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Arteriosclerosis was induced to rabbits by feeding with 1% cholesterol diet for various terms. After killing the rabbits, the surface of the thoracic aorta was measured and spotaneously released PGI2 from the thoracic aorta during 10 minutes incubation was determined by assay using platelet aggregation, which was demonstrated as pg/cm2/min. Plasma concentration of 6-keto PGF1α thromboxane B2 (TXB2) and TXB2 release from the washed platelets in the aggregatory response were determined by the radioimmunoassay.Arteriosclerotic plaque coverage in thoracic aorta was quantitatively determined by the planimetric procedure and they were divided into three groups, normal group (group A, n=16), arteriosclerotic group with less than 50% changes (group B, n=9) and arteriosclerotic group with more than 80% changes (group C, n=7). The PGI2 production of the aortic wall were 54±21 (A), 46±19 (B) and 41±22 (C)pg/cm2/min in each groups (statistically not significant). The microscopic examination of the aorta revealed preservation of the endothelium even at the site of arteriosclerotic lesion. The amount of released TXB2 from platelets showed no significant differences among three groups.PGI2 production was still preserved in advanced arteriosclerotic aortic wall of rabbits. Since the aortic endothelium is the main layer of the PGI2 production, arteriosclerotic lesion per se might not reduce PGI2 production of the aorta unless endothelium is damaged.
- 一般社団法人 日本血栓止血学会の論文
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