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Hemodynamic and vasoactive mediator response to experimental respiratory failure.


We determined the changes in hemodynamics and circulating concentrations of endogenous vasoactive mediators during acute respiratory failure in chronically catheterized unanesthetized sheep. Inhalation of a hypercarbic-hypoxic gas mixture for 2 h (pHa = 7.16, PaCO2 = 84 Torr, PaO2 = 48 Torr, n = 5) resulted in a doubling of cardiac output (thermodilution) and systemic and pulmonary hypertension. Systemic vascular resistance decreased, whereas pulmonary vascular resistance gradually increased throughout the 2-h experimental gas period. Pulmonary hypertension persisted for 45 min after return to room air breathing. Plasma renin activity tripled, and circulating bradykinin concentration increased 25-fold (radioimmunoassay). Plasma norepinephrine and epinephrine concentrations (radioenzymatic assay) dramatically increased with respective initial values (15 min) of 23.9 +/- 9.5 (SE) and 26.7 +/- 13.3 ng/ml (base line less than 0.2). Inhalation of hypoxic (n = 4) or hypercarbic-enriched O2 (n = 7) gas mixtures did not produce similar findings. We concluded that the hemodynamic response to experimental respiratory failure results from the combination of hypercarbic acidosis and hypoxia. These changes were mediated in part by increased sympathoadrenal activity and altered concentrations of H+, O2, and endogenous vasoactive mediators.

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