Modulation of pulmonary inflammation after endotoxin inhalation with a platelet-activating factor antagonist (48740 RP).
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.
Rylander
R
R
Department of Environmental Hygiene, University of Göteborg, Sweden.
Beijer
L
L
Lantz
R C
RC
Burrell
R
R
Sedivy
P
P
D000280:Administration, Inhalation; D000818:Animals; D002199:Capillary Permeability / Q000187:drug effects; D006224:Cricetinae; D004730:Endothelium, Vascular / Q000502:physiology; D004731:Endotoxins / Q000008:administration & dosage*; D005260:Female; D006168:Guinea Pigs; D008297:Male; D010972:Platelet Activating Factor / Q000037:antagonists & inhibitors*; D011014:Pneumonia / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D011725:Pyridines / Q000494:pharmacology*; D013844:Thiazoles / Q000494:pharmacology*
D004731:Endotoxins; D010972:Platelet Activating Factor; D011725:Pyridines; D013844:Thiazoles; C052520:3-(3-pyridinyl)-1H,3H-pyrrolo(1,2-c)thiazole-7-carboxamide