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- W2015459038 abstract "The mechanisms by which endothelin-1 (ET-1) modulate mucosal permeability were investigated by monitoring the blood-to-lumen clearance of 51Cr-ethylenediaminetetraacetic acid (51Cr-EDTA) in the rat small intestine. Different concentrations of ET-1 (100, 200, and 400 pmol/kg) were infused into the superior mesenteric artery for 10 min and mucosal permeability was monitored by measuring the 5ZCr-EDTA clearance for 60 min. Polymorphonuclear leukocyte (PMN) infiltration was monitored by measuring tissue myeloperoxidase (MPO) activities in intestinal samples. ET-I increased mucosal permeability in a dose-dependent fashion, with significant elevations in mucosal permeability were observed at a dose of 400 pmol/kg/min, A monoclonal antibody (mAb) directed against ICAM-I (MAb 1A29, 2mg/kg iv), anti-neutrophil serum (ANS; three intraperitoneal injections at 12 h intervals) and a platelet activating factor (PAF) antagonist (WEB2086, 10 mg/kg, iv) were each effective in attenuating the mucosal barrier dysfunction induced by ET-1. ET-1 administration also elevated tissue MPO activity, which was reduced by pretreatment with either the ICAM-1 mAb or ANS, but not by WEB2086. Overall, these findings suggest that the increased mucosal permeability elicited by ET-1 in the rat small intestine involves a mechanism that involves PAF and includes ICAM-I mediated adhesion of neutrophils to vascular endothelial ceils. Supported by TW00755 and HL26441." @default.
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- W2015459038 date "1998-04-01" @default.
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- W2015459038 title "Mechanisms of endothelin-1 induced mucosal dysfunction in the rat small intestine: Role of leukocytes" @default.
- W2015459038 doi "https://doi.org/10.1016/s0016-5085(98)81555-2" @default.
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