Role of spleen and liver for enhanced hemostatic competence following administration of adrenaline to humans.

This study evaluated by thrombelastography® (TEG) and Multiplate® analyses the role of the spleen and the liver for adrenaline-induced enhanced hemostatic competence. Eight splenectomized subjects and eight matched healthy control subjects were exposed to one-hour infusion of adrenaline (6 μg/kg/h). Administration of adrenaline to the healthy subjects reduced time to TEG-detected initial fibrin formation (by 22%) and increased rate of clot development (by 10%), maximal amplitude (by 8%), platelet count (by 30%), and Multiplate evaluated Ristocetin-induced platelet aggregation (by 21%) (all p ≤ 0.05), but infusion of adrenaline did not result in significant arterial to liver vein differences for plasma markers of coagulation. In the splenectomized subjects, adrenaline reduced the TEG-determined time to initial fibrin formation (by 17%; p = 0.005) whereas rate of clot development and maximum amplitude were unaffected. Also, 6 patients undergoing liver transplantation were exposed to infusion of adrenaline (4.8 μg/kg/h) during the anhepatic phase of the operation and that increased TEG-determined rate of clot formation (by 10%; p < 0.05), maximal amplitude (by 9%; p = 0.002) and tended to reduce time to initial fibrin formation (p = 0.1). In conclusion, adrenaline enhances hemostasis as evaluated by TEG in both healthy subjects and in anhepatic patients during liver transplantation and Ristocetin-induced aggregation in control subjects. In contrast, infusion of adrenaline reduces only time to initial fibrin formation in splenectomized subjects. These findings suggest that mobilization of platelets from the spleen dominates the adrenaline-induced enhanced hemostatic competence.