Intestinal stasis followed by mucosal barrier breakdown and the generation
of locally produced cytokines has been proposed as the cause of systemic in
fection and multiple organ failure following hemorrhagic shock. The aim of
this study was to investigate the underlying mechanisms of impaired intesti
nal muscle function leading to ileus following hemorrhagic shock. Rats were
subjected to severe hemorrhagic shock (mean arterial pressure 40 mm Hg) fo
llowed by resuscitation and were killed early at 4 h or late at 24 h. Other
groups consisted of control and sham animals. Intercellular adhesion molec
ule (ICAM-1) mRNA levels were significantly elevated in the muscularis but
not in the mucosa using the semiquantitative reverse transcriptase polymera
se chain reaction (RT-PCR). There was a marked infiltration of neutrophils
into the muscularis early and late after shock. Furthermore, smooth muscle
contractility in response to bethanechol was significantly decreased, being
more pronounced in the early group. Immunohistochemistry revealed signal f
or ICAM-1 in the muscularis microvasculature and on infiltrating cells. The
se results suggest that the expression of ICAM-1 within the muscularis vasc
ulature after hemorrhagic shock promotes the local recruitment of leukocyte
s and that this inflammatory response is accompanied by a subsequent impair
ment of intestinal contractility.