ANATOMY AND PHYSIOLOGY OF THE VASCULAR WALL 



88 3 



still are tight at low pressures [Schliiter (79)]. Further 

 degeneration makes them leaky at low pressures and 

 later they are so degenerated that only a small margin 

 remains or the valve leaflets are broken through. At 

 last they vanish completely. The effects of venous 

 valvular insufficiency are discussed in Chapter 36. 



The firm anchorage of the proximal part of the 

 veins may facilitate transmission of arterial pulsation 

 from arteries to their venae comitantes [Schade (78), 

 v. Lanz et al. (53)], but it seems also very convenient 

 for another task. Any distensible tube which stands 

 upright and is filled with fluid tends to pull down- 

 ward. The radius in the proximal part is then small 

 and the wall is stretched mainly in a longitudinal 

 direction. It is therefore necessary that the tube be 

 supported in the proximal part in the longitudinal 

 direction and be fixed to its surroundings. Such a 

 support may be formed in the veins by the bracing 

 straps (33, 53) and also by the longitudinal muscles. 

 In the distal part of such an upright tube the radius 

 is enlarged and the wall is stretched mainly in a 

 transverse direction. As indicated above, this is 

 countered by the increasing amount of circular 

 muscles. 



NUTRITION OF THE VASCULAR WALL 



The vascular wall is a living organ and its smooth 

 muscles need a source of energy. Their nutrition is 

 accomplished by two different means: diffusion from 

 the circulating blood from the inside of the vessel 

 toward the outside, and from the vasa vasorum 

 vessels which dip into the vascular wall from the 

 outside. These two supply routes meet in the vascular 

 wall. Miiller (64) has demonstrated a model in which 

 ten coaxial thin rubber tubes with increasing diam- 

 eters were telescoped and fixed so that the fluid 

 between the different sheets could not escape during 

 distention. This model satisfies very well the situation 

 in the vascular wall, which is also built from different 

 layers consisting of different materials. The pressure 

 between the sheets is equal to the negative radial 

 stress, and the tension of the different sheets of the 

 model decreases nearly linearly from the inside to 

 the outside at any given internal pressure. The inner- 

 most sheet has almost the same pressure as the filling 

 fluid, whereas the outermost sheet is at the ambient 

 pressure. This means that the vessels which supply 

 the vascular wall meet progressively higher pressures 

 the further they penetrate the wall. On the other 



hand, the pressure gradient from the inside toward 

 the outside facilitates the movement of materials 

 directly from the circulating blood through the wall. 

 The border between diffusion and vascular supply in 

 the vascular wall depends on the thickness of the 

 wall. The limit for diffusion is set by oxygen, which 

 is transported in the blood by the hemoglobin and 

 which can supply tissues adequately if the distance 

 from the hemoglobin, which stays in the blood, to 

 the tissue cells is not too great. This distance is, in 

 the vascular wall, about 500 ju [Linzbach (56)]. The 

 limit for the vasa vasorum is set by the pressure in 

 the wall. Since the vasa vasorum come mostly from 

 the adventitia, the pressure fall over the length of 

 the vasa vasorum allows them only to penetrate as 

 far as the pressure in the wall is less than the pressure 

 of the intramural capillaries. 



Diffusion from the Inside 



The whole circulatory system is lined with a single 

 layer of endothelium. This lining prevents extra- 

 vasation of blood even if the pressure in the vessels 

 exceeds by far the surrounding pressure. Any nutrient 

 material entering the vascular wall from the inside 

 must pass across this endothelial lining. Such pene- 

 tration is rendered possible either through the pres- 

 sure and concentration gradient between the blood 

 and the wall tissue or by means of active transport. 

 Chambers & Zweifach (21) assume that the individual 

 endothelial cells are held together by a cement 

 substance and that this cement substance makes 

 penetration possible. However, Linzbach (56) could 

 never find such a cement substance. He describes 

 cell branches which are near the basal side of the 

 endothelial cells, and with which the endothelial 

 cells are very tightly connected. The boundary 

 between the cells may form fissures, where capillary 

 attraction may be effective and render penetration 

 possible. Pappenheimer (65) suggests channels 

 between the endothelial cells with a diameter of 30 

 to 45 A, through which the materials can enter the 

 wall. All these mechanisms depend on a pressure 

 gradient between the blood and the wall tissue or an 

 osmotic concentration gradient of the different 

 materials. 



However, there may also be active transport. 

 Moore & Ruska (63) described small vacuoles on 

 the surface of the endothelial cells which contain 

 blood plasma. These vacuoles separate themselves 

 from the surface and wander through the cell sub- 



