Hemorrhagic shock inhibits lipopolysaccharide-induced myelopoiesis in both germ-free and conventional rats.

Background: Bacterial translocation has been implicated in the alteration of the immune response after shock and trauma. This study examined the effect of bacterial translocation on myelopoiesis after hemorrhagic shock in germ-free and conventional rats.

Methods: Awake, unrestrained germ-free and conventional rats were bled to a mean arterial pressure of 30 mm Hg until the animal required infusion of 10% of the shed blood. Rats were resuscitated with shed blood and crystalloid. Sham rats were catheterized but not bled. Twenty-four hours after shock or sham, rats were administered lipopolysaccharide 100 micrograms or saline intraperitoneally. Twenty-four hours later, bone marrow cells were cultured for growth of granulocyte-macrophage colony-stimulating factor (CFU-GM).

Results: Lipopolysaccharide increased the number of CFU-GM/femur in sham germ-free rats (801 +/- 129 versus 455 +/- 110; p less than 0.05) and conventional rats (1458 +/- 200 versus 492 +/- 59; p less than 0.05) compared with saline-treated rats. In contrast, hemorrhagic shock inhibited lipopolysaccharide-induced CFU-GM growth in both germ-free and conventional rats. Shock, itself, was a stimulus for CFU-GM growth in germ-free but not conventional rats. Bone marrow white blood cell counts were unaffected by shock, lipopolysaccharide administration, or the germ-free state.

Conclusions: Hemorrhagic shock inhibited lipopolysaccharide-induced CFU-GM proliferation independent of the germ-bearing status of the rat, and bacterial translocation exerted no influence on myelopoietic dysfunction after hemorrhagic shock.