A Novel Role of Gastric PGI2 in Gastric Cytoprotection

• Published in: Nihon Kyukyu Igakukai Zasshi 1998/04/15, Vol.9(4), pp.125-133
• Main Authors: Harada, Naoaki, Okajima, Kenji, Murakami, Kazunori, Isobe, Hirotaka, Tanaka, Keiichi, Okabe, Hiroaki
• Format: Article
• Language: English
• Subjects: gastric mucosal blood flow; gastric mucosal lesion; gastric prostacyclin (PGI2); leukocyte; water-immersion restraint
• ISSN: 0915-924X; 1883-3772
• DOI: 10.3893/jjaam.9.125

We investigated the role of gastric prostacyclin (PGI2) in water-immersion restraint stress-induced gastric mucosal injury in rats. Gastric 6-keto-PGF1α levels were increased after 30min of stress, followed by a decrease to below baseline after 6 to 8h of stress. Gastric mucosal blood flow (GMBF) was decreased with time after stress. Gastric myeloperoxidase (MPO) activity was significantly increased after 8h of stress. Pretreatment of the animals with indomethacin (IM) prevented the increase in the gastric level of 6-keto-PGF1α and markedly reduced the GMBF in animals subjected to stress. IM pretreatment markedly increased gastric MPO activity and exacerbated gastric mucosal injury in animals subjected to stress. Iloprost, a stable analog of PGI2, inhibited these IM-induced changes in stressed rats. Although nitrogen mustard-induced leukocytopenia inhibited both exacerbation of gastric mucosal injury and the increase in the gastric accumulation of leukocytes induced by IM in stressed animals, the IM-induced decrease in GMBF was not prevented in leukocytopenic animals. These observations strongly suggest that gastric PGI2 plays an important role in preventing formation of gastric mucosal lesions not only by maintaining the gastric mucosal blood flow, but by inhibiting the gastric accumulation of leukocytes.