Chronic hormone replacement therapy does not alter resting or maximal skin blood flow

1998 ◽  
Vol 85 (2) ◽  
pp. 505-510 ◽  
Author(s):  
E. M. Brooks-Asplund ◽  
W. L. Kenney
Keyword(s):  
Blood Flow ◽  
Replacement Therapy ◽  
Postmenopausal Women ◽  
Skin Blood Flow ◽  
Local Heating ◽  
Hormone Replacement ◽  
Venous Occlusion ◽  
Body Core Temperature ◽  
Vascular Conductance ◽  
Doppler Flowmetry

Postmenopausal women on estrogen replacement therapy (ERT) regulate body core temperature at a lower baseline level at rest in a thermoneutral environment. We conducted a series of studies to test whether, in a thermoneutral environment, chronic (≥2 yr) oral ERT significantly alters baseline skin blood flow (SkBF) and cutaneous vascular conductance (CVC) and whether ERT alters maximal CVC (CVCmax) and SkBF in postmenopausal women. In the first set of studies, forearm blood flow (FBF) was measured by venous-occlusion plethysmography in 24 postmenopausal women: 8 not taking exogenous hormone therapy (No HRT group), 8 on ERT, and 8 receiving combination of estrogen and progesterone therapy, at rest and during prolonged (1 h) local heating of the forearm at 42°C. Mean arterial pressure (MAP) was measured by brachial auscultation before each set of FBF measurements to calculate forearm vascular conductance (FVC = FBF/MAP). SkBF was measured by laser-Doppler flowmetry (LDF), and CVC was calculated as LDF/MAP and standardized as %CVCmax. Baseline FVC, %CVCmax, and maximal FVC were not significantly different among the three groups of women. In the second set of experiments, LDF in ERT and No HRT groups was measured at rest in both thermoneutral and warm environments. %CVCmax was again not significantly different between ERT and No HRT groups at thermoneutral ambient temperatures and increased similarly in the warm environment. Therefore, chronic exogenous ERT does not appear to influence either baseline or maximal SkBF.

Chronic hormone replacement therapy alters thermoregulatory and vasomotor function in postmenopausal women

1997 ◽  
Vol 83 (2) ◽  
pp. 477-484 ◽  
Author(s):  
E. M. Brooks ◽  
A. L. Morgan ◽  
J. M. Pierzga ◽  
S. L. Wladkowski ◽  
J. T. O’Gorman ◽  
...  
Keyword(s):  
Hormone Replacement Therapy ◽  
Replacement Therapy ◽  
Postmenopausal Women ◽  
Hormone Replacement ◽  
Venous Occlusion ◽  
Cycle Ergometer ◽  
Vascular Conductance ◽  
Mean Body Temperature ◽  
Doppler Flowmetry ◽  
Vasomotor Function

Brooks, E. M., A. L. Morgan, J. M. Pierzga, S. L. Wladkowski, J. T. O’Gorman, J. A. Derr, and W. L. Kenney. Chronic hormone replacement therapy alters thermoregulatory and vasomotor function in postmenopausal women. J. Appl. Physiol. 83(2): 477–484, 1997.—This investigation examined effects of chronic (≥2 yr) hormone replacement therapy (HRT), both estrogen replacement therapy (ERT) and estrogen plus progesterone therapy (E+P), on core temperature and skin blood flow responses of postmenopausal women. Twenty-five postmenopausal women [9 not on HRT (NO), 8 on ERT, 8 on E+P] exercised on a cycle ergometer for 1 h at an ambient temperature of 36°C. Cutaneous vascular conductance (CVC) was monitored by laser-Doppler flowmetry, and forearm vascular conductance (FVC) was measured by using venous occlusion plethysmography. Iontophoresis of bretylium tosylate was performed before exercise to block local vasoconstrictor (VC) activity at one skin site on the forearm. Rectal temperature (Tre) was ∼0.5°C lower for the ERT group ( P < 0.01) compared with E+P and NO groups at rest and throughout exercise. FVC: mean body temperature (Tb) and CVC: Tb curves were shifted ∼0.5°C leftward for the ERT group ( P < 0.0001). Baseline CVC was significantly higher in the ERT group ( P < 0.05), but there was no interaction between bretylium treatment and groups once exercise was initiated. These results suggest that 1) chronic ERT likely acts centrally to decrease Tre, 2) ERT lowers the Tre at which heat-loss effector mechanisms are initiated, primarily by actions on active cutaneous vasodilation, and 3) addition of exogenous progestins in HRT effectively blocks these effects.

Thermoregulatory reflexes and cutaneous active vasodilation during heat stress in hypertensive humans

1998 ◽  
Vol 85 (1) ◽  
pp. 175-180 ◽  
Author(s):  
D. L. Kellogg ◽  
S. R. Morris ◽  
S. B. Rodriguez ◽  
Y. Liu ◽  
M. Grossmann ◽  
...  
Keyword(s):  
Blood Flow ◽  
Heat Stress ◽  
Skin Blood Flow ◽  
Forearm Blood Flow ◽  
Venous Occlusion ◽  
Vascular Conductance ◽  
Doppler Flowmetry ◽  
Forearm Vascular Conductance ◽  
Normotensive Subjects ◽  
Cutaneous Vascular Conductance

During dynamic exercise in the heat, increases in skin blood flow are attenuated in hypertensive subjects when compared with normotensive subjects. We studied responses to passive heat stress (water-perfused suits) in eight hypertensive and eight normotensive subjects. Forearm blood flow was measured by venous-occlusion plethysmography, mean arterial pressure (MAP) was measured by Finapres, and forearm vascular conductance (FVC) was calculated. Bretylium tosylate (BT) iontophoresis was used to block active vasoconstriction in a small area of skin. Skin blood flow was indexed by laser-Doppler flowmetry at BT-treated and untreated sites, and cutaneous vascular conductance was calculated. In normothermia, FVC was lower in hypertensive than in normotensive subjects ( P < 0.01). During heat stress, FVC rose to similar levels in both groups ( P > 0.80); concurrent cutaneous vascular conductance increases were unaffected by BT treatment ( P > 0.60). MAP was greater in hypertensive than in normotensive subjects during normothermia ( P < 0.05, hypertensive vs. normotensive subjects). During hyperthermia, MAP fell in hypertensive subjects but showed no statistically significant change in normotensive subjects ( P < 0.05, hypertensive vs. normotensive subjects). The internal temperature at which vasodilation began did not differ between groups ( P> 0.80). FVC is reduced during normothermia in unmedicated hypertensive subjects; however, they respond to passive heat stress in a fashion no different from normotensive subjects.

scholarly journals Minimal role for H1 and H2 histamine receptors in cutaneous thermal hyperemia to local heating in humans

2006 ◽  
Vol 100 (2) ◽  
pp. 535-540 ◽  
Author(s):  
Brett J. Wong ◽  
Sarah J. Williams ◽  
Christopher T. Minson
Keyword(s):  
Blood Flow ◽  
Receptor Antagonist ◽  
Skin Blood Flow ◽  
Local Heating ◽  
Histamine Receptor ◽  
Receptor Activation ◽  
Control Site ◽  
Doppler Flowmetry ◽  
Histamine Receptor Antagonist ◽  
And Control

The precise mechanism(s) underlying the thermal hyperemic response to local heating of human skin are not fully understood. The purpose of this study was to investigate a potential role for H1 and H2 histamine-receptor activation in this response. Two groups of six subjects participated in two separate protocols and were instrumented with three microdialysis fibers on the ventral forearm. In both protocols, sites were randomly assigned to receive one of three treatments. In protocol 1, sites received 1) 500 μM pyrilamine maleate (H1-receptor antagonist), 2) 10 mM l-NAME to inhibit nitric oxide synthase, and 3) 500 μM pyrilamine with 10 mM NG-nitro-l-arginine methyl ester (l-NAME). In protocol 2, sites received 1) 2 mM cimetidine (H2 antagonist), 2) 10 mM l-NAME, and 3) 2 mM cimetidine with 10 mM l-NAME. A fourth site served as a control site (no microdialysis fiber). Skin sites were locally heated from a baseline of 33 to 42°C at a rate of 0.5°C/5 s, and skin blood flow was monitored using laser-Doppler flowmetry (LDF). Cutaneous vascular conductance was calculated as LDF/mean arterial pressure. To normalize skin blood flow to maximal vasodilation, microdialysis sites were perfused with 28 mM sodium nitroprusside, and control sites were heated to 43°C. In both H1 and H2 antagonist studies, no differences in initial peak or secondary plateau phase were observed between control and histamine-receptor antagonist only sites or between l-NAME and l-NAME with histamine receptor antagonist. There were no differences in nadir response between l-NAME and l-NAME with histamine-receptor antagonist. However, the nadir response in H1 antagonist sites was significantly reduced compared with control sites, but there was no effect of H2 antagonist on the nadir response. These data suggest only a modest role for H1-receptor activation in the cutaneous response to local heating as evidenced by a diminished nadir response and no role for H2-receptor activation.

Effect of functional electrostimulation on impaired skin vasodilator responses to local heating in spinal cord injury

2009 ◽  
Vol 106 (4) ◽  
pp. 1065-1071 ◽  
Author(s):  
Noortje T. L. Van Duijnhoven ◽  
Thomas W. J. Janssen ◽  
Daniel J. Green ◽  
Christopher T. Minson ◽  
Maria T. E. Hopman ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Blood Flow ◽  
Skin Blood Flow ◽  
Local Heating ◽  
Axon Reflex ◽  
Doppler Flowmetry ◽  
Cord Injury ◽  
Cutaneous Vascular Conductance ◽  
Functional Electrostimulation

Spinal cord injury (SCI) induces vascular adaptations below the level of the lesion, such as impaired cutaneous vasodilation. However, the mechanisms underlying these differences are unclear. The aim of this study is to examine arm and leg cutaneous vascular conductance (CVC) responses to local heating in 17 able-bodied controls (39 ± 13 yr) and 18 SCI subjects (42 ± 8 yr). SCI subjects were counterbalanced for functional electrostimulation (FES) cycling exercise (SCI-EX, n = 9) or control (SCI-C, n = 9) and reanalyzed after 8 wk. Arm and leg skin blood flow were measured by laser-Doppler flowmetry during local heating (42°C), resulting in an axon-reflex mediated first peak, nadir, and a primarily nitric oxide-dependent plateau phase. Data were expressed as a percentage of maximal CVC (44°C). CVC responses to local heating in the paralyzed leg, but also in the forearm of SCI subjects, were lower than in able-bodied controls ( P < 0.05 and 0.01, respectively). The 8-wk intervention did not change forearm and leg CVC responses to local heating in SCI-C and SCI-EX, but increased femoral artery diameter in SCI-EX ( P < 0.05). Interestingly, findings in skin microvessels contrast with conduit arteries, where physical (in)activity contributes to adaptations in SCI. The lower CVC responses in the paralyzed legs might suggest a role for inactivity in SCI, but the presence of impaired CVC responses in the normally active forearm suggests other mechanisms. This is supported by a lack of adaptation in skin microcirculation after FES cycle training. This might relate to the less frequent and smaller magnitude of skin blood flow responses to heat stimuli, compared with controls, than physical inactivity per se.

The role of baseline in the cutaneous vasoconstrictor responses during combined local and whole body cooling in humans

2007 ◽  
Vol 293 (5) ◽  
pp. H3187-H3192 ◽  
Author(s):  
Gary J. Hodges ◽  
Wojciech A. Kosiba ◽  
Kun Zhao ◽  
Guy E. Alvarez ◽  
John M. Johnson
Keyword(s):  
Blood Flow ◽  
Skin Blood Flow ◽  
Local Heating ◽  
Laser Doppler ◽  
Whole Body ◽  
Local Cooling ◽  
Doppler Flowmetry ◽  
Vasoconstrictor Response ◽  
Body Cooling ◽  
Whole Body Cooling

Previous work showed that local cooling (LC) attenuates the vasoconstrictor response to whole body cooling (WBC). We tested the extent to which this attenuation was due to the decreased baseline skin blood flow following LC. In eight subjects, skin blood flow was assessed using laser-Doppler flowmetry (LDF). Cutaneous vascular conductance (CVC) was expressed as LDF divided by blood pressure. Subjects were dressed in water-perfused suits to control WBC. Four forearm sites were prepared with microdialysis fibers, local heating/cooling probe holders, and laser-Doppler probes. Three sites were locally cooled from 34 to 28°C, reducing CVC to 45.9 ± 3.9, 42 ± 3.9, and 44.5 ± 4.8% of baseline ( P < 0.05 vs. baseline; P > 0.05 among sites). At two sites, CVC was restored to precooling baseline levels with sodium nitroprusside (SNP) or isoproterenol (Iso), increasing CVC to 106.4 ± 12.4 and 98.9 ± 10.1% of baseline, respectively ( P > 0.05 vs. precooling). Whole body skin temperature, apart from the area of blood flow measurement, was reduced from 34 to 31°C. Relative to the original baseline, CVC decreased ( P < 0.05) by 44.9 ± 2.8 (control), 11.3 ± 2.4 (LC only), 29 ± 3.7 (SNP), and 45.8 ± 8.7% (Iso). The reductions at LC only and SNP sites were less than at control or Iso sites ( P < 0.05); the responses at those latter sites were not different ( P > 0.05), suggesting that the baseline change in CVC with LC is important in the attenuation of reflex vasoconstrictor responses to WBC.

scholarly journals Cutaneous vasomotor responses in boys and men

2018 ◽  
Vol 43 (10) ◽  
pp. 1019-1026 ◽  
Author(s):  
Gary J. Hodges ◽  
Matthew C. Mueller ◽  
Stephen S. Cheung ◽  
Bareket Falk
Keyword(s):  
Blood Flow ◽  
Skin Blood Flow ◽  
Local Heating ◽  
Handgrip Exercise ◽  
Isometric Handgrip ◽  
Local Skin ◽  
Doppler Flowmetry ◽  
Age Related ◽  
Isometric Handgrip Exercise ◽  
Underlying Mechanisms

Few studies have investigated skin blood flow in children and age-related differences in the underlying mechanisms. We examined mechanisms of skin blood flow responses to local heating, postocclusive reactive hyperaemia (PORH), and isometric handgrip exercise in adult and prepubescent males, hypothesizing that skin blood flow responses would be greater in children compared with adults. We measured skin blood flow in 12 boys (age, 9 ± 1 years) and 12 men (age, 21 ± 1 years) using laser-Doppler flowmetry at rest, in response to 3-min PORH, 2-min isometric handgrip exercise, and local skin heating to 39 °C (submaximal) and 44 °C (maximal). Using wavelet analysis we assessed endothelial, neural, and myogenic activities. At rest and in response to local heating to 39 °C, children had higher skin blood flow and endothelial activity compared with men (d ≥ 1.1, p < 0.001) and similar neurogenic and myogenic activities (d < 0.2, p > 0.05). Maximal responses to 44 °C local skin heating, PORH, and isometric handgrip exercise did not differ between boys and men (all d ≤ 0.2, p > 0.05). During PORH children demonstrated greater endothelial activity compared with men (d ≥ 0.6, p < 0.05); in contrast, men had higher neurogenic activity (d = 1.0, p < 0.01). During isometric handgrip exercise there were no differences in endothelial, neurogenic, and myogenic activities (d < 0.2, p > 0.3), with boys and men demonstrating similar increases in endothelial activity and decreases in myogenic activity (d ≥ 0.8, p < 0.05). These data suggest that boys experience greater levels of skin blood flow at rest and in response to submaximal local heating compared with men, while maximal responses appear to be similar. Additionally, endothelial mediators seem to contribute more to vasodilatation in boys than in men.

scholarly journals Heat acclimation improves cutaneous vascular function and sweating in trained cyclists

2010 ◽  
Vol 109 (6) ◽  
pp. 1736-1743 ◽  
Author(s):  
Santiago Lorenzo ◽  
Christopher T. Minson
Keyword(s):  
Blood Flow ◽  
Skin Blood Flow ◽  
Vascular Function ◽  
Structural Changes ◽  
Forearm Blood Flow ◽  
Sweat Rate ◽  
Local Heating ◽  
Heat Acclimation ◽  
Control Group ◽  
Doppler Flowmetry

The aim of this study was to explore heat acclimation effects on cutaneous vascular responses and sweating to local ACh infusions and local heating. We also sought to examine whether heat acclimation altered maximal skin blood flow. ACh (1, 10, and 100 mM) was infused in 20 highly trained cyclists via microdialysis before and after a 10-day heat acclimation program [two 45-min exercise bouts at 50% maximal O2 uptake (V̇o2max) in 40°C ( n = 12)] or control conditions [two 45-min exercise bouts at 50% V̇o2max in 13°C ( n = 8)]. Skin blood flow was monitored via laser-Doppler flowmetry (LDF), and cutaneous vascular conductance (CVC) was calculated as LDF ÷ mean arterial pressure. Sweat rate was measured by resistance hygrometry. Maximal brachial artery blood flow (forearm blood flow) was obtained by heating the contralateral forearm in a water spray device and measured by Doppler ultrasound. Heat acclimation increased %CVCmax responses to 1, 10, and 100 mM ACh (43.5 ± 3.4 vs. 52.6 ± 2.6% CVCmax, 67.7 ± 3.4 vs. 78.0 ± 3.0% CVCmax, and 81.0 ± 3.8 vs. 88.5 ± 1.1% CVCmax, respectively, all P < 0.05). Maximal forearm blood flow remained unchanged after heat acclimation (290.9 ± 12.7 vs. 269.9 ± 23.6 ml/min). The experimental group showed significant increases in sweating responses to 10 and 100 mM ACh (0.21 ± 0.03 vs. 0.31 ± 0.03 mg·cm−2·min−1 and 0.45 ± 0.05 vs. 0.67 ± 0.06 mg·cm−2·min−1, respectively, all P < 0.05), but not to 1 mM ACh (0.13 ± 0.02 vs. 0.18 ± 0.02 mg·cm−2·min−1, P = 0.147). No differences in any of the variables were found in the control group. Heat acclimation in highly trained subjects induced local adaptations within the skin microcirculation and sweat gland apparatus. Furthermore, maximal skin blood flow was not altered by heat acclimation, demonstrating that the observed changes were attributable to improvement in cutaneous vascular function and not to structural changes that limit maximal vasodilator capacity.

Preserved reflex cutaneous vasodilation in cystic fibrosis does not include an enhanced nitric oxide-dependent mechanism

2007 ◽  
Vol 102 (6) ◽  
pp. 2301-2306 ◽  
Author(s):  
Brad W. Wilkins ◽  
Elizabeth A. Martin ◽  
Shelly K. Roberts ◽  
Michael J. Joyner
Keyword(s):  
Nitric Oxide ◽  
Cystic Fibrosis ◽  
Blood Flow ◽  
Skin Blood Flow ◽  
Local Heating ◽  
No Synthase ◽  
Local Skin ◽  
Doppler Flowmetry ◽  
Cutaneous Vasodilation ◽  
Reflex Cutaneous Vasodilation

In humans, vasoactive intestinal peptide (VIP) may play a role in reflex cutaneous vasodilation during body heating. We tested the hypothesis that the nitric oxide (NO)-dependent contribution to active vasodilation is enhanced in the skin of subjects with cystic fibrosis (CF), compensating for sparse levels of VIP. In 2 parallel protocols, microdialysis fibers were placed in the skin of 11 subjects with CF and 12 controls. Lactated Ringer was perfused at one microdialysis site and NG-nitro-l-arginine methyl ester (2.7 mg/ml) was perfused at a second microdialysis site. Skin blood flow was monitored over each site with laser-Doppler flowmetry. In protocol 1, local skin temperature was increased 0.5°C every 5 s to 42°C, and then it maintained at 42°C for ∼45 min. In protocol 2, subjects wore a tube-lined suit perfused with water at 50°C, sufficient to increase oral temperature (Tor) 0.8°C. Cutaneous vascular conductance (CVC) was calculated (flux/mean arterial pressure) and scaled as percent maximal CVC (sodium nitroprusside; 8.3 mg/ml). Vasodilation to local heating was similar between groups. The change (Δ%CVCmax) in CVC with NO synthase inhibition on the peak (9 ± 3 vs. 12 ± 5%CVCmax; P = 0.6) and the plateau (45 ± 3 vs. 35 ± 5%CVCmax; P = 0.1) phase of the skin blood flow response to local heating was similar in CF subjects and controls, respectively. Reflex cutaneous vasodilation increased CVC in CF subjects (58 ± 4%CVCmax) and controls (53 ± 4%CVCmax; P = 0.37) and NO synthase inhibition attenuated CVC in subjects with CF (37 ± 6%CVCmax) and controls (35 ± 5%CVCmax; P = 0.8) to a similar degree. Thus the preservation of cutaneous active vasodilation in subjects with CF is not associated with an enhanced NO-dependent vasodilation.

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