英文翻译200804030220.docVIP

阿司匹林, 卡洛芬 德拉昔布 美洛昔康 卡洛芬 德拉昔布 美洛昔康德拉昔布 卡洛芬美洛昔康德拉昔布 卡洛芬 德拉昔布美洛昔康 蛋白丢失性 肾上腺皮质机能亢进 卡洛芬 德拉昔布 美洛昔康多糖-蛋白质复合物 卡洛芬美洛昔康德拉昔布The Effects Of Aspirin, Carprofen, Deracoxib, And Meloxicam On Hemostasis And Systemic Prostaglandins In Dogs ABSTRACT Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used in veterinary medicine to provide analgesic and anti-inflammatory benefits to patients. The adverse effects associated with NSAID use are believed to be largely due to inhibition of the enzyme cyclooxygenase (COX)-l. As such, COX-2-selective NSAIDs were developed in attempt to limit the development of NSAID-associated adverse effects. Recent reports in the human medical literature have suggested an increased incidence of thromboembolic events associated with the use of COX-2 selective NSAIDs. There is speculation that COX-2 selective NSAIDs may lead to an imbalance in prostaglandin levels, with a relative increase in thromboxane versus prostacyclin. Thromboxane promotes platelet aggregation and vasoconstriction, while prostacyclin counteracts these effects. This study examined the effects of NSAIDs on hemostasis and cardiovascular prostaglandin levels in healthy dogs. Ten dogs were given four NSAIDs and one placebo in a cross-over design at dosages consistent with current therapeutic recommendations. The NSAIDs administered included aspirin, carprofen, deracoxib, and meloxicam. Parameters measured before and after 7 days of NSAID administration included platelet optical aggregometry, platelet function analysis (using the PFA-100), and plasma thromboxane and prostacyclin levels. Administration of NSAIDs did not cause a significant effect on platelet function measured by the PFA-100. Deracoxib did not affect platelet function measured by other aggregation studies and the PFA-100. Aspirin, carprofen, and meloxicam did not affect platelet function. Plasma thromboxane levels decreased after aspirin administration compared to after deracoxib administration, while NSAID administrati