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Am J Physiol Heart Circ Physiol 284: H535-H541, 2003. First published October 10, 2002; doi:10.1152/ajpheart.00311.2002
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Vol. 284, Issue 2, H535-H541, February 2003

Superoxide mediates endotoxin-induced platelet-endothelial cell adhesion in intestinal venules

Wolfgang H. Cerwinka1, Dianne Cooper1, Christian F. Krieglstein1,4, Chris R. Ross2, Joe M. McCord3, and D. Neil Granger1

1 Department of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, Louisiana 71130-3932; 2 Department of Anatomy and Physiology, College of Veterinary Medicine, Kansas State University, Manhattan, Kansas 66506-5612; 3 Webb-Waring Institute, University of Colorado Health Sciences Center, Denver, Colorado 80262; and 4 Department of General Surgery, Westphalian Wilhelms University, D48149 Muenster, Germany

Platelets have been implicated in the pathogenesis of different diseases of the vascular system, including atherosclerosis, sepsis, and ischemia-reperfusion injury; however, relatively little is known about the factors that regulate the interactions between circulating platelets and the vessel wall. The objective of this study was to define the contribution of superoxide to LPS-induced platelet-endothelial cell (P/E) adhesion in murine intestinal venules. The adhesion of rhodamine-6G-labeled murine platelets was monitored by intravital fluorescence microscopy. Four hours after LPS administration in control [wild-type (WT)] mice, an ~10-fold increase in P/E adhesion was detected. This response did not result from LPS-induced platelet activation. The LPS-induced P/E adhesion was greatly attenuated in NAD(P)H oxidase-deficient mice and in WT mice rendered neutropenic with anti-neutrophil serum, whereas the response was unchanged in WT mice receiving a CD18 blocking MAb or in CD18-deficient mice. A chimeric form of MnSOD that exhibits the binding properties of extracellular SOD also attenuated the LPS-induced response in WT mice. These findings indicate that neutrophil-derived superoxide plays a major role in the modulation of endotoxin-induced P/E adhesion.

endotoxemia; neutrophils; postcapillary venules


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