PROSTAGLANDIN E-1 DECREASES HUMAN ARTERIAL ACCUMULATION OF RADIOLABELED APO B-CONTAINING LIPOPROTEINS IN-VIVO

Citation
H. Kritz et al., PROSTAGLANDIN E-1 DECREASES HUMAN ARTERIAL ACCUMULATION OF RADIOLABELED APO B-CONTAINING LIPOPROTEINS IN-VIVO, European Journal of Clinical Pharmacology, 52(3), 1997, pp. 191-197
Citations number
31
Categorie Soggetti
Pharmacology & Pharmacy
ISSN journal
00316970
Volume
52
Issue
3
Year of publication
1997
Pages
191 - 197
Database
ISI
SICI code
0031-6970(1997)52:3<191:PEDHAA>2.0.ZU;2-T
Abstract
Objective: An increased apo B-containing lipoprotein influx and choles terol ester accumulation in arteries are well-known events in human at herogenesis. In vitro and experimental animal studies have provided ev idence of a beneficial effect of PGE(1) on both vascular apo B-contain ing lipoprotein accumulation and cholesterol ester content. Methods: W e examined the effect of PGE(1) (administered via an intravenous porta ble infusion pump at a rate of 5 ng PGE(1) kg(-1) min(-1) for 5 days a week, 6 h daily, over a total of 5 weeks) in ten patients (eight male s, two females) on I-123-apo B-containing lipoprotein accumulation int o the large arteries in vivo. Apo B-containing lipoprotein isolation w as carried out by immunoaffinity chromatography and radiolabeling with the iodine monochloride method. I-123-apo B-containing lipoprotein ac cumulation was imaged and quantified by means of special computer soft ware before and after 5 weeks of PGE(1) therapy Results: PGE(1) led to a significant decrease in maximal arterial apo B-containing lipoprote in retention. The mean decrease in the carotid and femoral arteries in type I lesions amounted to between 16.9% and 30.4%, and in type II le sions between 22.4% and 30.7%, 20 h after injection of radiolabeled ap o B-containing lipoprotein. The type of arterial apo B-containing lipo protein kinetic curves, however, remained unchanged. Conclusion: These findings indicate that PGE(1) decreases the apo B-containing lipoprot ein influx in the large arteries and the vascular cholesterol content, suggesting that PGE(1) may lead to regression of lipid-rich lesions i n human in vivo.