To study the effects of hemorrhagic shock with or without soft-tissue trauma on fracture healing capacity, as indicated by osteoblast function, we randomized male C3H/HeN mice into one of four groups (group 1: sham, group 2: fracture (FRA), group 3: fracture+hemorrhage (FRA+HEM), group 4: FRA+soft tissue trauma+HEM). The right tibia of animals in groups 2,3, and 4 was fractured by 3-point bending prior to HEM. Hemorrhaged animals (HEM) were bled to and maintained at a mean arterial blood pressure of 35±5mmHg for 90mins. The shed blood was then returned along with lactated Ringer's (2× the shed blood volume). At 72hrs after the experiment, all animals were sacrificed, blood was collected and plasma osteocalcin levels were determined by RIA. The results (meantSEM) were: Osteocalcin Level [ng/ml] Sham FRA FRA+HBM TRA+Soft-Tissue Trauma+HEM 6.7±0.3 8.2±1.3 4.6±0.4 #+ 2.4±0.2 #+ N-6/group, ANOVA, Student-Newman-Keuls test # p<0.05 vs. Shams, + p<0.05 vs. PRA, p<0.05 vs. FRA+HEM Fracture alone did not alter plasma osteocalcin levels. Hemorrhagic shock per se significantly decreased plasma osteocalcin levels and the additional soft-tissue trauma prior to hemorrhage further decreased osteoblast activity. Thus, severe hemorrhage significantly depresses osteoblast function which should compromise fracture healing under those conditions. Furthermore, fracture healing would be expected to be even more compromised if soft-tissue trauma occurs in conjunction with hemorrhage.