Modulation of pulmonary inflammation after endotoxin inhalation with a platelet-activating factor antagonist (48740 RP)

Ragnar Rylander; Lena Beijer; R. Clark Lantz; Robert Burrel; Pierrey Sediv

doi:10.1159/000234588

Modulation of pulmonary inflammation after endotoxin inhalation with a platelet-activating factor antagonist (48740 RP)

Ragnar Rylander, Lena Beijer, R. Clark Lantz, Robert Burrel, Pierrey Sediv

Cellular and Molecular Medicine

Research output: Contribution to journal › Article › peer-review

26 Scopus citations

Abstract

An acute pulmonary response was induced in guinea pigs and hamsters by inhalation of bacterial endotoxin in the form of a purified lipopolysaccharide (LPS). Pretreatment with the platelet-activating factor (PAF) antagonist, 48740 RP, inhibited damage to endothelial cells, decreased vascular permeability and the number of neutrophils in the airways 24 h after exposure to LPS. The increase in the number of platelets in the airways caused by endotoxin was not affected. The results suggest that PAF modulates early inflammation after endotoxin inhalation.

Original language	English (US)
Pages (from-to)	303-307
Number of pages	5
Journal	International Archives of Allergy and Immunology
Volume	86
Issue number	3
DOIs	https://doi.org/10.1159/000234588
State	Published - 1988

ASJC Scopus subject areas

Immunology and Allergy
Immunology

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abstract = "An acute pulmonary response was induced in guinea pigs and hamsters by inhalation of bacterial endotoxin in the form of a purified lipopolysaccharide (LPS). Pretreatment with the platelet-activating factor (PAF) antagonist, 48740 RP, inhibited damage to endothelial cells, decreased vascular permeability and the number of neutrophils in the airways 24 h after exposure to LPS. The increase in the number of platelets in the airways caused by endotoxin was not affected. The results suggest that PAF modulates early inflammation after endotoxin inhalation.",

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AU - Sediv, Pierrey

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AB - An acute pulmonary response was induced in guinea pigs and hamsters by inhalation of bacterial endotoxin in the form of a purified lipopolysaccharide (LPS). Pretreatment with the platelet-activating factor (PAF) antagonist, 48740 RP, inhibited damage to endothelial cells, decreased vascular permeability and the number of neutrophils in the airways 24 h after exposure to LPS. The increase in the number of platelets in the airways caused by endotoxin was not affected. The results suggest that PAF modulates early inflammation after endotoxin inhalation.

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Modulation of pulmonary inflammation after endotoxin inhalation with a platelet-activating factor antagonist (48740 RP)

Abstract

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