting schedule (on 0700-1900) with free access to food and water at 22°C. The protocols of this series of experiments were approved by the Animal Care Committee of Osaka University Faculty of Medicine.
All rats were ovariectomized using a dorsal approach. Anesthesia involved an intraperitoneal application of ketamine chloride (a 200 mg/kg loading dose plus 60 mg · kg
1 · h1 if necessary)
and inspired sevoflurane (15). Two weeks after the
ovariectomy, a Silastic tube (Dow Corning) containing 2 mg estradiol
benzoate was implanted (14) subcutaneously in 29 ovariectomized rats (replaced estrogen rats) under the same anesthesia
condition as the first surgery. In the other 27 rats, a tube of the
same size containing only saline was implanted (low estrogen rats). At
the same time, a sterilized biotelemetry device (PhysioTel, DataScience, St. Paul, MN) for measuring core temperature
(Tcore) and activity was implanted in the peritoneal
cavity. The estrous states of rats after tube implantation were
verified by examining vaginal smears at 2-day intervals. We started the
experiments when cornified vaginal smears were obtained in the replaced
estrogen rats three successive times, which indicates that the estrogen application was effective (16). Such vaginal smears were
obtained within 10 days of implantation of the estrogen tube. For the
low estrogen rats, we started the experiments 10 days after the second operation. Vaginal smears were obtained just after the completion of
each measurement. Each rat was used only once a day with an interval
between experiments of at least 2 days. All rats habituated to
experimental procedures after several training sessions. All measurements for a particular rat were completed 5 wk or less after the
first measurement. In preliminary experiments at night, we could hardly
estimate rats' thermoregulatory behavioral responses with the present
system because rats are too active in the nighttime. Therefore
experiments were conducted during the daytime.
Vasomotion. We used 16 low and 18 replaced estrogen rats in this experiment. At noon on the day of the experiment, a rat was put into an acrylic experimental box (35 × 25 × 20 cm) that was placed in a climatic chamber whose temperature was set at 13, 16, 19, 22, 25, 28, or 31°C. The order of chamber temperature for each rat was chosen at random. The Ta in the experimental box was measured by a Co-Cu thermocouple. A telemetry receiver board (CTR86, DataScience) was placed under the box for measuring Tcore and activity. Tail temperature (Ttail) measurement for these freely moving rats was done as previously described in detail (10). Briefly, a Co-Cu thermocouple was taped using medical adhesive plaster (Nichiban, Osaka, Japan) to the lateral surface of the tail 6 cm from the base. The thermocouple was protected by a T-shaped light acrylic tube. Its lead wires extended upward and out through a small slip ring in the ceiling of the experimental box. The lead wires did not restrict movement of the rat. Measurements started 2 h after the rat had been placed in the box and lasted for 3 h. Signals of Ttail, Ta, Tcore, and activity were fed into a computer at 1-min intervals.
O2.
The same rats as used in the experiment involving vasomotion were used
in the measurement of O2 at
Ta of 13, 22, and 31°C for 2 h. All measurements
were started 2 h after rats had been put in an experimental box
(30 cm long × 12 cm wide × 12 cm height) at noon. An
open-circuit method was used to measure
O2. The box was completely sealed except
one hole of 1-cm diameter on one side and nine holes of 5-mm diameter
on the other side. From the former hole, the air in the box was
continuously removed at a rate of 2 l/min and fed into an oxygen
analyzer (LC-700, Toray, Shiga, Japan) after passing through a
desiccator. Signals of O2 from the
oxygen analyzer were also fed into a computer and sampled at 1-min intervals.
Heat-escape behavior. We used the remaining 11 low estrogen and 11 replaced estrogen rats in this experiment. The system for testing behavioral thermoregulation (5) consisted of a chamber (60 long × 50 wide × 50 cm height) with an inlet and an outlet that received air from two air supply units (CAU-210, TABAI ESPEC, Osaka, Japan). One of them supplied cold air (0-30°C at a rate of 3 m3/min) and the other hot air (20-45°C at the same rate). The circulation of cold or hot air in the chamber was switched by computer-controlled valves. The rat was placed in a plastic box (50 long × 10 wide × 30 cm height) within the chamber. The top of the box was covered with metallic mesh, and the side of the box was perforated so that airflow over the animal was facilitated. The location of the rat within the box was monitored by light-emitting diodes 2 cm above the floor of the box, positioned at 10-cm intervals along the length of the box, and directed toward photoelectric cells on the opposite side. The position of the rat was thus located within one of five 10 × 10 cm2 areas. Air of high temperature, "load temperature" (TL), normally blew into the chamber. When the rat entered a predetermined "reward zone," the hot air was replaced with the "reward" cold air of 5°C for 30 s. To receive a subsequent reinforcement of cold air the rat had to leave the reward zone and reenter it. Tcore was measured by two telemetry receiver boards (CTR86) placed under the box. TL was changed in the sequence of 1) 25°C for 80 min, 2) 32°C for 80 min, 3) 36°C for 80 min, and finally 4) 40°C for 80 min. During the experiment, Ta, Tcore, and the position of the rat were recorded at 1-s intervals.
Estradiol determination.
After the final experiments, each rat was deeply anesthetized with an
overdose of anesthetic, and 5 ml of blood was obtained by cardiac
puncture. The blood was centrifuged, and the serum was stored at
20°C until the assay was performed. The concentration of estrogen
in the serum was measured by radioimmunoassay. The assay was performed
at Osaka Kessei (Osaka, Japan), and the coefficients of intra- and
interassays were both within 10%.
Statistical analysis.
Statistical significance was tested by ANOVA and Fisher's protected
least-significant difference test as post hoc test for the
experiments of vasomotion and O2. For
the analysis of number of rats with vasodilations of wide fluctuations,
a 
2 test was used. For the analysis of serum estradiol
levels, statistical significance was certified by a t-test.
In all statistical analyses, we regarded results as statistically
significant if P < 0.05. Values are expressed as
means ± SE.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Vasomotion and O2.
Typical recordings of Ttail and Tcore of the
low and the replaced estrogen rats are shown in Fig.
1. At a Ta of 13°C,
Ttail of both low and replaced estrogen rats stayed
slightly above the Ta, which indicates that the tails were
fully vasoconstricted. At Ta of 19°C, although the
Ttail of the replaced estrogen rat still stayed near the
Ta, the Ttail of the low estrogen rat showed a
spontaneous and sharp rise at around the 30th min, which reached as
high as 30°C (Fig. 1A). This rise in the Ttail
indicates a transient vasodilation of the tail. Such large
vasodilations at Ta of 19°C were observed more frequently
in low estrogen rats than in replaced estrogen rats. At Ta
of 25°C, the Ttail of the low estrogen rat stayed
well above 30°C and fluctuated only in a small temperature range,
which means that the tail was vasodilated most of the time. On the
contrary, the Ttail of the replaced estrogen rat fluctuated
widely in the temperature range from just above Ta to
31°C, which indicates an alteration between vasoconstriction and
vasodilation (Fig. 1C). Note that Ttail began to
rise when the Tcore was high, and the Tcore
decreased several minutes after the Ttail rise. Thus
Ttail and Tcore usually changed in a mirror image (compare Fig. 1, A and B, and C
and D).
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Ta as an index
of average vasomotor condition of the tail, which would be large when
the tail is vasodilated. This value was significantly greater in the
low estrogen rats than in the replaced estrogen rats at a
Ta of 19, 22, and 25°C (Fig.
2A). In general, the tail of a
rat fully vasoconstricts at a low Ta, fluctuates between
vasoconstriction and vasodilation at a mild Ta, and fully
vasodilates at a high Ta. When the tail fully vasodilates
or vasoconstricts, Ttail (thus Ttail Ta) is relatively constant. Fluctuation between
vasoconstriction and vasodilation is reflected as a large variation in
Ttail. Tail temperature measured at the similar site as in
the present study is >5°C degrees higher than Ta when
the tail is fully vasodilated (27). Thus we obtained the
number of rats at each Ta in which the difference between
highest and lowest Ttail in a 3-h measurement period was
>5°C. The number of rats showing large Ttail variations showed a bell-shaped distribution in both the low and the replaced estrogen rats (Fig. 2A, inset). The curve is
shifted to the left, to the lower temperature range, for the low
estrogen rats. At Ta of 19°C, the number of low estrogen
rats with large Ttail variation (11 of 16) was
significantly larger than that of replaced estrogen rats with large
Ttail variation (5 of 18). Note that the number is not zero
even at Ta of 13°C. Although Tcore of the
replaced estrogen rats tended to be higher than that of the low
estrogen rats especially at low Ta (Fig. 2B),
there were neither significant differences in Tcore at any
investigated Ta nor in overall effects between the low and
the replaced estrogen rats. There was also no significant difference in
the activity between the low and the replaced estrogen rats at any
investigated Ta.
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O2 at Ta of 13, 22, and 31°C was 22.5 ± 10.5, 17.0 ± 8.2, and 13.9 ± 6.9 ml · kg1 · min1,
respectively. These values also did not differ between the low and the
replaced estrogen rats at any Ta. The averaged
O2 decreased significantly in proportion
to the increase of Ta.
Heat-escape behavior.
Typical recording of the experiment of heat-escape behavior is
illustrated in Fig. 3. A transient sharp
decrease in Ta indicates that the rat entered the reward
zone and obtained cool reward air. Vigorous movements lasting several
10-min periods after the rat was put in the experimental chamber or
after TL was changed to a next level were due to
exploratory behaviors in response to the changed environment. Thus the
data depicted in Fig. 4 were taken from
the last 30-min period at TL of 25°C and the last 60-min period at TL of 32, 36, and 40°C. As the TL
increased, the frequency of obtaining rewards increased. At
TL of 40°C, the low estrogen rats obtained significantly
more rewards than the replaced estrogen rats (Fig. 4A), and
as a result the Ta became significantly lower (Fig.
4B). At TL of 36°C and lower, there were no
significant differences in the number of rewards and Ta.
Averaged Tcore at TL of 25, 32, 36, and 40°C
were 37.8 ± 0.1, 37.5 ± 0.1, 37.8 ± 0.1, and
37.7 ± 0.1°C, respectively. These values are not significantly different between the low and the replaced estrogen rats.
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Estradiol determination. Serum estradiol concentration of the replaced estrogen rats was 95.6 ± 5.6 pg/ml. This value is significantly higher than that of the low estrogen rats, which was below the detection limit (10 pg/ml).
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The tail is the major site for nonevaporative heat loss in rats.
Ttail depends on two factors, Ta and blood flow
of the tail. When blood vessels of the tail are fully constricted,
Ttail is close to Ta. On the contrary, when
they are fully dilated, Ttail is considerably higher than
Ta. So we took Ttail Ta as
an index of the vasomotor condition of the tail. This value was small
at low Ta and large at high Ta in both groups
of rats. At the lowest Ta (13 and 16°C) and at the
highest Ta (28 and 31°C), there was no significant
difference in Ttail Ta between the low
and replaced estrogen rats. This indicates that at the low
Ta the tail was close to full vasoconstriction and at the
high Ta it was close to full vasodilation.
In the temperature range between 19 and 25°C, Ttail Ta was significantly higher in the low estrogen rats
than in the replaced estrogen rats. Tail vasomotions of the rat occur
in an on-off fashion (26). Thus the tail blood vessels
fluctuate between full constriction and full dilation rather than
keeping a stable moderate tonus. Such fluctuation produces a large
variation of Ttail. The bell-shaped distribution in Fig.
2A, inset, certainly indicates that the tail
tended to vasoconstrict at low Ta, to vasodilate at high
Ta, and to fluctuate between vasoconstriction and
vasodilation at the Ta in between. The distribution is
shifted to the left, lower Ta range in the low estrogen
rats compared with the replaced estrogen rats. Therefore vasodilation
of the tail occurred at lower Ta in the low estrogen rats
than in the replaced estrogen rats. As a result, Ttail Ta in the middle Ta range was greater for
the low estrogen rats (Fig. 2A).
In the present experiments, more than half of the low estrogen rats showed vasodilation at Ta of 19°C (Fig. 2A, inset). Likewise more than half of the replaced estrogen rats showed tail vasodilation at Ta of 22°C. In previous studies done on restrained rats, tail vasodilation was observed only at a higher Ta range. For example, tail vasodilation occurred at Ta of 33°C in female rats locked in a narrow cage in which they could not turn around (26). Or when the female rat's tail was tightly fixed to a stainless tube, the tail vasodilated at Ta of 27°C (18). Tail vasomotor activity of the rat is controlled only by sympathetic nerves (17). Restraint is a strong stress for rats and would increase sympathetic tone. Thus in restrained animals tail vasodilation would occur only at such a high Ta that the thermoregulatory drive for vasodilation is strong enough to surpass the drive for vasoconstriction elicited by the stress. The present observations in unrestrained rats suggest that nonevaporative heat loss from the tail is brought into action at a lower Ta than previously considered, as low as 13°C in some rats (Fig. 2A, inset).
Changes of Ttail in aged rats of different reproductive statuses were reported previously. Aged, over 19-mo-old, rats in constant estrus or pseudopregnancy showed a tendency of vasodilation compared with young, below 7-mo-old, rats (20). However, Ttail was measured at only the two Ta, 24 and 30°C. Also, the rats were restrained and peripheral estrogen levels were not measured. Our experiments may be the first to report how estrogen affects thermoregulatory vasomotions at a wide range of Ta, using freely moving animals of matched age, with controlled peripheral estrogen levels.
The mechanisms that induce increased tail vasodilation in the low estrogen rats are still uncertain. One possibility is an effect of gonadotropin-releasing hormone (GnRH) that increases as a result of the decrease in systemic estrogen level (21). The participation of GnRH in thermoregulation was recently demonstrated by the fact that the injection of GnRH into the septal area, where GnRH receptors are densely located (1), elicits vasodilation in the tail of ovariectomized rats (10). The GnRH level in the low estrogen rats would be higher than in the replaced estrogen rats and therefore would cause a tendency toward vasodilation.
Estrogen had no effect on O2 at any
investigated Ta. This result coincides with previous
studies in which O2 was measured at
Ta of 22°C (8) or at Ta of 15 and 25°C (4). Ineffectiveness of estrogen on
Tcore is also consistent with previous studies made at
ambient temperatures between 15 and 30°C (4, 11, 14). In
our previous study (9), however, we observed significant difference in Tcore between low and replaced estrogen rats
at Ta of 13, 19, and 22°C. Because it became clear that
the apparatus for measuring Ttail and Tcore in
that experiment had placed considerable restraint on the rats, we
improved the apparatus and conducted the present series of experiments.
Therefore the contradiction concerning the effect of estrogen on
Tcore between the previous and present results might be due
to the difference in the stress induced by restraint.
Although there is no difference in O2
between the low and the replaced estrogen rats, heat loss from the skin
is facilitated in the low estrogen rats. Then why is there no
difference in Tcore? Although statistically insignificant,
Tcore of the replaced estrogen rats tended to stay higher
than Tcore of the low estrogen rats (Fig. 2B).
Indeed it is also reported that injection of 1 µg estradiol benzoate
increases rectal temperature of ovariectomized rats at room temperature
(16). The effect of estrogen on vasomotion, although
measurable, must not have been strong enough to have a clear influences
on Tcore.
The experiment of heat-escape behavior showed that the low estrogen
rats tended to keep Ta lower than the replaced estrogen rats when the heat was severe. At a Ta near or higher than
Tcore, nonevaporative heat dissipation through the tail
becomes ineffective and evaporative heat loss responses such as
salivation and grooming are fully activated (24).
Therefore at a Ta of 40°C, heat-escape behavior, if
available, might be a very important means for rats to prevent
Tcore from rising. The facilitation of heat-escape behavior
in the low estrogen rats is not simply due to an increase in the
sensitivity to stress. Evidence for this is provided by cold-escape
behavior experiments (23). In a situation opposite to that
of the present study, replaced estrogen rats tended to keep
Ta higher than the low estrogen rats in extreme cold
(7°C). Rewards of heat were provided by rat's pressing a lever.
The lack of estrogen apparently acted to modulate thermoregulatory
behavior so as to lower Ta. The low estrogen rats would
feel "hotter" than the replaced estrogen rats.
Although the peripheral estrogen level in the replaced estrogen rats was slightly higher than the estrogen levels of intact female rats (2), estrogen levels even higher than the level of the replaced estrogen rats were regarded as "physiological" in previous studies (11, 23).
On the basis of the present results of autonomic and behavioral experiments with controlled estrogen level, it can be concluded that lack of estrogen facilitates not only autonomic heat dissipation but also heat-escape thermoregulatory behavior.
Perspectives
Several investigators hypothesize that the tail vasodilation seen in ovariectomized rats can be regarded as a model of the human hot flush although their experiments used retrained animals only at a few ambient temperatures (11, 12, 19). The observations in the present experiments that the lack of estrogen facilitates skin vasodilation adds convincing support to the hypothesis. Furthermore, climacteric women are often eager for the behavioral cooling provided by air conditioning as well as by light clothing (13) during an attack of hot flushes. Both behaviors can be regarded as facilitation of heat-dissipating behavior. Therefore ovariectomized rats may mimic climacteric hot flushes not only with the autonomic vasomotion but also with the behavioral thermoregulation.| |
ACKNOWLEDGEMENTS |
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We thank Drs. Y.-H. Zhang and M. Nakano, Osaka University for technical help. We are also grateful to Dr. L. I. Crawshaw, Portland State University, for critical reading of this manuscript.
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FOOTNOTES |
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This study was partially supported by the Grant 10670062 from the Ministry of Education, Science, Culture and Sports of Japan.
Address for reprint requests and other correspondence: T. Hosono, c/o Prof. K. Kanosue, Dept. of Physiology, School of Allied Health Sciences, Osaka Univ. Faculty of Medicine, Yamadaoka 1-7, Suita, Osaka, 565-0871, Japan (E-mail: hosono{at}sahs.med.osaka-u.ac.jp).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received 17 April 2000; accepted in final form 4 January 2001.
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RESULTS
DISCUSSION
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and open column, low estrogen rats (n = 16). 
and filled column, replaced estrogen rats
(n = 18). *P < 0.05, low estrogen rats
vs. replaced estrogen rats at each Ta. Vertical bars
represent SE. B: Tcore at Ta between
13 and 31°C.
