Introduction: Previous work has shown that severe injury accompanied by sympathetic stimulation induces bone marrow (BM) dysfunction by both suppression of hematopoietic progenitor cell (HPC) growth within the BM and HPC mobilization to the peripheral circulation. The resultant anemia and immune system suppression can last for up to two weeks following injury. Our previous work has demonstrated that beta blockade given prior to lung injury reduced both HPC mobilization and restored HPC growth within the BM. This study aims to examine the effect of beta blockade prior to or at the time of hemorrhagic shock (HS).

Methods: Male Sprague-Dawley rats (wt 250 - 300 g) were assigned to four groups (N=4-8 per group). Three groups underwent hemorrhagic shock (HS) via blood withdrawal maintaining the MAP between 30 - 40 mmHg for 45 minutes after which shed blood was rein- fused and the animal was sacrificed at 3 hours. Two of the three groups received beta-blocker as follows: one group received a single daily IP propranolol dose (8-10mg/kg) for three days prior to HS (3dBB/HS), the other group received a single dose of IP propranolol (10 mg/kg) following HS during resuscitation (HS/BB). HPC growth was assessed via GEMM, BFU-E, and CFU-E colony growth in the BM at 3 hours. Blood pressure and heart rate were recorded (*p<0.05 by ANOVA and Tukey-Kramer analysis).

Results: Administration of beta blockers prior to injury or during resuscitation restored HPC growth similar to that of control levels (*p<0.05). This trend was similar for both GEMM and CFU-E colony growth. 3dBB/HS and HS/BB had a decrease in heart rate as compared to HS at the end of shock (360 bpm and 340 bpm vs. 490 bpm).

Conclusion: Administration of non-specific beta blockade at the time of resuscitation significantly reduces BM suppression following HS. The BM protection is identical to that observed when beta blockers are administered prior to injury. Therefore, beta blockade may play an important role in attenuating the BM dysfunction seen following shock.