Anti-inflammatory and anti-thrombotic effects of quinidine

We have studied the effects of quinidine, a class-1 anti-arrhythmic agent, on human platelet aggregation and arachidonic acid (AA) metabolism, and its in vivo effects on shock induced by AA and platelet activating factor (PAF ) in rabbits and on carrageenan-induced rat paw oedema. Quinidine strongly inhibited PAF-induced platelet aggregation, with lesser potency against AA- and adrenaline-induced aggregation, with IC50 values of 130 and 250, and 2 00 mu M, respectively. When tested against AA metabolism, quinidine selecti vely inhibited the production of thromboxane A(2) (TXA(2)) via the cyclooxy genase (COX) pathway in human platelets (IC50 210 +/- 20 mu M, n = 4) witho ut any effects on lipoxygenase products. Pre-treatment of rabbits with quin idine (50-100 mg/kg) prevented the lethal effects of intravenous PAF (II mu g/kg) or AA (2 mg/kg) in a dose-dependent fashion (P < 0.001). In addition , quinidine, at doses ranging from 50 to 200 mg/kg, inhibited carrageenan-i nduced rat paw oedema (P < 0.001). These findings point to a new facet of t he pharmacological actions of quinidine and indicate that it inhibits plate let aggregation induced by PAF AA and adrenaline in vitro and in vivo. Med Sci Res 27:621-624 (C) 1999 Lippincott Williams & Wilkins.