Myocardial and circulatory effects of E. coli endotoxin; modification of responses to catecholamines

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The predominant acute effect of E. coli endotoxin in anaesthetized, ventilated cats was pulmonary hypertension resulting from a 8–12 fold increase in pulmonary vascular resistance. This was followed by decreases in left ventricular (LV) and systemic arterial pressures and in LV dP/dt max. Recovery occurred within 2–4 min and was dependent upon increased sympathetic drive; recovery did not occur in cats treated with the β‐adrenoceptor blocking drug alprenolol. The pulmonary vasoconstriction was reduced in cats given compound 48/80 and evidence is presented that it results primarily from histamine release. Over the 2–3 h period following endotoxin injection, systemic arterial pressure tended to decrease and heart rate and myocardial metabolic heat production to increase. Myocardial blood flow and LV dP/dt remained fairly stable until the terminal stages of shock. The predominant delayed effects of E. coli endotoxin in cats were a markedly reduced stroke volume, an increase in peripheral vascular resistance and a severe metabolic acidosis (arterial base excess—20 mEq/litre). Arterial pO2 and pCO2 were not significantly affected. It is concluded that myocardial contractility is maintained at this time through the release of catecholamines and that endotoxin itself depresses contractility. The effects of adrenaline and noradrenaline infusions on systolic and diastolic blood pressures, heart rate, cardiac output, myocardial blood flow and LV dP/dt max were markedly reduced in the period 2–3 h after endotoxin. In a few animals some recovery of the response to noradrenaline occurred and was associated with a general circulatory improvement and a reduced metabolic acidosis. 1973 British Pharmacological Society

Original languageEnglish
Pages (from-to)12-25
Number of pages14
JournalBritish journal of pharmacology
Issue number1
Publication statusPublished - Jan 1973


ASJC Scopus subject areas

  • Pharmacology

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