Intimal hyperplasia producing thrombus organization in an experimental venous thrombosis model.

Abstract

A venous thrombosis animal model demonstrated similarities between intimal hyperplasia and thrombus organization. This has prompted the evaluation of a hypothesis that intimal hyperplasia may be the mechanism for thrombus organization in veins with normal pressure. Thrombi were produced in surgically exposed jugular veins of anesthetized, 18 to 20 kg pigs. Thrombosis was induced by a combination of devascularization, electric injury produced by a low amperage, direct current, and permanent partial ligation (50% diameter reduction). Vein segments were harvested at 0, 1, 2, 7, 14, and 60 days and histologically examined for fibrin, red blood cells, platelets, smooth muscle cells, endothelial cells, elastic fibers, and collagen deposits. Forty vein segments in 20 pigs were evaluated. Luminal thrombi with thickened walls developed in all specimens. All luminal thrombi demonstrated partial spontaneous thrombolysis over the period of observation. Intimal thickening consisting primarily of smooth muscle cells by day 2 was apparent and progressed until about 2 weeks, when collagen deposits became prominent within the neointima. The neointima frequently comprised half the cross-sectional area of the veins. Endothelial cells were present in the intima as single cells or as lining for clefts formed within the thickened intima. Smooth muscle cell proliferation with collagen deposition characteristic of intimal hyperplasia seemed to be the mechanism of thrombus organization in the experimental thrombosis model used in this study in which extensive stimulation was used to produce thrombosis.