Prostaglandin Derivatives and Platelet-specific Proteins During Transluminal Coronary Angioplasty

Abstract

There is much speculation about the role of prostaglandins and thromboxanes in ischemic heart disease. These endogenous compounds are potent modulators of vascular smooth muscle tone and platelet aggregability. During platelet activation platelets generate a potent vasoconstrictor, thromboxane A₂ (TXA₂), whereas prostaglandin I₂ (PGI₂), produced by the vessel wall, is a potent vasodilator and inhibits platelet aggregation [5]. Both PGI₂ and TXA₂ are unstable and spontaneously convert to the inactive metabolites 6-Oxo-prostaglandin F₁ α (6-Oxo-PGF₁ α;) and thromboxane B₂ (TXB₂), respectively [2, 7]. In addition, the measurement of plasma concentrations of β-thromboglobulin (βTG), a specific protein, which is extruded from well-defined platelet granules into the surrounding medium, might reflect in vivo platelet activation [4].