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FELINE ENDOTOXIN SHOCK: EFFECTS OF METHYLPREDNISOLONE ON KININOGEN‐DEPLETION, ON THE PULMONARY CIRCULATION AND ON SURVIVAL
Author(s) -
ALKAISI NAHLA,
PARRATT J.R.,
SIDDIQUI H.H.,
ZEITLIN I.J.
Publication year - 1977
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.1476-5381.1977.tb07524.x
Subject(s) - shock (circulatory) , methylprednisolone , medicine , kininogen , pharmacology , cardiology , chemistry , bradykinin , receptor
1 Escherichia coli endotoxin, administered intravenously in a dose of 2mg/kg to pentobarbitone‐anaesthetized, artificially ventilated cats resulted in pulmonary hypertension, systemic hypotension and an immediate (1‐2 min) 30‐40% reduction in plasma kininogen, an effect which probably indicates a release of plasma kinins. 2 Methylprednisolone (30 mg/kg), when administered 30 min before endotoxin, did not influence the endotoxin‐induced pulmonary hypertension or systemic hypotension but completely prevented the depletion of plasma kininogen. 3 In spontaneously breathing cats, methylprednisolone, administered 30 min after endotoxin, caused a rapid repletion of kininogen and prolonged survival (47% at 6 h compared to 10% in the endotoxinalone animals). Methylprednisolone did not appear to influence lactate production or the hyperventilation observed during the delayed endotoxin shock phase. 4 It is concluded that methylprednisolone does not prevent the release, by endotoxin, of a pulmonary vasoconstrictor prostaglandin, or its effects, but that perhaps by preventing kinin release it may reduce endotoxin‐induced capillary leakage.