Abstract

Administration of catechol amines together with endotoxin to normal rabbits results in a greater degree of inflammation and necrosis of cardiac muscle than is produced by either agent alone. The damage is prevented or markedly reduced by pretreatment with dibenamine. It can be produced by endotoxin in shocked animals without the catechol amines, presumably because the amines are already present in high concentration. Although the data obtained do not demonstrate that a specific cardiac lesion attributable to endotoxin is a key factor in development of irreversibility to transfusion in hemorrhagic shock, they are not inconsistent with such a hypothesis.

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