Background: Pentoxifylline 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.
Objective: To 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.
Methods: Seven 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.
Results: Based 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.
Conclusions: Pentoxifylline 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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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8604144 | PMC |
http://dx.doi.org/10.1002/vms3.595 | DOI Listing |
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