Platelet activating factor (PAF-acether) is released into rat pulmonary alveolar fluid as a consequence of hypoxia | Research - Institut Pasteur

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Evolution of aspartyl proteases by gene duplication: the mouse renin gene is organized in two homologous clusters of four exons

Study of the conidial development and cleistothecium-like structure of some strains of Fonsecaea pedrosoi. Comparison with other close Dematiaeae

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Published in Biochemical and biophysical research communications - 29 Feb 1984

Prevost MC, Cariven C, Simon MF, Chap H, Douste-Blazy L

Link to Pubmed [PMID] – 6422938

Biochem. Biophys. Res. Commun. 1984 Feb;119(1):58-63

Hypoxia provokes pulmonary constriction and because PAF-acether is a very strong pulmonary constrictor, we looked for PAF-acether in lung alveolar lavage (LAL) with a biological method based on the measurement of rabbit platelet aggregation. We first demonstrated a PAF-acether secretion during bronchoalveolar lavage with sterile isotonic NaCl (pH 7.2). PAF-acether secretion was completely suppressed with isotonic NaCl containing 5 mM EDTA but lyso-PAF-acether was still present (1.9 +/- 0.55 nmoles). Upon hypobaric hypoxia, PAF-acether was detected in LAL (1.05 +/- 0.25 10(-2)nmoles). The amount of lyso-PAF-acether increased by 6 times (12.1 +/- 4.1 nmoles). These results are given for 10(4) nmoles phospholipids of LAL. They indicate that alveolar macrophages might be activated by hypobaric hypoxia, so they produce PAF-acether in the alveole. Such a process could be involved in the well-known bronchoconstriction accompanying hypoxia.

Published on: 29 Feb 1984