Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3775_Библиотеки_им_академика_М_И_Перельмана

All blood vessels have an inner layer, the intima, lined by endothelium with subjacent connective tissue; a middle layer, the media, composed of smooth muscle, elastic tissue and collagen embedded in ground substance (see Fig. 2.10); and an outer layer, the adventitia, composed of elastic and fibrous tissue.

The ability of blood vessel to accommodate or influence changes in blood flow and intraluminal pressure by contraction or relaxation relies largely on the smooth muscle component of their wall, moderated by connective tissue elements and a complex of vasoactive substances and the

addition, fibronectin acts as regulator of smooth muscle cell contractility. Smooth muscle, in con­trast to skeletal or cardiac muscle, will replicate and proliferate under appropriate stimuli as seen, for example, in the repair processes, in response to inflammation or in altered haemodynamic con­ditions such as venous hypertension and turbu­lent flow.

tissue (the elastica) is composed of another fibrous protein (elastin). It is a prominent compo­nent of vessel walls, particularly well shown by appropriate staining methods where it is concen­trated to form the fenestrated lamella (internal elastic membrane or lamina).

We know from classical physiology that the relationship between vein volume and pressure is characterized by a significant increase in volume with little change in pressure during the filling phase, in which the vein is distended by the increase in blood volume without experimenting

an increase of pressure, just adapting to the vol­ume [6, 7, 64–67, 72, 73]. In other words, during this first phase, the pressure and volume relation­ship is not linear. Instead, during the distension phase following the filling phase, further increases in volume are proportionally reflected by pressure increases, so that linearity of the vol­ume/pressure relationship in veins can be demon­strated starting from pressure values around 20 mmHg (Fig. 2.14).

(maximum effect, grade of contraction), respec­tively, in control tissue, great saphenous vein in early stages of varicose vein illness (only visible veins, C2), great saphenous veins in later stages (skin changes, C4) and finally varicose tributar­ies, of dose-dependent concentrations, respec­tively, of norepinephrine (NE), endothelin (ET1) and angiotensin (Ang II). The maximum effect that could be evoked by the stimulants was reduced progressively with the increasing sever­ity of the disease in the great saphenous vein as well as in tributaries, which raised the tributary assay to statistical significance for both NE and Ang II (P < 0.05). We also measured the affinity of, respectively, NE, ET1 and Ang II for their specific receptors (pEC50, the negative logarithm to base 10 of the molar concentration of the ago­nist, which produces the 50% of the maximal effect). Surprisingly, a marked reduction of Ang II apparent affinity was already evident in tissues that were taken from patients in an early stage of the disease (P < 0.05) and confirmed also in later stages and in the GSV tributaries (Fig. 2.15).

of remodelling. Accentuated local enzymatic degradation of Ang II seems unlikely, but no data are available to exclude this possibility. The intracellular smooth muscle machinery that sub­serves contraction appears to be efficient because NE and ET-1 and also high concentrations of Ang II evoke maximal contractions.

In this chapter reduced mechanical wall prop-