Septic shock: hemodynamics of endotoxin and inflammation

Observations were made in 53 mongrel dogs, in which a nonseptic inflammatory lesion was induced by intramuscular injection of 10% calcium chloride into 1 thigh, to evaluate the relationship between bacterial endotoxin and the active hyperemia of inflammation. 4 days after lesion induction, the inflammatory lesion was associated with an increase in blood flow (91% greater than in normal limb) and a corresponding reduction in vascular resistance in the limb. The arteriovenous oxygen difference was decreased, and the calculated oxygen consumption was 26% greater than that in the normal limb. E. coli endotoxin administration (.2 mg/kg) was associated with a marked reduction in blood flow and increased vascular resistance in both inflamed and normal limbs. Prior administration of methylprednisolone (30 mg/kg) or phenoxybenzamine (1 mg/kg) did not greatly alter these changes. Expansion of the circulating blood volume with dextran -70 solution was followed by a marked increase in flow and reduction in vascular resistance in the normal and inflamed limbs. Therefore, the active hyperemia of inflammation may add significantly to demands on circulation. The hyperdynamic state is reduced after administration of endotoxin and returns when the circulating blood volume is increased above normal by the infusion of dextran. A discussion by a panel follows the article.