In-vitro hypocoagulability on whole blood thromboelastometry associated with in-vivo expansion of red cell mass in an equine model.

In several species, there is a strong correlation between indicators of red cell mass (RCM) and thromboelastometry results. The horse has a reliable, temporary, polycythemia in response to phenylephrine infusion. Our objective was to evaluate the effects of an in-vivo increase in circulating RCM on thromboelastometry results in an equine model of transient polycythemia. Six healthy research horses had whole blood thromboelastometry with contact activator and tissue factor initiation after recalcification of citrated samples. Additional samples were frozen for thrombin-antithrombin (TAT). Complete blood count biochemical analysis, fibrinogen, activated partial thromboplastin time (aPTT), and prothrombin time (PT) were performed. Additional samples were taken at 5 min and 2 h after phenylephrine infusion. Thromboelastometry was performed separately on four horses not receiving phenylephrine with the samples divided and spiked with phenylephrine ex vivo. Red cell count (P<0.001) and hematocrit (P<0.001) were significantly higher at 5 min after phenylephrine compared with baseline and 2 h. There was no change in platelet count, fibrinogen, PT, aPTT, or TAT at any time point. Both ex-tem and in-tem parameters were hypocoagulable at 5 min after phenylephrine compared to baseline and 2 h. There was no effect of phenylephrine in the ex-vivo spiking studies on any of the thromboelastometry parameters. Whole blood thromboelastometry results were hypocoagulable in this equine model of in-vivo transient polycythemia only during the polycythemic phase. All other coagulation parameters were unchanged. In the absence of other indicators of hypocoagulability, this may point to an artifact of thromboelastometry. Alternatively, the data may reflect true in-vivo hypocoagulability in patients with increased circulating RCM.