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pubmed-article:9142146pubmed:abstractTextWe have shown that therapy directed at polymorphonuclear neutrophil (PMN) CD18 receptors attenuates sequelae associated with a post-trauma endotoxin (lipopolysaccharide [LPS]) challenge. Platelet activating factor (PAF) stimulates PMNs by CD18-independent pathways, and WEB-2086, a PAF receptor antagonist, blunts septic symptoms in many experimental models. This study tested the hypothesis that the blockade of non-CD18 dependent PMN adherence attenuates trauma- and LPS-evoked pulmonary dysfunction.lld:pubmed
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pubmed-article:9142146pubmed:articleTitleUnexpected action of platelet activating factor antagonism after fluid resuscitation from traumatic shock.lld:pubmed
pubmed-article:9142146pubmed:affiliationDepartment of Surgery (Trauma Division), University of Tennessee Health Science Center, Memphis, USA.lld:pubmed
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