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The release of prostanoids during the acute pulmonary response to E. coli endotoxin in anaesthetized cats
Author(s) -
Coker Susan J.,
Hughes Bernadette,
Parratt J.R.,
Rodger I.W.,
Zeitlin I.J.
Publication year - 1983
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1983.tb08816.x
Subject(s) - pulmonary artery , thromboxane , medicine , thromboxane b2 , cats , pulmonary hypertension , radioimmunoassay , prostacyclin , prostaglandin , shock (circulatory) , thromboxane a2 , endocrinology , anesthesia , platelet
1 The administration of E. coli endotoxin (2 mg/kg i.v.) to anaesthetized cats results in a characteristic acute pulmonary response. This consists of increases in pulmonary artery pressure and airways resistance and a reduction in lung compliance. 2 Plasma concentrations of prostaglandin E 2 (PGE 2 ), PGF 2α , thromboxane B 2 and 6‐keto PGF 1α were measured by radioimmunoassay in aortic and pulmonary arterial blood samples before, during and after the acute pulmonary response to endotoxin. 3 Endotoxin administration resulted in the rapid release of PGF 2α and thromboxane B 2 from the lungs. The time course of this release was parallel to that of the pulmonary hypertensive and airways responses to endotoxin. PGE 2 and 6‐keto PGF 1α were released more gradually and with greater variations between individual animals. 4 During the delayed shock phase (2 h after endotoxin) the concentrations of PGE 2 , PGF 2α and 6‐keto PGF 1α were once again elevated in both the aorta and pulmonary artery. Thromboxane B 2 concentrations were not increased at this time. 5 These results suggest that PGF 2α and thromboxane A 2 may be mediators of the acute pulmonary responses to endotoxin.