Although the thymus is an important organ in the ontogeny of T-cells, little is known about the effect of hemorrhage and/or trauma on this organ. To study this, male C3H/HeN mice underwent either sham opérât ion, hemorrhagic shock (MABF 35±5mniHg for 90mins, fol lowed by fluid resuscitation; HEM), fracture of the right tibia (FRA), or fracture plus hemorrhage (FRA+HEM), respectively. At 72h after the operation, thymocyte apopcosis (by flow cytometry), total viable thymocyte yield and thymocyte cytokine-release (IL 3 bioassay; GM-CSF ELISA) were: Sham HEM FRA HEM + FRA TC yield (1 × 107) 4.30 ± 0.30 1.92±0,365.13±0.46 1.57±0.22Apoptotic TC (%) 1.26±7 2 20±0.251.32±0.21 2,70±0.39IL-3 (ConA-,U/ml) 1.43 ± 0.35 0 42±0.191.01±0.28 0.43±0.14IL-3 (ConA+,U/ml) 8.30±1.26 3 47±0.985.00±0.72 3.42±0.50GM-CSF (ng/mD 1.82 ± 0.30 2.92±0.58 2.17±0.38 4.76±0.70N-6-8/group, Menn + SEM. ANOVA, Student-Newman-Keuls Test,p<0.05 vs. Sham Our results demonstrate that : (1) there is a significant decrease in total viable thymocyte yield and an increase in thymocyte apoptonis following HEM or FRA+ HEM; (2) thymocyte IL-1 release was significantly reduced after HEM and FRA+HEM; (3) t.tiymuG-derived GM-CSF was significantly increased only after FRA+HEM, but not with HEM alone. Thus, it appears that severe hemorrhage alone and coupled with fracture can induce thymus atrophy via apoptosis. n addition, the decreased IL-3 release suggests that apoptot.ic thymic involution may be as much due to the lack of growth factor support as it is due to active negative select ion. Such dyshomeostasis may contribute to inappropriate/inadequate T-cell maturation leading to host immune suppression following trauma-hemorrhage, Increased thymus-derived GM-CSF might be in part responsible for the systemic inflammatory response following trauma-hemorrhage.