Veins

VEINS (venae), constitute the centripetal portion of the circulatory system—a network of tubes carrying blood toward the heart. Just as in the arterial system, the sum of the lumens of peripheral branches is greater than that of the main trunks. The capacity of the venous bed exceeds that of the arterial, since the arteries of the limbs and trunk are mostly accompanied by two veins, and their subcutaneous superficial network, where veins do not accompany arteries, is more developed. Only in the lesser circulation is the capacity of the venous and arterial systems approximately equal. Three networks are distinguished: superficial veins—venae superficiales s. subcutaneae, deep veins accompanying arteries—venae profundae s. comites, and visceral veins—venae viscerales. Despite numerous attempts to establish topographic relationships between veins and arteries, it must be admitted that veins (this especially concerns superficial ones) vary extremely in their origin and course, and only the point of entry of superficial veins into deep ones is relatively constant. Veins anastomose widely, both within a single trunk, forming so-called windows and plexuses, and between different trunks and networks: the superficial network communicates not only with the deep but also with visceral veins. Such a widely developed network of anastomoses explains the ease of collateral circulation and the impossibility, in certain areas (for example, the basin of v. jugularis int.), of achieving reduced circulation by simultaneous ligation of artery and vein (see). Plexuses are especially developed in the pelvic region, along the spinal canal, and on the base of the skull (plexus pterygoideus superior et inf., occipitalis, plexus foram.oval. and others). Additionally, in the region of the nail phalanges, direct transitions (without capillaries) from arteries (arterioles) to veins are noted. The walls of veins are thin, easily compressible, and due to the negative pressure within them, collapse when cut. However, in certain areas (v. subclavia, v. anonyma, axillaris, femoralis), the outer coat is significantly developed or fused with surrounding vessel fasciae, so that when cut, their lumen gapes and air entry is possible (air embolism). The movement of blood through the veins is facilitated by the suction action of the chest during respiratory excursions and, to a large extent, by the contraction of muscles between which the deep veins are located. Additionally, the anatomical peculiarity of vein structure—venous valves, or flaps, resembling pockets with the free edge directed along the blood flow—exerts its influence. In large veins, two such valves are located at the same level, in smaller veins there is one valve. With reverse blood flow, the valve opens and closes the lumen, preventing regurgitation. Such valves are located both at the mouths of branches flowing into larger trunks (valvulae ostiales) and along their course (valvulae parietales). They are especially numerous in the veins of the lower extremities and are completely absent in the hollow veins, renal, hepatic, pulmonary, portal vein, splenic, uterine, umbilical, veins of the spinal cord, deep veins of the head, and SKIN veins.

N. Kupriyanov. Histological Structure. In the typical vein, the wall, like that of an artery, consists of three layers: inner (intima), middle (media), or muscular, and outer (adventitia). In details, the structure of the venous wall exhibits even greater diversity than that of the artery, especially in large-caliber veins. In typically constructed veins, a thin endothelial layer consisting of wide angular cells can be distinguished; the internal elastic membrane characteristic of arteries is not found in veins, only a small number of elastic fibers forming a fine-meshed network at the boundary of the inner and middle layers are present; in the intima of some veins (iliac, femoral), longitudinal bundles of smooth muscle fibers can be found; the middle layer consists of a few rows of circular smooth muscle cells, after which a relatively powerful layer of adventitia begins, i.e., the outer connective tissue coat forming the main thickness of the venous wall. Compared to the arterial wall, the entire combination of these layers is significantly weaker, and the inner coat of veins never forms scallops as in arteries (see color plate to Portal vein, fig. 3). The smallest veins, immediately after their formation from the confluence of capillary vessels, usually consist of only two layers: endothelium and a thin connective tissue layer composed of collagen fibers and a small amount of elastic fibers (venule). Some veins even of relatively large caliber, for example, veins of the meninges, spleen, bone veins, etc., are also completely devoid of a muscular middle layer; veins of the abdominal cavity, veins of the lower extremities, besides the circular muscular layer (better developed in the veins of the lower extremities, especially in v. poplitea), contain numerous smooth muscle fibers in the adventitia; here these fibers form bundles that prevent the stretching of veins under the action of the blood column. Well-developed, longitudinally arranged bundles of smooth muscle fibers are also present in the adventitia of the portal and renal veins. According to Eberth, v. cava inf., azygos, portae, hepaticae, spermatica int., renalis and axillaris have internal circular and external longitudinal musculature; v. iliaca, cruralis, poplitea, mesenterica and umbilicalis—internal and external longitudinal and middle circular; veins of the upper and partly lower extremities, small veins of the neck and chest—exclusively circular musculature, and veins of the pregnant uterus—longitudinal. The valves of veins on both their surfaces are covered with endothelial cells, between which lies a layer of collagen bundles, elastic fibers, and bundles of smooth muscle fibers extending here from the middle layer. The sections closest to the heart of the hollow veins and the pulmonary vein also contain specially constructed striated muscle fibers penetrating here from the myocardium. To veins should also be attributed the venous sinuses of the dura mater, representing wide cavities lined with endothelium; their walls, however, lack a muscular layer and consist of fibrous connective tissue. Lit.: Handbuch d. mikroskopischen Anatomie, herausgegeben v. W. MOUendorl, B. VI.

V. Fomin. Pathology of Veins. Developmental defects of the venous system in the vast majority of cases belong to the category of so-called anatomical variations, which are extremely numerous and diverse here. The exception is some abnormalities in the development of large venous trunks (vena cava, pulmonary veins), but they are usually associated with either incorrect positioning of the internal organs or, even more often, with developmental defects of the heart (see), in connection with which they are also considered (disorders of venous circulation, see Hyperemia, Thromb). Atrophic processes in the walls of veins mainly affect the muscular elements (to a lesser extent - elastic tissue) and for the most part reduce to their simple atrophy with replacement by connective tissue. In addition to phlebosclerosis and phlebectasias (see), these processes can be observed in the physiological obliteration of certain venous trunks, such as: v. umbilicalis, ductus venosus Arantii, many veins of the uterus in the postpartum period, etc. Hyaline degeneration, as well as the rarer degenerative obesity and calcification, are part of the picture of phlebosclerosis. Hypertrophic processes, affecting all components of the wall, occur physiologically in the veins of the uterus during pregnancy, and pathologically - with all more or less significant demands on increasing the carrying capacity of the venous tubes. A classic example of changes of the latter kind is the hypertrophy of the veins of the stomach and esophagus or vv. epigastric, et mammar. intern, in case of difficulty in portal circulation due to liver diseases or of the portal vein (cirrhosis of the liver, thrombosis of v. portae, etc.). The group of hypertrophic processes should also include those proliferations of connective tissue elements of the venous wall that are observed in the organization of thrombi and in the healing of wounds. Both the first and the second, in essence, do not differ in any way from the corresponding processes in the arteries. Finally, mention should also be made here of the connective tissue hyperplasias that characterize various forms of phlebosclerosis. Among the inflammations of the veins, both acute and chronic forms are distinguished. The former are most often based on infection by pus-forming cocci (especially streptococcus) and, according to the course of development of the changes, are divided into peri- and endophlebitis. In periphlebitis, the infection spreads to the veins from the surrounding parts, and the changes in the wall develop from the outside inward. They are initially expressed in hyperemia of the perivascular and adventitial tissue, edema and more or less less infiltration of it. Subsequently, the resulting exudate, both liquid and cellular, in addition to passing to the middle coat, very readily spreads along the lymphatic vessels and tissue spaces along the wall of the vein, dissecting its elements and forming between them significant accumulations, often passing into abscesses. Sometimes, as a result, the vein is found, as it were, for a considerable extent dissected away from the surrounding tissues by the purulent process. Usually simultaneously with the middle coat, the inner coat is also affected, which leads to the formation of a thrombus, and hence the often used name "thrombophlebitis" (it would be more correct in these cases to speak of phlebothrombosis), while the intima most often undergoes necrosis. In endophlebitis, the process begins with the fixation of bacteria contained in the blood on the intima, its necrosis and the formation of a thrombus (thrombophlebitis in the proper sense of the word, or thromboendophlebitis). This is usually followed by phlegmonous impregnation of the remaining layers of the wall, and then the histological picture takes on exactly the same character as in periphlebitis. As for the thrombotic masses, only in very rare cases, when the causative agent dies and the process subsides, they retain, even in the peripheral layers, their characteristic consistency, in order to subsequently undergo organization or petrification. Much more often, there is a purulent melting of the thrombi, most often with subsequent generalization of the process by septic embolism. Thrombophlebitis is most often observed: 1) in the veins of the uterus, vv. spermaticae, hypogastricae et femorales in postpartum infections; 2) in the sinuses of the dura mater (sinus sigmoideus et transversus) in otitis complicated by mastoiditis or osteomyelitis of the pyramid of the temporal bone; 3) in the umbilical vein in umbilical infections in newborns and 4) in the portal vein and its roots in ulcerative or purulent processes in the abdominal cavity (appendicitis, dysentery, typhoid fever, etc.). It should be noted that the term "thrombophlebitis" is often incorrectly used to denote a simple thrombosis of the vein with subsequent reactive changes in its wall, which do not have the character of phlebitis in the direct sense of the word.---To the chronic forms of inflammation of the veins belong: chronic productive phlebitis, or endophlebitis chronica productiva s. hyperplastica, s. obliterans, by some authors referred to phleboscleroses; it leads to a sharp thickening and fibrohyaline transformation of the walls of the veins with narrowing of their lumen or complete obliteration; often observed in the area of venae saphenae. 1. Tuberculous endo- and periphlebitides. Regarding them, approximately the same can be said as was said about the corresponding lesions of the arteries (see), with the only difference that in the veins the formation of intimal tubercles occurs much more often. The cause of this is, on the one hand, the significantly slower blood flow, often interrupted even by short stops (e.g., during strong coughing), which greatly facilitates the fixation of bacilli suspended in the blood on the venous wall and 72S