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EFFECTS OF ORAL BERAPROST SODIUM, A PROSTAGLANDIN I 2 ANALOGUE, ON ENDOTHELIUM DEPENDENT VASODILATATION IN THE FOREARM OF PATIENTS WITH CORONARY ARTERY DISEASE
Author(s) -
Ohata Shuzo,
Ishibashi Yutaka,
Shimada Toshio,
Takahashi Nobuyuki,
Sugamori Takashi,
Sakane Takeshi,
Hirano Yoshifumi,
Oyake Nobuyuki,
Murakami Yo,
Higami Tetsuya
Publication year - 2006
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.2006.04379.x
Subject(s) - vasodilation , forearm , medicine , coronary artery disease , brachial artery , cardiology , prostaglandin , endothelium , surgery , blood pressure
SUMMARY1 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 mg/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 2a (8‐iso‐PGF 2a ) 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 2a 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 2a 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 2a ( 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.