NE and EPI promote platelet production and activation. (A) Flow cytometric analysis of platelet production from MKs induced by NE or EPI. CD34⁺ cells were cultured with rhTPO for 13 days and then treated with NE (1 μM) or EPI (1 μM) for 24 hours. (B) Mean percentages of culture-derived platelets induced by NE or EPI. (C-D) Western blot analysis of ERK1/2 phosphorylation in isolated platelets from the health donors treated with NE or EPI for different times. (E-F) Flow cytometry analysis of the time-course changes of in CD62p expression in isolated platelets induced by NE (10 μM) or EPI (10 μM). (G-H) CD62p expression in isolated platelets treated with yohimbine (10 μM) and U0126 (10 μM) before NE and EPI stimulation. (I) Schematic illustration of the role of sympathetic stress in regulating thrombopoiesis and its pathophysiological implications. The elevated NE and EPI levels induced by sympathetic stress stimulate thrombopoiesis and platelet activation via α2-adrenoceptor–mediated ERK1/2 signaling. As a result, the increased platelet counts and activation promote 2 different outcomes (hemostasis facilitation or thrombosis aggravation) under different pathophysiological conditions. *P < .05, **P < .01, vs control; #P < .05, ##P < .01, vs NE or EPI treatment group.