Abstract

BackgroundPentoxifylline can decrease platelet function in humans, but the anti‐platelet effects of pentoxifylline in dogs is unknown. The addition of a luciferin–luciferase reagent during platelet aggregometry can induce a dose‐dependent potentiation of platelet aggregation.ObjectiveTo determine if exposure to pentoxifylline, without the addition of a luciferin–luciferase reagent during aggregometry, causes canine platelet dysfunction. Our hypotheses were that pentoxifylline would inhibit platelet function, and that the addition of a luciferin–luciferase reagent would obscure detection of pentoxifylline‐induced platelet dysfunction as measured via aggregometry.MethodsSeven healthy Walker hound dogs. Platelet‐rich plasma (PRP) and whole blood were treated for 30 minutes with pentoxifylline: 0 (control), 1 and 2 μg/mL. The platelet aggregation was determined using optical (maximum amplitude) and impedance (ohms) aggregometry using collagen as the agonists, with and without a luciferin–luciferase reagent. Four samples were analysed per concentration and the results were averaged.ResultsBased on optical aggregometry, there was no difference (p = 0.964) in the mean maximum amplitude at any pentoxifylline concentration, with and without the luciferin–luciferase reagent. During impedance aggregometry, the addition of a luciferin–luciferase reagent was associated with significantly (p < 0.001) greater platelet aggregation in response to a collagen agonist, regardless of the presence or absence of pentoxifylline.ConclusionsPentoxifylline does not exert an in vitro anti‐platelet effect on canine platelet aggregation when collagen is used as an agonist, but it is unknown if long‐term oral drug administration will inhibit platelet aggregation. The addition of a luciferin–luciferase reagent during platelet aggregometry can artificially enhance canine platelet aggregation.

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