DEPRESSED SPLENIC FUNCTION AFTER HEMORRHAGE RESULTS FROM GASTROINTESTINAL-TRACT STIMULATION OF HEPATIC-MEDIATOR RELEASE - CORRECTION WITH PORTACAVAL-SHUNT

Objective: To determine whether redirecting intestinal blood flow away from the liver via a portacaval shunt would protect distal immune res ponses in the spleen after hemorrhage. Design: Type C3H/HeN male mice in which a portacaval shunt had been established Z to 3 weeks before t he experiment were bled, their blood pressure was maintained at 35 mm Hg for 1 hour, and then they were resuscitated. Twenty-four hours late r, the mice were killed, and mixed and adherent splenocyte cultures we re established. The proliferative capacity of splenocytes, the release of interleukin-2 and interleukin-dr, and the ability of splenic macro phages to present the antigen, conalbumin, were then determined as ind exes of immunocompetence.Results and Conclusions: The results indicate that splenocyte proliferation and splenocyte interleukin-2, but not i nterleukin-4, release were decreased and that splenic macrophage antig en presentation declined after hemorrhage. However, animals in which a portacaval shunt had been established before hemorrhage showed no suc h changes in their splenocyte or splenic macrophage functions. Thus, t he decline of splenic immune responses after hemorrhage seems to be du e to mediators released from the gut. Such mediators, in turn, stimula te Kupffer cells to secrete additional agents that produce immunosuppr essive exocrine effects on splenic immune functions. Results and Concl usions: The results indicate that splenocyte proliferation and splenoc yte interleukin-2, but not interleukin-4, release were decreased and t hat splenic macrophage antigen presentation declined after hemorrhage. However, animals in which a portacaval shunt had been established bef ore hemorrhage showed no such changes in their splenocyte or splenic m acrophage functions. Thus, the decline of splenic immune responses aft er hemorrhage seems to be due to mediators released from the gut. Such mediators, in turn, stimulate Kupffer cells to secrete additional age nts that produce immunosuppressive exocrine effects on splenic immune functions.