Gut ischemia induces bone marrow failure and increases risk of infection.

Hemorrhagic shock leads to bone marrow (BM) failure and renders the host susceptible to infection. We hypothesized that splanchnic hypoperfusion may play a mechanistic role in this process. BM was harvested from normal rats and, on Postprocedure Days 1 and 3, from rats that had undergone laparotomy (LAP) or gut ischemia/reperfusion (I/R; 45 min superior mesentery artery occlusion). Granulocyte-macrophage colony-forming unit (CFU-GM) proliferation, a measure of BM myeloid progenitors, was quantitated using a standard soft agar culture technique. On Postprocedure Days 1 and 3, BM proliferation of CFU-GM was depressed in gut I/R rats, compared to control and LAP animals (P < 0.05). Next, six rats were subjected to I/R, LAP, ANEST (anesthesia control), or no treatment (NL, normal control); 1 day later, 3.5 x 10(7) Staphylococcus aureus, suspended in 0.25 ml of saline, were injected subcutaneously in four sites on the back of each animal. Five days later, the NL rats had developed 23 abscesses, ANEST 23, and LAP 22, while the gut I/R rats had 24. The abscesses were excised, weighed, and measured. The weight and size of abscesses were greater in the gut I/R animals (P < 0.05). In summary, gut I/R depressed BM proliferation and rendered animals susceptible to infection in a manner similar to that observed following hemorrhagic shock. These data suggest that splanchnic hypoperfusion, a common sequela of hemorrhagic shock, may play a mechanistic role in BM failure and infection after hemorrhage.