The artery blood structure?

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Answer 1

Blood Vessel Structure

In general the circulatory system of blood vessels may be broken down into those vessels that deliver oxygenated blood to tissues: the arteries, arterioles, and capillaries, and those vessels that return blood with carbon dioxide for gas exchange: the veins and venules. The basic structure of all these vessels can be broken down into three layers:

1. The Intima
2. The Media
3. The Adventia

It is the materials that make up these layers and the size of these three layers themselves that differentiates arteries from veins and indeed even one artery from another artery or one vein from another vein. A schematic from Fung's "Mechanical Properties of Living Tissues" shown below gives an overview of the different structures in the different types of blood vessels:

Here is the composition of each layer of a blood vessel:

Intima:

Innermost layer
Contains endothelial cells
Basal lamina (80 nm thick)
Subendothelia layer with collagenous bundles, some elastin

Media:

Middle Layer
Contains mainly smooth muscle cells
Collagenous fibrils (type III collagen)
Divided from adventia by elastin layer (elastin is a protein which is very elastic, can undergo a
stretch ratio of 1.6, about 80% strain)

Adventia:

Outermost layer
Collagen fibers (mainly type III, differ in amino acid sequence from I and II)
Ground substance
Fibroblasts

Answer 2

Abstract

The occurrence of natural menopause may indicate that a woman is entering a period of increased risk for cardiovascular disease, due to both chronologic aging and lower levels of estrogen. This brief review aims to demonstrate the relevance of changes in blood pressure and large artery structure and function occurring after menopause. These changes, i.e., thickening and stiffening of large arteries (which, in turn would also result in increased systolic and pulse pressures), were found to predict subsequent cardiovascular events, independently of other known cardiovascular risk. The benefits of early hormone replacement therapy on the life expectancy of women have dramatically lost consensus since publication of the Women's Health Initiative study results. However, the authors believe that those results should increase the attention paid by clinicians and public health researchers to the individualization of hormone replacement therapy prescription for postmenopausal women, and to a better characterization of those vascular parameters and profiles identifying post-menopausal women who are most likely to benefit from specific hormone replacement therapy in terms of cardiovascular protection.
Introduction

A 2001 statement from the American Heart Association[1] recommended that hormone replacement therapy (HRT) should not be used for secondary prevention of cardiovascular disease (CVD). Later, the July 17, 2002 issue of JAMA presented the results from the Women's Health Initiative (WHI) study.[2] The strength of the WHI study findings, supported by the rigorous design, the large sample size, and the long follow-up, appears to have put the word "end" to the use of HRT for prevention of CVD in postmenopausal women.

We have neither the authority nor clear evidence to provide an alternative approach to the statement reported in the paper by the WHI study investigators. However, as noted in an editorial relating to the WHI Study,[3] 46 million prescriptions for conjugated estrogens (Premarin) were written in the United States in 2000. The idea that so many doctors prescribed an "inappropriate" treatment for so many years is difficult to accept.

For example, increasing attention should be paid to exploring criteria that could be used for a greater individualization of HRT prescriptions for postmenopausal women and better-characterized risk factor profiles that would identify postmenopausal women who are most likely to benefit from specific HRT in terms of cardiovascular protection.

The results of this clinical trial are certainly true for oral HRT administration, but current clinical practices are often based on transdermal administration. Some preliminary data suggest that the two treatment approaches may not be equivalent.

The goal of the present manuscript is to very briefly underline some issues still to be addressed with regard to the effects of HRT on large artery structure and function and, thus, on the individual risk of cardiovascular events.