The gravity of Gram-negative bacteremia has long been recognized,1,2 but it is only recently that the lethal effect of these organisms when present in the systemic circulation has been correlated with their ability to produce shock3. The ability to cause shock in man, as well as in a variety of laboratory animals, is apparently dependent upon a lipoprotein-carbohydrate complex, or endotoxin, which is liberated at death from the cell wall of the Gram-negative bacteria.4 While the mechanism by which endotoxin causes shock is not clear, there is increasing evidence that its faculty of causing profound vasospasm in the small blood vessels5,6 is intimately linked with its capacity to cause shock. In the dog, hemoconcentration, plasma loss, increased plasma hemoglobin, bloody diarrhea, and hemorrhagic necrosis of the bowel mucosa regularly follow the injection of endotoxin and are apparently the result of the vasospastic effect of endotoxin
LILLEHEI RC, MacLEAN LD. Physiological Approach to Successful Treatment of Endotoxin Shock in the Experimental Animal. AMA Arch Surg. 1959;78(3):464–471. doi:10.1001/archsurg.1959.04320030108018
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