| [ Summary ] |
It has been proposed that neutrophils play an important roleIn the pathogenesis of gastric mucosal injury induced by nonsteroidal anti-inflammatory drugs (NSAID). Superoxide dismutase and catalase pro-tect against NSAlD-induced gastric mucosal lesions through scavenging of active oxyen species and by inhibiting lipid peroxidation. In vivo studies have indi-cated that aspirin may increase surface expression of CDI11b/CD18 on neutrophils and may induce neutrophil adherence to endothelial cells followed by neutrophilmediated endothelialcellinjury. In vivo studies have demonstrated that aspirin and indomethacin also promote leukocyte rolling and adherence in rat mesenteric venules. Finally, rendering animals neutropenic or interfering with neutrophil adhesive interactions with the microvasculature largely prevents epithelial cell and microvascular injury after administration of NSAID. Together, these studies inclicate that aspirin and other NSAID produce gastritis by promoting neutrophil-endotheiial cell adhesive interaction that ultimately result in neutrophil-mediated tissue injury. |