[Study of acute gastric mucosal lesion induced by endotoxemia].
Acute gastric mucosal lesion (AGML) was induced six hours after the administration of endotoxin. The decrease of gastric mucosal blood flow, used to be supposed as an important factor of the formation of AGML, was not found, but thiobarbituric acid (TBA) reactants in the gastric mucosa were increased three hours after endotoxin injection, 198 +/- 18.2 (vs control 130 +/- 18.2). The administration of platelet activating factor (PAF) inhibitor, CV3988, reduced the formation of AGML and increase of the TBA reactants. These results suggested that the chemical mediator like PAF and free radicals may play an important role in the pathogenesis of gastric mucosal injury induced by endotoxemia, without the decrease of mucosal blood flow.
Maeda
Y
Y
First Department of Surgery, Yamanashi Medical College.
D000818:Animals; D004731:Endotoxins / Q000097:blood*; D004926:Escherichia coli; D005609:Free Radicals; D005753:Gastric Mucosa / Q000378:metabolism / Q000473:pathology*; D008297:Male; D010972:Platelet Activating Factor / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D013858:Thiobarbiturates / Q000378:metabolism; D014115:Toxemia / Q000378:metabolism / Q000473:pathology*
D004731:Endotoxins; D005609:Free Radicals; D010972:Platelet Activating Factor; D013858:Thiobarbiturates; C029684:thiobarbituric acid