Abstract
Summary
The pulmonary vascular resistance in herbivores has been reported to increase threefold in endotoxin shock; poor cardiac output has been attributed to cor pulmonale. The poor cardiac output in dogs has been attributed to splanchnic pooling. However, we previously reported that splanchnic pooling was brief, and had resolved, while cardiac output remained low. In the present study of 27 anesthetized dogs we found a marked reduction in cardiac output and aortic pressure following endotoxin, and an increase in systemic resistance to only 125%. Pulmonary arterial resistance rose to a peak of 450% of normal at 5 min, but by 30 min had fallen to 200% of control. The relative contractility of the two ventricles, based on Vmax was equal to or greater than control for most of the 4 hr. Although the afterload for the right ventricle is actually increased, in contrast to a reduction for the left ventricle, contractility for both ventricles 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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