GUT ISCHEMIA INDUCES BONE-MARROW FAILURE AND INCREASES RISK OF INFECTION

Hemorrhagic shock leads to bone marrow (BM) failure and renders the ho st susceptible to infection. We hypothesized that splanchnic hypoperfu sion may play a mechanistic role in this process. BM was harvested fro m normal rats and, on Postprocedure Days 1 and 3, from rats that had u ndergone laparotomy (LAP) or gut ischemia/reperfusion (I/R; 45 min sup erior mesentery artery occlusion). Granulocyte-macrophage colony-formi ng unit (CFU-GM) proliferation, a measure of BM myeloid progenitors, w as quantitated using a standard soft agar culture technique. On Postpr ocedure 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 ra ts were subjected to I/R, LAP, ANEST (anesthesia control), or no treat ment (NL, normal control); 1 day later, 3.5 x 10(7) Staphylococcus aur eus, suspended in 0.25 ml of saline, were injected subcutaneously in f our 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 su sceptible 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 B M failure and infection after hemorrhage. (C) 1994 Academic Press, Inc .