DEPRESSED SPLENIC FUNCTION AFTER HEMORRHAGE RESULTS FROM GASTROINTESTINAL-TRACT STIMULATION OF HEPATIC-MEDIATOR RELEASE - CORRECTION WITH PORTACAVAL-SHUNT
A. Ayala et al., DEPRESSED SPLENIC FUNCTION AFTER HEMORRHAGE RESULTS FROM GASTROINTESTINAL-TRACT STIMULATION OF HEPATIC-MEDIATOR RELEASE - CORRECTION WITH PORTACAVAL-SHUNT, Archives of surgery, 131(11), 1996, pp. 1209-1214
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.