Depressed splenic function after hemorrhage results from gastrointestinal tract stimulation of hepatic-mediator release. Correction with portacaval shunt
A. Ayala, Y. Tu, M. W. Flye and I. H. Chaudry
Department of Surgery, Michigan State University, East Lansing, USA.
OBJECTIVE: To determine whether redirecting intestinal blood flow away from
the liver via a portacaval shunt would protect distal immune responses in
the spleen after hemorrhage. DESIGN: Type C3H/HeN male mice in which a
portacaval shunt had been established 2 to 3 weeks before the experiment
were bled, their blood pressure was maintained at 35 mm Hg for 1 hour, and
then they were resuscitated. Twenty-four hours later, the mice were killed,
and mixed and adherent splenocyte cultures were established. The
proliferative capacity of splenocytes, the release of interleukin-2 and
interleukin-4, and the ability of splenic macrophages to present the
antigen, conalbumin, were then determined as indexes of immunocompetence.
RESULTS AND CONCLUSIONS: The results indicate that splenocyte proliferation
and splenocyte interleukin-2, but not interleukin-4, release were decreased
and that splenic macrophage antigen presentation declined after hemorrhage.
However, animals in which a portacaval shunt had been established before
hemorrhage showed no such changes in their splenocyte or splenic macrophage
functions. Thus, the decline of splenic immune responses after hemorrhage
seems to be due to mediators released from the gut. Such mediators, in
turn, stimulate Kupffer cells to secrete additional agents that produce
immunosuppressive exocrine effects on splenic immune functions.
