title: Effects of oral beraprost sodium, a prostaglandin I2 analogue, on endothelium dependent vasodilatation in the forearm of patients with coronary artery disease.
abstract: 1. Previous clinical studies with prostaglandin I(2) (PGI(2)) analogue beraprost sodium suggested the potential effects on protection of cardiovascular events in patients with peripheral artery disease. Although the mechanism is not well known, experimental studies have shown protective effects of endothelial cells. This study was designed to examine the effects of beraprost sodium on vascular endothelial function in the forearm of patients with coronary artery disease. 2. Beraprost sodium (120 microg/day) was orally administered to 14 coronary artery disease patients for 4 weeks and then stopped for 4 weeks. Eleven control patients did not receive beraprost sodium treatment. Reactive hyperemia was induced in the forearm, endothelium-dependent vasodilatation was assessed by plethysmography, and urinary 8-iso-prostaglandin F(2alpha) (8-iso-PGF(2alpha)) was measured at baseline, 4 weeks and 8 weeks. 3. Both groups had similar reactive hyperemic responses at baseline. In the control group, reactive hyperemic response and urinary 8-iso-PGF(2alpha) remained unchanged for 8 weeks. In the beraprost group, maximum forearm blood flow increased significantly (P = 0.01) after 4 weeks of treatment and returned to baseline at 8 weeks. Duration of hyperemia increased significantly (P = 0.003) after 4 weeks, and remained greater than baseline at 8 weeks (P = 0.02). Urinary 8-iso-PGF(2alpha) decreased significantly (P = 0.03) after 4 weeks, and tended to be lower at 8 weeks (P = 0.07). Changes in reactive hyperemia correlated weakly but significantly with changes in 8-iso-PGF(2alpha) (P < 0.001). 4. Beraprost sodium decreased oxidative stress and improved forearm endothelium-dependent vasodilatation in coronary artery disease patients. The favorable effects on vascular endothelium could potentially lead to a decrease in vascular events.
authors.affiliation: Division of Cardiovascular Medicine, Department of Internal Medicine, Shimane University Faculty of Medicine, Izumo City, Shimane, Japan.
authors.forename: Shuzo
authors.initials: S
authors.lastname: Ohata
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Ishibashi
authors.forename: Toshio
authors.initials: T
authors.lastname: Shimada
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Takahashi
authors.forename: Takashi
authors.initials: T
authors.lastname: Sugamori
authors.forename: Takeshi
authors.initials: T
authors.lastname: Sakane
authors.forename: Yoshifumi
authors.initials: Y
authors.lastname: Hirano
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Oyake
authors.forename: Yo
authors.initials: Y
authors.lastname: Murakami
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Higami
mesh_terms: D000368:Aged; D003324:Coronary Artery Disease / Q000503:physiopathology*; D015237:Dinoprost / Q000031:analogs & derivatives / Q000494:pharmacology; D004311:Double-Blind Method; D004730:Endothelium, Vascular / Q000502:physiology*; D011464:Epoprostenol / Q000031:analogs & derivatives* / Q000494:pharmacology; D005260:Female; D005542:Forearm / Q000098:blood supply*; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D006940:Hyperemia / Q000503:physiopathology; D008297:Male; D011446:Prospective Studies; D012039:Regional Blood Flow / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects*; D014665:Vasodilator Agents / Q000494:pharmacology*
chemical_list: D014665:Vasodilator Agents; C075750:8-epi-prostaglandin F2alpha; C048081:beraprost; D015237:Dinoprost; D011464:Epoprostenol