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Estrogen and the blood vessel wall.
Mendelsohn ME, Karas RH.
Source

Molecular Cardiology Research Center, Tufts University School of Medicine, Boston, Massachusetts.
Abstract

This article reviews historical studies and recent advances regarding the direct effects of estrogen on the blood vessel wall. It is organized into two sections that summarize effects of estrogen on vasomotor tone and on vascular cell growth and atherogenesis, based on two recognized actions of estrogen on the vasculature: a rapid vasodilatory effect, and an atheroprotective effect involving inhibition of smooth-muscle cell proliferation. These effects are likely mediated by different mechanisms. The rapid vasodilatory effects of estrogen are probably nongenomic, whereas the antiproliferative effects of estrogen are likely due to estrogen receptor-dependent alterations in gene expression. Overlap between these two mechanisms also exists, in that genes regulating the production of two important vasodilators synthesized by the vessel wall (prostacyclin and nitric oxide) can be up-regulated by estrogen. Potential molecular mechanisms by which estrogen exerts its effects are discussed, and future directions in this rapidly evolving area of research are considered.

Compressed air massage causes capillary dilation in untraumatised skeletal muscle: a morphometric and ultrastructural study

M.A. Gregorya,
M. Marsb, Corresponding author contact information, E-mail the corresponding author

a Electron Microscopy Unit, University of KwaZulu-Natal, Congella, South Africa
b Department of TeleHealth, Nelson R. Mandela School of Medicine, University of KwaZulu-Natal, Pvt Bag 7, Congella 4013, South Africa

Available online 3 February 2005.

http://dx.doi.org/10.1016/j.physio.2004.11.007, How to Cite or Link Using DOI
Cited by in Scopus (3)

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Abstract
Objectives

Massage is thought to encourage the healing of soft tissue injuries by improving blood flow to the damaged region. This study used light microscopy, transmission electron microscopy and morphometry to determine whether: (a) compressed air massage causes capillary vasodilation; (b) such dilation persists for an extended period of time; and (c) the treatment damages capillaries.
Design

Animal model involving 12 New Zealand white rabbits.
Setting

Electron microscopy unit of the University of KwaZulu-Natal, South Africa.
Interventions

The rabbits were anaesthetised and treated for 15 minutes using compressed air massage at 1 bar (100 kPa).
Main outcome measures

Biopsies were taken from the treated vastus lateralis within 10 minutes (n = 4), 24 hours (n = 4) and 6 days (n = 4) after treatment and control biopsies were taken from the vastus lateralis of the untreated limb. The samples were stained with toluidine blue for light microscopy, and the external cross-sectional area of at least 60 capillaries was measured from each specimen using image analysis software. Ultra-thin sections were prepared for transmission electron microscopy from biopsies taken from control and treated limbs within 10 minutes (n = 2) and 24 hours (n = 2) after treatment. At least 25 capillaries were collected from each specimen. Endothelial cell thickness and the external and luminal diameters were measured and cross-sectional areas were calculated.
Results

On light microscopy, mean external cross-sectional diameter had increased by 8% immediately after treatment, from 4.96 ± 1.09 μm (95% confidence interval: 4.85–5.08) to 5.33 ± 1.21 μm (95% confidence interval: 5.22–5.45) (P < 0.001), and by 11% 24 hours later, from 5.00 ± 1.22 μm (95% confidence interval: 4.87–5.13) to 5.52 ± 1.22 μm (95% confidence interval: 5.37–5.67) (P < 0.001), returning to normal at 6 days. On electron microscopy, luminal cross-sectional area had increased by 35% immediately after treatment, from 20.29 ± 9.07 μm2 (95% confidence interval: 19.37–21.2) to 23.50 ± 11.83 μm2 (95% confidence interval: 22.35–24.66) (P < 0.05), and remained 30% larger, 24 hours later, from 20.77 ± 10.88 μm2 (95% confidence interval: 19.60–21.95) to 25.66 ± 16.03 μm2 (95% confidence interval: 23.99–27.33) (P < 0.05). While capillaries were larger, endothelial cell thickness was reduced in all post-massage specimens, suggesting vasodilation. No pathomorphology was noted in any capillary apart from mild oedema in one specimen.
Conclusions

Compressed air massage of muscle causes vasodilation of skeletal muscle capillaries and this persists for at least 24 hours after treatment.

Impaired microvascular perfusion: a consequence of vascular dysfunction and a potential cause of insulin resistance in muscle

Michael G. Clark

+ Author Affiliations

Menzies Research Institute, University of Tasmania, Hobart, Australia

Address for reprint requests and other correspondence: M. G. Clark, Menzies Research Institute, Univ. of Tasmania, Private Bag 58, Hobart 7001, Australia (e-mail: Michael.Clark@utas.edu.au)

Submitted 29 May 2008.
Accepted 7 July 2008.


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Abstract

Insulin has an exercise-like action to increase microvascular perfusion of skeletal muscle and thereby enhance delivery of hormone and nutrient to the myocytes. With insulin resistance, insulin's action to increase microvascular perfusion is markedly impaired. This review examines the present status of these observations and techniques available to measure such changes as well as the possible underpinning mechanisms. Low physiological doses of insulin and light exercise have been shown to increase microvascular perfusion without increasing bulk blood flow. In these circumstances, blood flow is proposed to be redirected from the nonnutritive route to the nutritive route with flow becoming dominant in the nonnutritive route when insulin resistance has developed. Increased vasomotion controlled by vascular smooth muscle may be part of the explanation by which insulin mediates an increase in microvascular perfusion, as seen from the effects of insulin on both muscle and skin microvascular blood flow. In addition, vascular dysfunction appears to be an early development in the onset of insulin resistance, with the consequence that impaired glucose delivery, more so than insulin delivery, accounts for the diminished glucose uptake by insulin-resistant muscle. Regular exercise may prevent and ameliorate insulin resistance by increasing “vascular fitness” and thereby recovering insulin-mediated capillary recruitment.

Changes in the control of skin blood flow with exercise training: where do cutaneous vascular adaptations fit in?
Simmons GH, Wong BJ, Holowatz LA, Kenney WL.
Source
Department of Biomedical Sciences, University of Missouri, Columbia, MO 65211, USA. simmonsgh@missouri.edu

Abstract
Heat is the most abundant byproduct of cellular metabolism. As such, dynamic exercise in which a significant percentage of muscle mass is engaged generates thermoregulatory demands that are met in part by increases in skin blood flow. Increased skin blood flow during exercise adds to the demands on cardiac output and confers additional circulatory strain beyond that associated with perfusion of active muscle alone. Endurance exercise training results in a number of physiological adaptations which ultimately reduce circulatory strain and shift thermoregulatory control of skin blood flow to higher levels of blood flow for a given core temperature. In addition, exercise training induces peripheral vascular adaptations within the cutaneous microvasculature indicative of enhanced endothelium-dependent vasomotor function. However, it is not currently clear how (or if) these local vascular adaptations contribute to the beneficial changes in thermoregulatory control of skin blood flow following exercise training. The purpose of this Hot Topic Review is to synthesize the literature pertaining to exercise training-mediated changes in cutaneous microvascular reactivity and thermoregulatory control of skin blood flow. In addition, we address mechanisms driving changes in cutaneous microvascular reactivity and thermoregulatory control of skin blood flow, and pose the question: what (if any) is the functional role of increased cutaneous microvascular reactivity following exercise training?