{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,4]],"date-time":"2026-02-04T15:19:58Z","timestamp":1770218398165,"version":"3.49.0"},"reference-count":74,"publisher":"European Respiratory Society (ERS)","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur Respir J"],"accepted":{"date-parts":[[2004,12,27]]},"published-print":{"date-parts":[[2005,5]]},"abstract":"<jats:p>Platelet-activating factor (PAF) is a pro-inflammatory lipid mediator that increases vascular permeability by simultaneous activation of two pathways, one dependent on the cyclooxygenase metabolite prostaglandin E<jats:sub>2<\/jats:sub>and the other on the sphingomyelinase metabolite ceramide. The hypothesis that part of the PAF-induced oedema is mediated<jats:italic>via<\/jats:italic>the inositol 1,4,5-trisphosphate (IP<jats:sub>3<\/jats:sub>) pathway or Rho kinase pathway was investigated.<\/jats:p><jats:p>Oedema formation was induced in isolated perfused rat lungs by injection of 5\u2005nmol PAF into the pulmonary artery. Lungs were pre-treated with specific inhibitors: edelfosine (L108) to block phosphatidyl-inositol-specific phospholipase C, xestospongin to block the IP<jats:sub>3<\/jats:sub>receptor, 5-iodonaphthalene-1-sulphonyl-homopiperazine (ML-7) to block myosin light chain kinase, and (+)-<jats:italic>R<\/jats:italic>-trans-4-(aminoethyl)-<jats:italic>N<\/jats:italic>-(4-pyridyl)cyclohexanecarboxamide (Y27632) to block Rho-associated protein kinase.<\/jats:p><jats:p>Pre-treatment with L108 or xestospongin reduced PAF-induced oedema formation by 58 and 56%, respectively. The effect of L108 was additive to that of the cyclooxygenase inhibitor acetyl salicylic acid (88% oedema reduction). PAF-induced oedema formation was also reduced if extracellular calcium concentrations were lowered. Furthermore, treatment with ML-7 reduced oedema formation by 54%, whereas Y27632 was without effect.<\/jats:p><jats:p>It is concluded that platelet-activating-factor-triggered oedema is mediated by activation of the inositol 1,4,5-trisphosphate pathway, influx of extracellular calcium and subsequent activation of a myosin light chain kinase-dependent and Rho-associated-protein-kinase-independent mechanism.<\/jats:p>","DOI":"10.1183\/09031936.05.00069804","type":"journal-article","created":{"date-parts":[[2005,4,29]],"date-time":"2005-04-29T17:38:11Z","timestamp":1114796291000},"page":"849-857","source":"Crossref","is-referenced-by-count":27,"title":["The inositol trisphosphate pathway mediates platelet-activating-factor-induced pulmonary oedema"],"prefix":"10.1183","volume":"25","author":[{"given":"R.","family":"G\u00f6ggel","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S.","family":"Uhlig","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"81","published-online":{"date-parts":[[2005,5,1]]},"reference":[{"key":"2024101811155867000_25.5.849.1","doi-asserted-by":"crossref","unstructured":"Hosford D, Koltai M, Paubert-Braquet M, Braquet P. 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