BACKGROUND: Pentoxifylline (PTX) possesses a number of vasomotor, immunomodulatory, and hemorheologic properties. Based upon the hypothesis that equine laminitis and navicular disease result from microthrombosis, the inhibitory effects of PTX on inflammatory cytokines, and its inhibitory effects on human platelet aggregation, PTX has been widely used to treat equine endotoxemia, navicular disease, and laminitis. Despite this, the effects of PTX on equine platelet aggregation have not been investigated previously. HYPOTHESIS: PTX decreases platelet aggregation in equine whole blood at concentrations approximating those achieved in horses given clinically relevant doses of PTX. ANIMALS: Seven healthy adult horses from a research herd. METHODS: Whole blood impedance aggregometry using whole equine blood incubated with varying concentrations of PTX. Adenosine diphosphate (ADP) and collagen were used to initiate aggregation. RESULTS: The onset time of collagen-induced equine platelet aggregation was significantly shortened by PTX. The maximum slope of resistance change (dR/dt) and total resistance change of collagen-induced platelet aggregation were unaffected by PTX. No effects of PTX on ADP-induced onset time of aggregation, dR/dt, or total resistance change were observed. CONCLUSIONS AND CLINICAL IMPORTANCE: Our hypothesis is not supported by the results. PTX hastens the onset of collagen-induced platelet aggregation in equine whole blood, but has no effect on the rate of collagen-induced aggregation. PTX does not affect ADP-dependent equine platelet aggregation. Given these findings, PTX may not be a reasonable therapeutic option to decrease platelet aggregation in horses.
BACKGROUND:Pentoxifylline (PTX) possesses a number of vasomotor, immunomodulatory, and hemorheologic properties. Based upon the hypothesis that equinelaminitis and navicular disease result from microthrombosis, the inhibitory effects of PTX on inflammatory cytokines, and its inhibitory effects on humanplatelet aggregation, PTX has been widely used to treat equineendotoxemia, navicular disease, and laminitis. Despite this, the effects of PTX on equineplatelet aggregation have not been investigated previously. HYPOTHESIS: PTXdecreases platelet aggregation in equine whole blood at concentrations approximating those achieved in horses given clinically relevant doses of PTX. ANIMALS: Seven healthy adult horses from a research herd. METHODS: Whole blood impedance aggregometry using whole equine blood incubated with varying concentrations of PTX. Adenosine diphosphate (ADP) and collagen were used to initiate aggregation. RESULTS: The onset time of collagen-induced equineplatelet aggregation was significantly shortened by PTX. The maximum slope of resistance change (dR/dt) and total resistance change of collagen-induced platelet aggregation were unaffected by PTX. No effects of PTX on ADP-induced onset time of aggregation, dR/dt, or total resistance change were observed. CONCLUSIONS AND CLINICAL IMPORTANCE: Our hypothesis is not supported by the results. PTX hastens the onset of collagen-induced platelet aggregation in equine whole blood, but has no effect on the rate of collagen-induced aggregation. PTX does not affect ADP-dependent equineplatelet aggregation. Given these findings, PTX may not be a reasonable therapeutic option to decrease platelet aggregation in horses.