| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Noll Physiological Research Center and Graduate Program in Physiology, The Pennsylvania State University, University Park, Pennsylvania 16802-6900
 |
ABSTRACT |
|---|
 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
To examine the influence of chronic hormone replacement therapy (HRT) on the central and peripheral cardiovascular responses of postmenopausal women to direct passive heating, seven women taking estrogen replacement therapy, seven women taking estrogen and progesterone therapy, and seven women not taking HRT were passively heated with water-perfused suits to their individual limit of thermal tolerance. Measurements included heart rate (HR), cardiac output, blood pressure, skin blood flow, splanchnic blood flow, renal blood flow, esophageal temperature, and mean skin temperature. Cardiac output was higher in women taking estrogen and progesterone therapy than in women not taking HRT (7.12 ± 0.70 vs. 5.02 ± 0.57 l/min at the limit of thermal tolerance, respectively; P < 0.05) because of a higher HR. However, when the HR data were plotted as a percentage of the maximum HR or percentage of HR reserve, there were no differences among the three groups of women. Neither splanchnic nor renal blood flow differed among the groups of women. These data suggest that HRT has little effect on the cardiovascular responses to direct passive heating.
aging; cardiac output; skin blood flow; cardiovascular responses; hyperthermia
| |
INTRODUCTION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
DURING HEAT
STRESS, blood flow to the cutaneous vasculature increases
dramatically to move heat away from the core and dissipate it to the
environment. To support this increase in skin blood flow
(SkBF), cardiac output (
c) increases, and blood is
distributed away from the splanchnic and renal vascular beds.
Our laboratory recently reported that, during passive heat stress to
the limit of thermal tolerance, older men (64-81 yr), compared
with younger men (19-28 yr), responded with a lower SkBF, which
was associated with both a lower c and a reduced
ability to redistribute blood from their combined splanchnic and renal vascular beds (12). The lower c
in the older men was due primarily to a lower stroke volume (SV).
Numerous studies have shown that both endogenous and exogenous female steroid hormones can affect cardiovascular and thermoregulatory function in young women. Both during a normal menstrual cycle and during oral contraceptive use, changes in core temperature and the SkBF response to heating correspond to changes in the estrogen-to-progesterone ratio (2, 18).
There is also evidence that hormone replacement therapy (HRT) in postmenopausal women may affect the cardiovascular mechanisms that underlie human thermoregulatory control. Women taking estrogen replacement therapy (ERT) have lower core temperatures at rest and during exercise in a warm environment compared with women not taking any HRT (1, 19). Additionally, women taking ERT have a higher SkBF at any given core temperature than women not taking any HRT (1). These alterations due to ERT were blocked by the addition of progestins to the HRT.
It is unknown, however, how control of central hemodynamic function and
blood flow to visceral organs may be affected by HRT during direct
passive heating. In several animal models, ERT has been shown to cause
increased c via increased SV (7,
9, 16). Additionally, in humans,
c is increased during pregnancy, a time when
estrogen levels are elevated (10, 13). In a
recent study of postmenopausal women, c, SV, and
ejection fraction (EF) were increased at rest after 16 wk of estrogen
and progesterone (E+P) replacement therapy (17). Although
an increase in plasma volume (PV) could have accounted for the increase
in SV in that study, it could not account for the increase in EF. Thus
there is evidence that HRT can increase resting c by
increasing the inotropic function of the heart. An increase in
inotropic function of the heart could attenuate the age-related decline
in the c response to direct passive heating.
HRT also has the potential to impact peripheral hemodynamic responses to heating. HRT in postmenopausal women has been shown to increase blood flow to several vascular beds, including the heart and uterus (6). It is unknown whether HRT also increases blood flow to the splanchnic and renal vascular beds and whether it would affect the vasoconstriction that occurs in these vascular beds during a heat stress. For example, more vasoconstriction in the viscera may be needed to support the increase in cutaneous blood flow seen with ERT.
Therefore, the purpose of this investigation was to examine the
influence of chronic ERT and E+P on the central and peripheral hemodynamic responses to prolonged direct passive heating. It was
hypothesized that women taking ERT and E+P would have a higher c at the limit of thermal tolerance because of a
higher SV.
| |
METHODS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Subjects
All procedures used in this investigation were approved in advance by the Committee for the Protection of Human Subjects of the Office of Regulatory Compliance at The Pennsylvania State University. After approved informed consent procedures, 21 postmenopausal women (aged 52-80 yr) volunteered for the present investigation. Seven women were not receiving HRT (No HRT), seven women were receiving chronic ERT, and seven women were receiving chronic E+P. Chronic HRT was defined as continuous therapy for at least 2 yr. All but one woman taking ERT received 0.625 mg of Premarin (Wyeth-Ayerst Laboratories, Philadelphia, PA). The one exception was a woman using an estrogen patch (Estraderm, Novartis Pharmaceuticals, East Hanover, NJ). Four of the women in the E+P group were receiving PremPro (Wyeth-Ayerst Laboratories), which contains 0.625 mg of Premarin and 2.5 mg medroxyprogesterone acetate (Provera, Upjohn, Kalamazoo, MI). The other three women in the E+P group received 0.625 mg of Premarin for the first 25 days of the month and received either 5 mg (2 women) or 10 mg (1 women) of Provera on days 14-25. Women who were not receiving HRT were defined as postmenopausal by the following criteria: 1) circulating follicle-stimulating hormone >30 IU/ml (11), 2) circulating 17
-estradiol <25 pg/ml (11), and 3) cessation of menses for at least 1 yr. Women who had both a hysterectomy and oophorectomy were
considered postmenopausal. All women were healthy nonsmokers not taking
any medication that could affect the thermoregulatory or cardiovascular
variables of interest.
Before participating in the experimental protocol, subjects
underwent a screening procedure. This procedure included a medical examination by a physician, measurement of skinfold thickness as an
estimate of adiposity, a resting 12-lead electrocardiogram, blood tests
to establish normal liver and kidney function, and blood pressure
measurement. Subjects also underwent a maximal graded exercise test on
a treadmill to determine maximal heart rate (HR) and maximal oxygen
consumption (
O2 max).
Subject characteristics are presented in Table
1. The three groups of subjects were
matched for height, weight, adiposity, surface area,
O2 max, PV, and blood volume. The No
HRT group was older than the E+P group and thus had a lower maximal HR.
As expected, women taking ERT and E+P had higher serum estradiol concentrations and lower FSH concentrations than did the women in the
No HRT group. Additionally, the initial esophageal temperature (Tes) measured during the first minute of the baseline
period was lower in the ERT group than in either the E+P or No HRT
groups.
|
Experimental Procedures
Instrumentation. Subjects reported to the laboratory at 0800 after an 8-h fast. They were asked to refrain from ingesting alcohol for 24 h before the test and caffeine for 12 h before the test and were encouraged to drink plenty of fluids in the 24 h before the experiment. Subjects were weighed before and after the experiment to estimate sweat loss. A catheter was inserted into an antecubital or forearm vein of the right arm for infusion of a solution containing indocyanine green (ICG) and p-aminohippurate (PAH) for the measurement of splanchnic blood flow (SBF) and renal blood flow (RBF), respectively. A second catheter was placed in a vein distal to the site of infusion in either the left or right arm for blood sampling.
With assistance, the subjects inserted a thermistor located in a sealed pediatric feeding tube for measurement of Tes. To aid insertion, subjects drank 2.5 ml/kg of water. Eight copper-constantan thermocouples were affixed to the subjects' skin on the upper and lower back and on the left side and right sides of the chest, stomach, shoulder, thigh, and calf. Mean skin temperature (
sk) was calculated as the unweighted average of
these eight thermocouples.
Two blood pressure cuffs and a mercury-in-Silastic strain gauge were
placed on the left forearm for measurement of forearm blood flow (FBF)
via venous occlusion plethysmography (24). Under
conditions of passive heating, increases in FBF represent increases in
SkBF because underlying muscle blood flow does not change
(3). The FBF measurement at each time point was calculated as the average of three to four traces. The upper blood pressure cuff
was also used to measure blood pressure by brachial auscultation. HR
was measured via a three-lead electrocardiogram.
c was determined with the acetylene-rebreathing
technique (20) by using a mass spectrometer for analysis
of gas concentrations. SV was calculated as c/HR.
Total peripheral resistance (TPR) was calculated as mean arterial
pressure (MAP)/c.
Protocol. After instrumentation, subjects donned a water-perfused suit and plastic coverall to prevent evaporative cooling. Subjects wore only shorts and a sports bra under the suit. The water-perfused suit covered the entire body except for the head, feet, and arms below the elbow. Subjects were supine throughout the experiment, and, to begin the protocol, thermoneutral water (~34°C) was circulated through the suit for 45 min, during which baseline data were collected. After the baseline period, the temperature of the water circulating through the suit was changed to ~50°C, and this temperature was maintained until each subject's individual limit of thermal tolerance was reached. The limit of thermal tolerance was defined as either the point at which subjects expressed that they were too uncomfortable to continue or when Tes reached 39°C. At this time, the subjects were cooled with 15°C water for at least 15 min.
Tes,sk, and HR were measured
continuously throughout the protocol. All other measurements were taken
every 15 min throughout the protocol. The measurement of
c and a 7-ml blood draw were performed
simultaneously, followed sequentially by FBF measurement and then blood
pressure measurement.
SBF and RBF. In this study, SBF and RBF were measured from constant infusion of ICG and PAH, respectively. At the beginning of the baseline period, 20 ml of blood were drawn to serve as a blank. Then, a priming dose of ICG (0.10 mg/kg body wt) and PAH (8.0 mg/kg body wt) was injected into the infusion catheter. For the remainder of the protocol, a constant infusion of 0.5 mg/ml ICG and 12 mg/ml PAH was maintained at a rate of 1.0 ml/min. As described in Protocol, blood was drawn every 15 min after the start of the infusion for the entire protocol. Plasma concentration of ICG was measured spectrophotometrically (absorbency 805 nm), and plasma concentration of PAH was determined with the color reagent N-(1-naphthyl)-ethylenediammonium dichloride. Additionally, the blood samples were used to calculate changes in plasma volume via changes in hematocrit (Hct) and hemoglobin concentrations (4).
SBF changes during passive heating, and thus corrections for non-steady-state conditions in the calculation of SBF were necessary because dye removal rate does not equal dye infusion rate. Therefore, splanchnic plasma flow was calculated as (15)
![SPF<IT>=</IT>{I<IT>−</IT>[(C<SUB>a2</SUB><IT>−</IT>C<SUB>a1</SUB>)<IT>/&Dgr;t</IT>]<IT> · </IT>PV}<IT>/</IT>(ER<IT> · </IT>C<SUB>a</SUB>)](/content/vol89/issue1/fulltext/97/img002.gif)
|
t is the change in time between samples (15 min); ER is
the individual extraction ratio for ICG (see Determination of
ER); and Ca is the arterial dye concentration. SBF was
calculated as SPF/(1 
Hct).
Because of the short protocol and rapid changes in RBF, urine
collection of PAH (which is the preferred method to measure RBF) was
not possible in this study. Additionally, the same constraints for the
measurement of SBF also apply to the measurement of RBF; i.e., the
assumption of equality between excretion rate and infusion rate does
not hold. Therefore, corrections were also made in the calculation of
RBF. Renal plasma flow was calculated as
![RPF<IT>=</IT>{I<IT>−</IT>[(C<SUB>a2</SUB><IT>−</IT>C<SUB>a1</SUB>)<IT>/&Dgr;t</IT>]<IT> · </IT>PV}<IT>/</IT>C<SUB>a</SUB>](/content/vol89/issue1/fulltext/97/img003.gif)
|
Hct).
Determination of ER
On a day separate from the experimental protocol, the resting ER for ICG was measured. ER was measured in each subject by an intravenous bolus injection technique based on a two-compartment model of ICG removal from plasma by the liver (8). After the subjects had been supine for 30 min, an aliquot of venous blood was drawn to serve as a spectrophotometer blank. Then, a bolus of 0.5 mg/kg body wt ICG was injected into an antecubital vein. Five minutes after the bolus injection, a 5-ml venous sample was collected in a lithium-heparin-treated tube, followed by venous samples every 3 min for 30 min. Samples were centrifuged at 3,000 rpm for 20 min, and the plasma concentration of ICG was determined spectrophotometrically (absorbancy of 805 nm). ER was calculated for each subject from the two slopes of the plasma disappearance curve of ICG. Heating does not appear to alter ER (14), and thus the ER determined on this day was used in the calculations of SBF during the heating protocol.Determination of PV
On a day separate from the experimental protocol and the ER determination, baseline PV was determined via injection of Evans blue dye (EBD) (5). After the subjects had been supine for 30 min, an aliquot of venous blood was drawn as a spectrophotometer blank. Then, a bolus of EBD was injected into an antecubital vein. Venous blood samples were collected every 10 min for 30 min. Samples were centrifuged at 3,000 rpm for 20 min, and the plasma concentration of EBD was determined spectrophotometrically (absorbancy of 620 nm).Statistical Analyses
Significant differences between subject characteristics were determined by using a one-way ANOVA. A two-way repeated-measures ANOVA (main effect of HRT group, main effect of time, and group × time interaction) was performed on all variables from baseline through the first 60 min of heating. To account for differences in the time to the limit of thermal tolerance, each individual's final 15 min of heating were also used to calculate a group mean, and another two-way repeated-measures ANOVA was performed on these data. Homogeneity of variance and normality of the data were verified before the ANOVA. Post hoc analyses with a Bonferroni correction were used to evaluate significance of specific pairwise comparisons. The level of significance was set at P < 0.05. Values are presented as means ± SE.| |
RESULTS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Temperature Variables
The time to reach thermal tolerance varied widely among individuals (45-105 min), but there was no significant difference among the three groups (69 ± 8, 71 ± 6, and 76 ± 7 min for E+P, ERT, and No HRT groups, respectively; P = 0.77). There were no significant group differences in Tes or
sk at baseline or at any time during the heating
protocol (Fig. 1). ERT has been shown to
lower baseline Tes (1, 19). Table
1 shows that, during the first minute of the baseline period,
Tes was lower in the ERT group compared with both the No
HRT and E+P groups. However, the water-perfused suit is designed to
tightly control skin temperature, and the plastic coverall prevents
evaporative heat loss. This experimental manipulation could have caused
temperatures in the three groups of women to not differ statistically
by the end of the baseline period. It is also possible that the sample
size in this study was too small to detect the small difference in temperature. Sweating rate did not differ significantly among the three
groups of women (442 ± 48, 444 ± 81, and 441 ± 32 g/h in ERT, E+P, and No HRT groups, respectively; P = 0.99)
|
Cardiac Responses
c (Fig. 2) was
significantly increased in all three groups of women after 30 min of
heating (P < 0.05). The E+P group had higher
c than did the No HRT group throughout the entire
protocol (7.12 ± 0.70 vs. 5.02 ± 0.57 l/min at the limit of
thermal tolerance, respectively; P < 0.05).
|
The higher c in the E+P group was due to a higher HR
response (Fig. 2). HR in the E+P group was significantly higher than in
both the ERT and No HRT groups beginning at 15 min of heating (107 ± 5 vs. 90 ± 3 and 86 ± 5 beats/min at the limit of
thermal tolerance in E+P vs. ERT and No HRT groups, respectively;
P < 0.05). HR was significantly elevated above
baseline in all three groups of women beginning at 15 min of heating
(P < 0.05). SV was not significantly different among
the three groups at any time during the protocol, and SV did not change
significantly during the heating (Fig. 2).
The higher HR response in the E+P group can be explained by their
higher maximal HRs (Table 1). When the HR data are plotted either as a
percentage of the maximal HR or as a percentage of the HR reserve (Fig.
3), there are no longer any statistically significant group differences in the HR response (63 ± 1, 57 ± 3, and 57 ± 3% of maximal HR at the limit of thermal
tolerance in E+P, ERT, and No HRT groups, respectively;
P = 0.29 for group effect, P = 0.19 for
group × time interaction; 39 ± 4, 28 ± 4, and 30 ± 6% of HR reserve at the limit of thermal tolerance in E+P, ERT, and
No HRT groups, respectively; P = 0.63 for group effect,
P = 0.29 for group × time interaction).
|
Other Cardiovascular Variables
FBF (Fig. 4) increased significantly in all three groups of women after the first 15 min of heating (P < 0.05), but there were no significant differences among the groups in FBF at any time during the protocol.
|
SBF (Fig. 4) was significantly higher in the E+P group than in the ERT or No HRT groups at baseline (1,131 ± 43 vs. 889 ± 90 and 980 ± 117 ml/min, respectively; P < 0.05) but not during heating. SBF decreased significantly below baseline values for all groups after the first 15 min of heating (P < 0.05). RBF (Fig. 4) decreased significantly after the first 15 min of heating in all three groups of women (P < 0.05), but there were no significant differences in RBF among the groups at any time during the protocol.
MAP (Fig. 5) was well maintained during
the heating in all three groups of women. There were no significant
differences in MAP among the three groups at baseline (100 ± 4, 92 ± 4, and 93 ± 2 mmHg in E+P, ERT, and No HRT groups,
respectively) or during heating (100 ± 4, 91 ± 2, and
93 ± 2 mmHg at the limit of thermal tolerance in E+P, ERT, and No
HRT groups, respectively; P = 0.12 for group main
effect, P = 0.37 for group × time interaction). TPR (Fig. 5) fell significantly during the protocol in all three groups
of women (P < 0.05). There were no significant
differences in TPR among the three groups of women during the protocol
(14.7 ± 1.2, 15.1 ± 1.0, and 21.1 ± 2.1 mmHg · min · l
1 at the limit of thermal tolerance in E+P,
ERT, and No HRT groups, respectively; P = 0.17 for
group main effect, P = 0.83 for group × time
interaction).
|
| |
DISCUSSION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
The main finding of the present study was that chronic HRT, either
ERT alone or in combination with progestins, does not affect the
cardiac or hemodynamic responses of postmenopausal women to direct
passive heating. The E+P group did have a higher
c than did the No HRT group throughout the
entire protocol because of a higher HR. However, the women in the E+P
group were younger than the women in the No HRT group and thus had a
higher maximal HR. Consequently, when the HR data were plotted as a
percentage of the maximal HR, there were no significant differences
observed among the three groups of women. Thus the higher
c response in the E+P group seems to be an
artifact of the group characteristics [specifically, age (12)] rather
than an effect of the HRT. There were no differences in any of the
other hemodynamic variables among the groups during the heating
protocol, and, therefore, it seems that HRT does not affect the
hemodynamic responses to direct passive heating.
It appears that the "extra" c in the E+P
group was evenly distributed throughout the vascular beds examined in
this study. The E+P group had the highest flows to the cutaneous,
splanchnic, and renal vascular beds consistently throughout the entire
protocol, although these group differences were not statistically
significant (Fig. 3).
In a previous study from our laboratory (12), the increase
in c directed to the skin during direct
passive heating was smaller in older men compared
with younger men. SV fell in the older men, but not in the
younger men, meaning that the older men had to rely more heavily on an
increase in chronotropic function, and operated at a higher percentage
of their HR reserve during passive heating, than did the younger men.
We believe that this increased HR response may put older individuals,
especially those with coronary artery disease, at a greater risk for
cardiac events during heat stress. Thus an increase in inotropic
function of the heart could be beneficial during heat stress. We
hypothesized that chronic HRT would increase c
during direct passive heating by increasing SV (i.e., by increasing
inotropic function). There are no data examining the effects of HRT on
cardiac or hemodynamic function during heat stress, and this hypothesis
was based on resting data from various studies of HRT using both human
and animal models. Many of these studies have suggested that ERT could increase cardiac inotropic function (6, 9,
17, 22). However, in most of those studies,
the estrogen administration was not prolonged enough to allow PV and
blood volume to return to baseline. That is, for the first several
months of ERT, PV is expanded. If ERT is continued beyond several
months, PV returns to pre-ERT values. Thus the observed increases in PV
and blood volume in the previous studies could have, at least
partially, accounted for the observed increases in c
and SV.
The present study also showed no differences between women taking HRT and women not taking HRT with respect to SBF and RBF. From these data, it does not appear that HRT increases resting blood flow to these vascular beds, in contrast to some other vascular beds, namely the heart and uterus (6). It also does not appear that HRT affects the vasoconstriction that occurs in these vascular beds during heating to redistribute flow to the skin.
It has been consistently shown that ERT in postmenopausal women decreases core temperature at rest (1), during exercise in the heat (1, 19), and during passive heating (E. M. Brooks-Asplund, personal communication). These same studies showed that ERT shifts the threshold for cutaneous active vasodilation such that, at any given core temperature, women taking ERT have a higher SkBF response. Both of these thermoregulatory effects of ERT are blocked by the addition of progestins to the HRT. In this study, there were no differences in core temperature or FBF by the end of the baseline period or during the heating protocol. This is most likely due to the use of the water-perfused suit and plastic coverall, which very tightly control skin temperature and, by convective heat transfer, core temperature during the heating. In fact, Tes was lower in women taking ERT than in either of the other two groups of women at the start of the baseline period (Table 1), but these differences lost statistical significance by the end of the 45-min baseline period. All women had 34°C water circulated through the suit during the baseline period. This caused a slight increase in skin and core temperatures in the ERT group and slight decreases in these temperatures in the other two groups of women. It is also possible that the sample size in this study was not large enough to detect the small difference in temperature that existed at the end of the baseline period.
Charkoudian and Johnson (2) have used a whole body heating protocol with a water-perfused suit and coverall. In contrast to our results, they did show thermoregulatory effects of estrogen in the form of oral contraceptives. However, they do not report the temperature of the water circulating through the suit, if any, during the baseline period. They also did not elevate skin or core temperatures as much as in this study. Additionally, they measured SkBF via laser-Doppler flowmetry as opposed to venous occlusion plethysmography used in this study. These protocol differences may explain the differences in results between their study and ours.
In summary, the purpose of this investigation was to examine the effect
of HRT on the cardiac and hemodynamic responses during direct passive
heating to the limits of thermal tolerance in postmenopausal women.
There were no differences among the groups in blood flow to the skin or
visceral circulation. c was higher in women
taking E+P due to a higher HR, but this can be explained by a higher maximal HR in this group of women, a function of their slightly younger
mean age.
| |
ACKNOWLEDGEMENTS |
|---|
The authors greatly appreciate the assistance of Jane Pierzga, Gretchen Keisling, Laurie Aquilino, and Mark Dunbar and the scientific input of Drs. James Pawelczyk, Peter Farrell, Dan Deaver, and E. R. Buskirk. The medical assistance provided by the General Clinical Research Center is also appreciated.
| |
FOOTNOTES |
|---|
This research was supported by National Institute on Aging Grant R01-AG-07004-09. S. L. Dunbar was supported by National Institute of General Medical Sciences Predoctoral Training Grant T32-GM-08619.
Address for reprint requests and other correspondence: W. L. Kenney, 102 Noll Laboratory, Pennsylvania State University, University Park, PA 16802-6900.
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. §1734 solely to indicate this fact.
Received 16 August 1999; accepted in final form 29 February 2000.
| |
REFERENCES |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
1.
Brooks, EM,
Morgan AL,
Pierzga JM,
Wladkowski SL,
O'Gorman JT,
Derr JA,
and
Kenney WL.
Chronic hormone replacement therapy alters thermoregulatory and vasomotor function in postmenopausal women.
J Appl Physiol
83:
477-484,
1997
2.
Charkoudian, N,
and
Johnson JM.
Modification of active cutaneous vasodilation by oral contraceptive hormones.
J Appl Physiol
83:
2012-2018,
1997
3.
Detry, JR,
Brengelmann GL,
Rowell LB,
and
Wyss C.
Skin and muscle components of forearm blood flow in directly heated resting man.
J Appl Physiol
32:
506-511,
1972
4.
Dill, DB,
and
Costill DL.
Calculation of percentage changes in volume of blood, plasma, and red cells in dehydration.
J Appl Physiol
37:
247-248,
1974
5.
El-Sayed, H,
Goodall SR,
and
Hainsworth R.
Re-evaluation of Evans blue dye dilution method of plasma volume measurement.
Clin Lab Haematol
17:
189-194,
1995[ISI][Medline].
6.
Ganger, KF,
Vyas S,
and
Whitehead M.
Pulsatility index in internal carotid artery in relation to transdermal oestradiol and time since menopause.
Lancet
338:
839-842,
1991[ISI][Medline].
7.
Giraud, GD,
Morton MJ,
Davis LE,
Paul MS,
and
Thornburg KL.
Estrogen-induced left ventricular chamber enlargement in ewes.
Am J Physiol Endocrinol Metab
264:
E490-E496,
1993
8.
Grainger, SL,
Keeling PWN,
Brown IMH,
Marigold JH,
and
Thompson RPH
Clearance and noninvasive determination of the hepatic extraction of indocyanine green in baboons and man.
Clin Sci (Lond)
64:
207-212,
1983[Medline].
9.
Hart, MV,
Hosenpud JD,
Hohimer AR,
and
Morton MJ.
Hemodynamics during pregnancy and sex steroid administration in guinea pigs.
Am J Physiol Regulatory Integrative Comp Physiol
249:
R179-R185,
1985
10.
Katz, K,
Karliner JS,
and
Resnik R.
Effects of a natural volume overload state (pregnancy) on left ventricular performance in normal human subjects.
Circulation
58:
434-441,
1978
11.
Longcope, C,
Franz C,
Morello C,
Baker R,
and
Johnston CC, Jr.
Steroid and gonadotropin levels in women during the peri-menopausal years.
Maturitas
8:
189-196,
1986[ISI][Medline].
12.
Minson, CT,
Wladkowski SL,
Cardell AF,
Pawelczyk JA,
and
Kenney WL.
Age alters the cardiovascular response to direct passive heating.
J Appl Physiol
84:
1323-1332,
1998
13.
Robson, SC,
Hunter S,
Boys RJ,
and
Dunlop W.
Serial study of factors influencing changes in cardiac output during human pregnancy.
Am J Physiol Heart Circ Physiol
256:
H1060-H1065,
1989
14.
Rowell, LB,
Brengelmann GL,
Blackmon JR,
and
Murray JA.
Redistribution of blood flow during sustained high skin temperature in resting man.
J Appl Physiol
28:
413-420,
1970.
15.
Rowell, LB,
Detry JR,
Blackmon JR,
and
Wyss C.
Importance of the splanchnic vascular bed in human blood pressure regulation.
J Appl Physiol
32:
213-220,
1972
16.
Scheuer, J,
Malhotra A.,
Schaible TF,
and
Capasso T.
Effects of gonadectomy and hormonal replacement on rat hearts.
Circ Res
61:
12-19,
1987
17.
Sites, CK,
Tischler MD,
Blackman JA,
Niggel J,
Fairbank JT,
O'Connell M,
and
Ashikaga T.
Effect of short-term hormone replacement therapy on left ventricular mass and contractile function.
Fertil Steril
71:
137-143,
1999[ISI][Medline].
18.
Stephenson, LA,
and
Kolka MA.
Menstrual cycle phase and time of day alter reference signal controlling arm blood flow and sweating.
Am J Physiol Regulatory Integrative Comp Physiol
249:
R186-R191,
1985
19.
Tankersely, CG,
Nicholas WC,
Deaver DR,
Mikita D,
and
Kenney WL.
Estrogen replacement in middle-aged women: thermoregulatory responses to exercise in the heat.
J Appl Physiol
73:
1238-1245,
1992
20.
Treibwasser, JH,
Johnson RL,
Burpo RP,
Campbell JC,
Reardon WC,
and
Blomqvist CG.
Noninvasive determination of cardiac output by a modified acetylene rebreathing procedure utilizing mass spectrometer measurements.
Aviat Space Environ Med
48:
203-209,
1977[Medline].
21.
Van Acker, BA,
Koomen GCM,
and
Arisz L.
Drawbacks of the constant-infusion technique for measurement of renal function.
Am J Physiol Renal Fluid Electrolyte Physiol
268:
F543-F552,
1995
22.
Voutilainen, S,
Hippelainen M,
Hulkko S,
Karppinen K,
Ventila M,
and
Kupari M.
Left ventricular diastolic function by Doppler echocardiography in relation to hormonal replacement therapy in healthy postmenopausal women.
Am J Cardiol
71:
614-616,
1993[ISI][Medline].
23.
Wesson, LG.
Electrolyte excretion in relation to diurnal cycle of renal function.
Medicine (Baltimore)
43:
547-592,
1964.
24.
Whitney, RJ.
The measurement of volume changes in human limbs.
J Physiol (Lond)
121:
1-27,
1953.
This article has been cited by other articles:
|
|
 |
|
  D. S. Hydock, C.-Y. Lien, C. M. Schneider, and R. Hayward Effects of voluntary wheel running on cardiac function and myosin heavy chain in chemically gonadectomized rats Am J Physiol Heart Circ Physiol, December 1, 2007; 293(6): H3254 - H3264. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. L. Kenney and T. A. Munce Invited Review: Aging and human temperature regulation J Appl Physiol, December 1, 2003; 95(6): 2598 - 2603. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
Values under brackets are significantly different from baseline
for all 3 groups of women, P < 0.05.
