TP (thromboxane-A2 /prostaglandin-endoperoxide)-receptor blockade with terutroban decreases portal pressure in cirrhosis[3]. Terutroban is a selective TP receptor antagonist, i.e. a specific antagonist of the thromboxane A(2) and prostaglandin endoperoxide receptors, shown to improve endothelial function after a single administration in patients with coronary artery disease. It can chronically improve endothelium-dependent vasodilatation and inhibiting platelet aggregation[4]. Terutroban prevents the development of aorta hyperplasia and has beneficial effects on fibrotic processes by affecting TGF-β and heat shock protein-47 expression in SHRSPs(spontaneously hypertensive stroke-prone rats)[5]. Terutroban significantly protected retinal vascularity from ischaemia in experimental diabetes, and this result could be attributed not only to its antiplatelet/antithrombotic activities but also to its vascular properties[6]. In PAD (peripheral arterial disease) patients, terutroban dose-dependently inhibited platelet aggregation 24 h after dosing, and was at least as effective as aspirin at 5, 10 and 30 mg day(-1). Terutroban was well tolerated[7].
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