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Lymphostasis in the aortic wall has been produced experimentally. It has been proved that the disturbance of the lymph circulation results in changes of the aortic wall e.g. oedematic transformation of muscle cells, demarcation of parts of them, formation of ghost bodies and eventually total necrosis of muscle cells. The necrosis of muscle cells usually is followed by proliferation and development of sclerosis.

Characteristic features of the smooth muscles cell migration and ghost body formation observed in vascular lesions induced by intravenous administration of Lipofundin-S (Braun, Melsungen) were studied and compared to lesions seen in other models. Phenomena revealed can be explained by alterations of the cell environment. The cell, producing ghost body looses a part of the cytoplasm and complies with the new environment. Thus ghost bodies play an active part in maintaining the equilibrium between the cell and its environment.

Characteristic features of the smooth muscle cell migration and ghost body formation observed in vascular lesions induced by intravenous administration of Lipofundin-S were studied and compared to lesions seen in other models. Phenomena revealed can be explained by alterations of the cell environment. The cell, producing ghost body looses a part of the cytoplasm and complies with the new environment. Thus ghost bodies play an active part in maintaining the equilibrium between the cell and it's environment.

In our previous studies performed in rats sclerotic alterations were induced in the vessel wall by Lipofundin-S 20% (Braun, Melsungen) administration for 8 or 16 days, respectively. In order to elucidate eventual species dependency, studies on rabbits were also performed. Alterations were examined in rabbits after Lipofundin treatment for 8 days. Electron microscopic studies revealed the accumulation of granular basement membrane-like material in the subendothelial space due to the activity of immigrated smooth muscle cells. The formation of elastic granules and elastic laminae was also observed among others due to the coalescence of microfibrillary structures formed from glycoseaminoglycans. The lesion developed was similar to that observed in the rat, the only difference was that in the rabbit the accumulation of the collagen fibres was more prominent. Results of our studies obtained in rabbits appear to support our previous findings: Lipofundin-S treatment induces aortic smooth muscle cell mobilization, fibrillogenesis and enlargement of the subendothelial space, namely sclerotic manifestations are induced.

Be the ligature of lymphatic vessels lymphostasis has been produced and the consequences of it in the myocardium were studied. Lymphatics of the myocardium in lymphostasis were compared with those in the normal one. It was found that the space between lymphatics and myocardial fibers filled mainly with connective tissue due to accumulation of oedema fluid enlarges and the collagen fibers disintegrate. At the same time accumulation of fluid and dilatation of lymphatics takes also place. Pinocytotic activity of endothelial cells increases. Due to oedema vacuolization of myocardial cells occurs. Disturbance of the capillary circulation leads to swelling of endothelial cells and narrowing the capillary lumen. This lies on the basis of hypoxia and fatty degeneration of the myocardium. The coronary vessels have also shown alterations. In the subendothelial space accumulation of plasma constituents, in the smooth muscle cells of the vessel wall oedema was found. Thus, lymphostasis in the myocardium results in significant alterations.

Lesions in the arterial wall induced in rats by means of intravenous injection of Lipofundin-S were studied by electron microscopy. The morphological changes in this model are the enlargement of the subendothelial space, proliferation of smooth muscle and accumulation of basement membrane-like material. These changes are a closer model for the fibro-proliferative aspects of human atherosclerosis than those seen in short-term (2-3 month) cholesterol feeding. Moreover, such changes are produced in 8 days rather than 2-3 month. These factors indicate that the Lipofundin-S model may be of value in testing anti-atherosclerotic drugs.