Pulmonary Vascular Resistance and Right Ventricular Function in Canine Endotoxin Shock

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Abstract
The pulmonary vascular resistance in herbivores was reported to increase 3-fold in endotoxin shock; poor cardiac output was attributed to cor pulmonale. The poor cardiac output in dogs was attributed to splanchnic pooling. It was previously reported that splanchnic pooling was brief and had resolved, while cardiac output remained low. In the present study of 27 anesthetized dogs, a marked reduction in cardiac output and aortic pressure following endotoxin, and an increase in systemic resistance to only 125% was found. Pulmonary arterial resistance rose to a peak of 450% of normal at 5 min, but by 30 min fell to 200% of control. The relative contractility of the 2 ventricles, based on Vmax was equal to or greater than control for most of the 4 h. Although the afterload for the right ventricle is actually increased, in contrast to a reduction for the left ventricle, contractility for both ventricules was maintained. Treatment with Dextran transiently restored cardiac output, but caused a significant gradual reduction in arterial PO2 as a result of extravasation.

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