Remarkable increase of VV accompanies the most severe forms of varices as well as all cases of the extreme grades of phlebosclerosis, medial hyperplasia and thrombosis. We hypothesize that this increase in VV is rather a secondary vascular reaction to the impaired metabolic conditions within the venous wall than a primary varicogenic factor.

AbstractThe vascular supply of the wall of human vena saphena magna was qualitatively studied by the use of several morphological methods on both normal and pathologically changed veins. The material was obtained from patients undergoing aortocoronary bypass or surgery of the varices, and material from cadavers. Under physiological conditions, the wall of vena saphena magna is supplied by delicate system of vasa vasorum, organized in a form of feeding vessels branched into an irregular loose adventitial mesh and continuing further as a microcirculatory network supplying the two outer thirds of the media. Small local dilatations and tortuosities of adventitial veins were found on heavy varicose veins. Slight increase of vasa vasorum growing into the innermost layer of media was detected, but the hyperplastic intima remained avascular. In patients with recurrent varices or with vein thrombophlebitis intimal hyperplasia, degradation of media and thrombosis, were found. Apparent massive increase of vasa vasorum growing into the whole media, hyperplastic intima and into the organizing thrombi, were regularly observed. The increase of vasa vasorum is a part of the complex of pathophysiological reactions of the vein wall on the hypoxia developing during the most serious pathological changes, and not as the primary varicogenic factor. The vascular supply of the wall of the human vena saphena magna was qualitatively studied by the use of several morphological methods on both normal and pathologically changed veins. The material was obtained from patients undergoing aortocoronary bypass grafting or surgery of varices, as well as materials from cadavers. Under physiological conditions the wall of vena saphena magna is supplied by a delicate system of vasa vasorum. It is organized in a form of feeding vessels branched into an irregular loose adventitial mesh, which continues further as a microcirculatory network supplying the outer two thirds of the media. Small local dilatations and tortuosities of adventitial veins were found on severe varicose veins. A slight increase of the vasa vasorum growing into the innermost layer of media was detected, but the hyperplastic intima remained avascular. In patients with recurrent varices or vein thrombophlebitis, intimal hyperplasia, degradation of media and thrombosis, were found. It was regularly observed that there was an apparent, massive increase of the vasa vasorum growing into the entire media, hyperplastic intima, and into the organizing thrombi. The increase of the vasa vasorum is due to the pathophysiological reaction of the vein wall as a result of hypoxia, which develops during the most serious pathological changes. The increase is not the primary varicogenic factor.