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This article is part of the supplement: 18th International Symposium on Intensive Care and Emergency Medicine

Meeting abstract

Antibodies to ICAM-1 and PECAM-1 ameliorate pulmonary injury after intestinal ischemia-reperfusion in the rat

A Börjesson, XD Wang and R Andersson

Department of Surgery, Lund University Hospital, 221 85 Lund, Sweden

from 18th International Symposium on Intensive Care and Emergency Medicine
Brussels, Belgium. 17–20 March 1998

Critical Care 1998, 2(Suppl 1):P011doi:10.1186/cc141

Published: 1 March 1998

© 1998 Current Science Ltd

Full text

Intestinal ischemia-reperfusion (I/R) gives rise to acute lung injury characterized by neutrophil sequestration and microvascular injury. Important mediators of I/R-associated injury include neutrophils and platelet-activating factor (PAF). During conditions of inflammation neutrophils and endothelial cells show an increased expression of adhesion molecules. ICAM-1 on endothelial cells is needed for high affinity bonds between neutrophils and endothelial cells, necessary for the further transmigration of neutrophils, where PECAM-1 is involved.

In the present study, a significant increase in albumin leakage over the pulmonary capillaries, as well as increased pulmonary MPO (myeloperoxidase)-content was found in rats subjected to 30 min intestinal ischemia (by clamping the superior mesenteric artery) followed by 12 h reperfusion. Treatment with anti-ICAM-1 or anti-PECAM-1 monoclonal antibodies significantly reduced the otherwise occuring increase in both albumin leakage and pulmonary MPO-content in pancreatitis animals. There was also an increase in serum IL-1β levels after intestinal I/R, which could be prevented by use of antibodies to ICAM-1 and PECAM-1.

In conclusion we found that the acute lung injury seen after intestinal I/R in the rat to a large extent could be prevented by blocking the adhesion/transmigration process of pulmonary leukocytes.

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