Prostacyclin (PGI2)-generation by different types of human atherosclerotic lesions.
Unaltered human arterial tissue as well as different types of macroscopically and microscopically characterized atherosclerotic lesions were microdissected under a preparation microscope. The prostacyclin formation was examined using its potent platelet aggregation inhibition in vitro according to Moncada's bioassay. In contrast to different PGI2-formation in various experimental animal models the generation in the different lesion types in terms of wet weight was statistically significantly (p less than 0.001) diminished in comparison to normal control tissue. However, the PGI2- formation in different lesion types is comparable. Accepting the hypothesis delivered earlier by us, that the arterial wall is able to react upon exogenous noxes with a temporarily enhanced PGI2-formation, followed (after ceasing) by a decrease of PGI2-synthesis (exhaustion phenomenon) it can be concluded, that the critical stage is prior to the fatty streak formation, which is a preatherosclerotic lesion. Therefore, PGI2-generation-exhaustion might be mainly responsible for initiation and progression of atherosclerosis, probably before any detectable morphological alterations.
D000368:Aged; D001158:Arteries / Q000378:metabolism* / Q000473:pathology; D001161:Arteriosclerosis / Q000378:metabolism* / Q000473:pathology; D001681:Biological Assay; D011464:Epoprostenol / Q000096:biosynthesis* / Q000494:pharmacology; D005260:Female; D005263:Femoral Artery; D006801:Humans; D007083:Iliac Artery; D008297:Male; D008875:Middle Aged; D010974:Platelet Aggregation / Q000187:drug effects; D011453:Prostaglandins / Q000096:biosynthesis*
D011453:Prostaglandins; D011464:Epoprostenol