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Modification by steroids of pulmonary oedema and prostaglandin E 2 pharmacokinetics induced by endotoxin in rats
Author(s) -
Izumi T.,
Bakhle Y.S.
Publication year - 1988
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.1476-5381.1988.tb11485.x
Subject(s) - methylprednisolone , pharmacokinetics , prostaglandin e2 , lung , corticosteroid , sepsis , prostaglandin , medicine , budesonide , pharmacology , prostaglandin e , anesthesia , endocrinology
1 A single i.p. injection of bacterial endotoxin in rats (3.5 mg kg −1 ) caused lung injury assessed as changes in lung dry: wet weight ratio and leukopaenia over the subsequent 28 h. 2 This treatment also slowed the efflux of 14 C from [ 14 C]‐prostaglandin E 2 (PGE 2 ), i.e., increased t 1/2 and increased the survival of PGE 2 in isolated perfused lungs over the same period. 3 These effects of endotoxin were reversed by methylprednisolone (30 mg kg −1 ), given 30 min after the endotoxin. 4 Another synthetic corticosteroid, budesonide (1.2 mg kg −1 ) given 1 h before endotoxin partially prevented the lung injury and leukopaenia but did not affect the increased t 1/2 for PGE 2 nor its survival. 5 The reversal by methylprednisolone of both the physical signs of lung injury and the changes in PGE 2 pharmacokinetics caused by endotoxin suggests that changes in PGE 2 pharmacokinetics could serve as an index of acute lung injury following sepsis.