The ultrastructural changes of cutaneous and subcutaneous capillaries and venules in 6 cases of severe, chronic venous insufficiency were examined. The findings in all cases consisted of numerous and characteristic alterations of the vessel wall structure and of the pericapillary space which are supposed to be due to the increased intravenous pressure. The intercellular spaces are enlarged to wide channels through which erythrocytes pass into the perivascular spaces. Microvesicles occur in great numbers, they are arranged in chain-like formations and seem to come together to form transendothelial channels. Around the capillaries, edematous fluid with proteins and erythrocytes accumulates. Phagocytosis of erythrocytes, siderosomes and collagen fibrils by macrophages is observed. Within the endothelial cells there is an abundance of Weibel-Palade bodies and of multivesicular bodies. The former are frequently seen in contact with the luminal cell membrane. Weibel-Palade bodies are believed to be involved in the clotting mechanism.
The organization of thrombi and emboli may be performed exclusively by mononuclear blood cells which represent precursors of various mesenchymal cell types. Between the 10th and 20th day after the onset of blood clotting, mononuclear cells within the fibrinous matrix differentiate into (1) macrophages responsible for hematoclasia and hematophagocytosis, (2) endothelial cells lining autolytic slits in the fibrinous matrix and forming new capillaries, and (3) fibroblasts and even smooth muscle cells building up a young mesenchymal connective tissue.
In organizing thrombi angiogenesis is not dependent on invasion of vasa vasora from the vascular wall. Mononuclear cells of the monohistiocytic system are always present within the clotted blood and are capable of differentiation into various types of mesenchymal cells, including endothelial cells. At first autolytic slits and clefts appear in the fibrinous superficial areas of the thrombus. They are gradually lined by spindle-shaped "pre-endothelial" cells that already possess immunohistological properties of endothelial cells but still resemble primitive mesenchymal cells ultrastructurally. Later these cells gain connection with each other by pseudopodia, overlapping and interdigitation until the channels in the fibrinous matrix are covered by an uninterrupted layer of cells. These cells are now characterized ultrastructurally by the appearance of specific endothelial organelles (Weibel-Palade bodies). Circulation within these channels begins from the blood stream. In addition, angiogenesis by sprouting of vasa vasora from the vascular wall occurs in those areas of the thrombus in contact with the vessel wall. In blood vessels with on unimpaired intimal layer, angiogenesis by invasion of capillaries occurs at an earlier date than capillary formation by mononuclear cells.
The case history of a 23-year-old man presenting with a progressive tender swelling in both temporal regions is described. Eosinophilia varied between 28% and 48% and IgE was markedly increased (1,380 U/l). Arteriography revealed tortuous, enlarged temporal and occipital arteries intersected by stenoses. The pathology diagnosis was chronic necrotizing panarteritis of the temporal artery with pseudoaneurysms, fibrinoid necroses, scar tissue, occasional giant cells, and abundant hypereosinophilia.
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