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Articles in PresS, published online ahead of print October 10, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00311.2002
Submitted on April 8, 2002
Accepted on October 3, 2002
1 Department of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, LA, USA
2 Department of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, LA, USA; Department of General Surgery, Westphalian Wilhelms-University, Muenster, Germany
3 Department of Anatomy and Physiology, Kansas State University, College of Veterinary Medicine, Manhattan, KS, USA
4 Department of Webb-Waring Institute, University of Colorado Health Sciences Center, Denver, CO, USA
* To whom correspondence should be addressed. E-mail: dgrang{at}lsuhsc.edu.
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 lipopolysaccharide (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, about a 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, while the response was unchanged in WT mice receiving a CD18 blocking monoclonal antibody or in CD18-deficient mice. A chimeric form of manganese superoxide dismutase (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.
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