Pathomechanisms of atherosclerosis beneficially affected by prostaglandin E1 (PGE1)--an update.
The antiplatelet action of PGE1 was the basic concept for introducing this substance into clinical therapy of atherosclerosis. However, in the meanwhile a variety of other mechanisms have been discovered, which might be of importance, especially concerning the long-term benefit seen after treatment with PGE1, such as stabilization of endothelial lining, reflected by a decreased number of circulating endothelial cells and a decreased thrombogenicity (potentiated by endogenous EDRF-release), an inhibitory action on smooth muscle cells of the vessel wall such as decrease in mitotic and proliferative activity associated with a diminished extracellular matrix formation, an increase in fibrinolytic capacity, beneficial effects on white and red blood cells and some beneficial effects on the lipid metabolism by decreasing the arterial wall cholesterol content and upregulation of LDL-receptors as well as a moderate drop in serum cholesterol, seen in severe hypercholesterolemics only. It is assumed, that especially the vascular effects together with the hypolipidemic actions of PGE1 might be of major importance underlying the long-term benefit.
Sinzinger
H
H
Virgolini
I
I
Fitscha
P
P
D000527:Alprostadil / Q000494:pharmacology* / Q000627:therapeutic use; D001161:Arteriosclerosis / Q000188:drug therapy*; D001792:Blood Platelets / Q000187:drug effects*; D004730:Endothelium, Vascular / Q000187:drug effects; D004912:Erythrocytes / Q000187:drug effects; D006801:Humans; D007962:Leukocytes / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects
D000527:Alprostadil