Hemorrhagic shock results in intestinal muscularis intercellular adhesion molecule (ICAM-1) expression, neutrophil infiltration, and smooth muscle dysfunction

Abstract

Intestinal stasis followed by mucosal barrier breakdown and the generation of locally produced cytokines has been proposed as the cause of systemic infection and multiple organ failure following hemorrhagic shock. The aim of this study was to investigate the underlying mechanisms of impaired intestinal muscle function leading to ileus following hemorrhagic shock. Rats were subjected to severe hemorrhagic shock (mean arterial pressure 40 mm Hg) followed by resuscitation and were killed early at 4 h or late at 24 h. Other groups consisted of control and sham animals. Intercellular adhesion molecule (ICAM-1) mRNA levels were significantly elevated in the muscularis but not in the mucosa using the semiquantitative reverse transcriptase polymerase 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 for ICAM-1 in the muscularis microvasculature and on infiltrating cells. These results suggest that the expression of ICAM-1 within the muscularis vasculature after hemorrhagic shock promotes the local recruitment of leukocytes and that this inflammatory response is accompanied by a subsequent impairment of intestinal contractility.

Influence of Immunosuppression on Alloresponse, Inflammation and Contractile Function of Graft After Intestinal Transplantation

“…This is consistent with our previous reports (12,23) (25) and graft-infiltrating macrophages are one of the main players of rejection reaction (26). ICAM-1 is also involved in leukocyte extravasation in intestinal muscularis (27) and acute rejection (28,29 Intestinal macrophages in muscularis propria contribute to postoperative ileus and dysmotility of graft after SBTx through the release of NO from iNOS and prostanoid synthesis (10,14). As shown in Figures 5G and H (31,32) and impairment of ICC is suggested to be involved in the dysmotility of the intestine in some clinical settings (33)(34)(35).…”

Colonic Postoperative Inflammatory Ileus in the Rat

“…It has previously been shown that the initiation of leukocyte recruitment in the small intestinal muscularis after manipulation or hemorrhagic shock is mediated through the expression of adhesion molecules, such as ICAM-1. 10,22 In addition, we recently showed that lipopolysaccharide induces monocyte extravasation in the small intestinal muscularis through the expression of macrophage-derived MCP-1. 21 Quantification of the postoperative mRNA expression for both mediators revealed a distinct upregulation, thus providing evidence for the importance of both ICAM-1 and MCP-1 as important mediators controlling the targeted transmigration of immunocompetent cells into the intestinal muscularis after surgical manipulation.…”

Acute intestinal pseudo-obstruction

“…Disturbances of the hypothalamic-pituitary axis have also been invoked in some contexts [50]. Recently, Bauer et al [51][52][53] have suggested an important contribution for peripheral events in the pathogenesis of motor dysfunction in response to surgery and shock. They noted a significant relationship between the local inflammatory response, neutrophil infiltration and smooth-muscle dysfunction.…”