Prostaglandins and thromboxane in the delayed phase of shock induced by Serratia marcescens endotoxin

J. R. Parratt, N. Sharma, I. J. Zeitlin

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Abstract

The cardiovascular and metabolic effects of an endotoxin derived from Serratia marcescens were examined in anaesthetized, spontaneously‐breathing cats. There was a marked initial elevation of right atrial pressure (the result of pulmonary vasoconstriction) and decreases in systemic arterial pressure and in arterial PO2. The ‘delayed’ effects of endotoxin shock in this species (1–8 h) consisted of a reduced cardiac output and decreased urinary excretion. Blood pressure and myocardial contractility (assessed from measurement of left ventricular (LV) dP/dt and LV end‐diastolic pressure) were maintained throughout this phase. There was evidence of a metabolic (lactic) acidosis largely compensated by hyperventilation. Plasma levels (both arterial and mixed venous blood samples) of prostaglandin (PG)E2, PGF, 6‐keto PGF and thromboxane (TX)B2 were measured by radioimmunoassay techniques. Endotoxin administration caused substantial increases in the plasma levels of all four derivatives of arachidonic acid, especially between 1 and 6 h. Separation of the endotoxin‐treated cats into survivors and non‐survivors showed that the non‐survivors had significantly higher circulating levels of PGE2, TXB2 and PGF. It is suggested that TXB2 and PGF might contribute to some of the detrimental effects of endotoxin (e.g. pulmonary, mesenteric, renal vasoconstriction; platelet aggregation with resulting organ failure) and that prostacyclin may be beneficial in endotoxin shock in this species. 1984 British Pharmacological Society

Original languageEnglish
Pages (from-to)281-288
Number of pages8
JournalBritish journal of pharmacology
Volume82
Issue number1
DOIs
Publication statusPublished - May 1984

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ASJC Scopus subject areas

  • Pharmacology

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