THE POSSIBLE ROLES OF HISTAMINE, 5‐HYDROXYTRYPTAMINE AND PROSTAGLANDIN F AS MEDIATORS OF THE ACUTE PULMONARY EFFECTS OF ENDOTOXIN

J. R. PARRATT, R. M. STURGESS

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Abstract

In an attempt to investigate the possible role of released vasoactive substances in mediating the pulmonary pressor responses to E. coli endotoxin, cats were pretreated with histamine, 5‐hydroxytryptamine (5‐HT) or prostaglandin antagonists, with a histamine depleting agent (compound 48/80) or with an inhibitor of prostaglandin synthetase (sodium meclofenamate). The administration of endotoxin (2 mg/kg) resulted in a rapidly developing pulmonary hypertension (pressure twice normal after 2–3 min), increases in right atrial and intratracheal pressures, systemic hypotension and bradycardia. These effects were unaffected by methysergide in a dose sufficient to prevent the effects of intravenously administered 5‐HT. Endotoxin responses were also unaffected by a combination of mepyramine and burimamide in doses sufficient to reduce markedly the effects of intravenously‐administered histamine. In cats pretreated (chronically or acutely) with compound 48/80, endotoxin induced a transient pulmonary pressor response which was not maintained. The pulmonary and systemic responses to endotoxin were prevented by the prior administration of the prostaglandin antagonist, polyphloretin phosphate and by pretreatment with the prostaglandin synthetase inhibitor, sodium meclofenamate. It is concluded that a pulmonary vasoconstrictor prostaglandin is involved in the acute response to endotoxin in the cat. 1977 British Pharmacological Society

Original languageEnglish
Pages (from-to)209-219
Number of pages11
JournalBritish journal of pharmacology
Volume60
Issue number2
DOIs
Publication statusPublished - Jun 1977

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ASJC Scopus subject areas

  • Pharmacology

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