title: [Cause and significance of increased endothelial permeability in the development of arteriosclerosis].
abstract: The above survey described the physiological and pathological transport of molecules through the arterial endothelium. The barrier function of the endothelium can be interrupted by the humoral substances and such ones be longing to the vascular wall as well as by haemodynamic stress. With the intercellular junctions being opened by destruction or contraction of the endothelium, macromolecular plasma constituents get into the subendothelium where they are retained. By this retentive effect an increased endothelial permeability causes, even with physiological plasma-lipid concentrations, an accumulation of lipoproteins and other large plasma particles in the intima and upper media. The continuous plasma insudation consequently leads to the formation of an intimal regneration tissue, the intimal proliferation. Under the conditions of pathological plasma-lipid concentrations there is to be noticed an acceleration of regeneration processes. Though the new experimental results characterize the endothelial alteration as an initial process, the individual reaction of the vascular wall forms the biochemical and structural correlate of arteriosclerosis. From the results described it can be concluded that the inhibition of permeability disturbances and the involved proliferation processes of the arterial wall as well as the prevention of a hyperlipoproteinaemia are a causative therapeutical basis of prophylaxis and metaphylaxis of arteriosclerosis.
mesh_terms: D001158:Arteries / Q000378:metabolism / Q000503:physiopathology; D001161:Arteriosclerosis / Q000209:etiology* / Q000378:metabolism; D001679:Biogenic Amines / Q000378:metabolism; D002463:Cell Membrane Permeability; D004727:Endothelium / Q000378:metabolism / Q000503:physiopathology*; D006801:Humans; D050356:Lipid Metabolism; D010455:Peptides / Q000378:metabolism
chemical_list: D001679:Biogenic Amines; D010455:Peptides
vernacular_title: Ursachen und Bedeutung der gesteigerten Endothelpermeabilität für die Entstehung der Arteriosklerose