Role of polymorphonuclear leukocytes and oxygen-derived free radicals in the formation of gastric mucosal lesions induced by platelet-activating factor

• Published in: Nippon Shōkakibyō Gakkai zasshi Vol. 86; no. 4; p. 858
• Main Authors: Yoshikawa, T, Yoshida, N, Yasuda, M, Ichikawa, H, Takano, H, Takahashi, S, Tazaki, N, Ando, T, Naito, Y, Ueda, S
• Format: Journal Article
• Language: Japanese
• Published: Japan 1989
• Subjects: Animals; Free Radicals; Gastric Mucosa - blood supply; Gastric Mucosa - drug effects; Gastric Mucosa - pathology; Male; Neutrophils - metabolism; Platelet Activating Factor - physiology; Rats; Regional Blood Flow; Superoxides - metabolism; Superoxides - toxicity
• ISSN: 0446-6586
• DOI: 10.11405/nisshoshi1964.86.858

Gastric hemorrhagic erosions were induced by the administration of platelet-activating factor (PAF). Gastric wall blood flow was decreased and thiobarbituric acid (TBA) reactants in the gastric mucosa were increased 10 min after PAF injection. SOD and catalase reduced gastric mucosal lesions and TBA reactants, but had no influence on gastric blood flow. In polymorphonuclear leukocytes (PMN)-depleted rats, gastric mucosal lesions and TBA reactants in the gastric mucosa were reduced and gastric blood flow were increased. PAF induced the superoxide production from rat PMN in a dose dependent manner. These results suggest that oxygen-derived free radicals produced by PMN and lipid peroxidation may play an important role in the pathogenesis of gastric mucosal injury induced by PAF.