作者: Timothy D. Warner , Sven Nylander , Carl Whatling
DOI: 10.1111/J.1365-2125.2011.03943.X
关键词:
摘要: Aspirin and P2Y12 antagonists are commonly used anti-platelet agents. produces its effects through inhibition of thromboxane A2 (TXA2) production, while attenuate the secondary responses to ADP released by activated platelets. The aspirin a antagonist often considered be separately additive. However, there is evidence an overlap in effects, that high level receptor can blunt TXA2 signalling platelets reduce platelet production TXA2. Against this background, addition aspirin, particularly at higher doses, could cause significant reductions prostanoids other tissues, e.g. prostaglandin I2 from blood vessel wall. This review summarizes data clinical studies which dose-dependent on prostanoid have been evaluated both plasma urinary measures. It also addresses biology underlying cardiovascular influences upon throughout body. then considers whether, presence newer, more refined antagonists, may offer less benefit than might predicted earlier trials using variable antagonists. possibility reflected upon, when combined with blockade net effect doses removal anti-thrombotic vasodilating so lessening effectiveness treatment.