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February 3, 1962


JAMA. 1962;179(5):369. doi:10.1001/jama.1962.03050050059011

In the belief that adrenergic vasoconstriction may aggravate the development of shock, Gourzis et al.,1 postulated that the damage to tissues exposed to endotoxins is not due to a direct toxic effect but is secondary to an increased responsiveness to adrenergic stimuli. In one experiment they showed that pretreatment with Escherichia coli endotoxin increases the pressor response to epinephrine and levarterenol in rabbits. When strips of aorta from freshly killed rabbits were exposed to the endotoxin in a medium that contained whole blood or blood cells, the response of the muscle to epinephrine was augmented. When the medium contained not blood but a physiologic saline solution or plasma this increased response did not occur. The effects of the endotoxin appeared to be mediated through or dependent on peripheral adrenergic mechanisms. The nature of the interaction between the endotoxin and the blood elements that enhanced the response to adrenergic stimuli