Gezielte Überdehnung der Aorta abdominalis am normo- und hypercholesterinaemischen Kaninchen
- 1 January 1963
- journal article
- research article
- Published by S. Karger AG in Pathobiology
- Vol. 26 (2) , 129-148
- https://doi.org/10.1159/000161361
Abstract
A segment of the rabbit abdominal aorta was over-dilatated by means of a balloon-catheter introduced through a femoral artery. The dilatation is standardized by applying equal pressures for equal periods of time. The sequence of structural changes occurring in the injured segment was studied in 22 normo- and 18 hypercholesterolemic rabbits. Stages from 1 day to 28 weeks after over-dilatation were histologically examined. Over-dilatation causes destruction of the intima and necrosis of the smooth muscle cells of the media. In hypercholesterolemic animals fat is seen to be spread diffusely in fine drops in the inner part of the media as early as 1 day after over-dilatation. Towards the end of the 1st week an intense regeneration takes place in both normo- and hypercholesterolemic animals, i.e. new nuclei appear in the media as well as in the quickly proliferating intima. Increase of elastic fibers and smooth muscle cells in the thickened intima also point to a regenerative process. In hypercholesterolemic animals an increase in the inter-stitially deposited fat is observed. Whereas the newly formed tissue elements of the intima consolidate in the normocholesterolemic animals during the following weeks, in cholesterol fed animals these elements are displaced by increasing masses of fat and are finally destroyed secondarily 18 or more weeks after over-dilatation. The combination of lipemia with structural alteration of the vessel wall is extremely unfavourable for the organism, as in the injured wall fat infiltration occurs earlier and fat deposits are larger than in the undamaged vascular wall. The fat in turn severely interferes with the healing-process. This disadvantageous correlation between humoral and arterial wall-factor might have a significance for the pathogenesis of arteriosclerosis in the sense of a vicious circle.Keywords
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