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Glucocorticoid protection against PAF‐acether toxicity in mice
Author(s) -
Myers Adam,
Ramey Estelle,
Ramwell Peter
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.tb11034.x
Subject(s) - platelet activating factor , verapamil , nifedipine , toxicity , pharmacology , in vivo , glucocorticoid , mechanism of action , chemistry , endocrinology , medicine , extracellular , calcium , biology , in vitro , biochemistry , microbiology and biotechnology
1 Intravenous platelet activating factor (PAF‐acether, 10 to 25 μg/kg body weight) produced dose‐dependent mortality in both male and female mice. 2 Pretreatment with indomethacin (50 mg/kg), verapamil (40 mg/kg) or nifedipine (4 mg/kg) failed to inhibit the lethal effect of 20 μg/kg PAF‐acether. This suggests that neither arachidonate cyclo‐oxygenase products nor availability of extracellular Ca 2+ mediate the toxic action. 3 In contrast, pretreatment with 100 mg/kg cortisone acetate (s.c.) daily for four days exerted a highly protective effect, i.e. 100% and 93% survival in males and females, compared to 13% and 7% respectively, in untreated animals. 4 PAF‐acether‐induced death may be a useful model for the in vivo evaluation of pharmacological agents in anaphylactic shock.