Lethal Endotoxin Shock

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Abstract
Recent studies by Crowel1and Smith1and Rush et al2have drawn attention to the significance of the oxygen deficit incurred during hemorrhagic shock. The results of these investigations support the concept of progressive stagnant hypoxia as the final pathway of irreversible hemorrhagic shock.3Endotoxin shock is thought to produce death in a similar fashion, ie, vasoactive substances are released which lead to venous pooling, decreased venous return, decreased cardiac output, and poor tissue perfusion. The latter results in stagnant hypoxia with eventual cellular death. The following experiments were undertaken to quantitate the hypoxia sustained during lethal endotoxin shock by measuring oxygen deficit and lactate production following the administration ofEscherichia coliendotoxin. The data reported in this paper were derived from animals that did not develop a pyrogenic response to the endotoxin. If shock was accompanied by fever, oxygen consumption rose, despite progressive deterioration terminating in

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