Abstract
DURING the course of our investigations on the mechanism of enhanced susceptibility to endotoxin after adrenalectomy in dogs, it was found that a transferable shock-inducing factor develops in the absence of glucocorticoids. The shock induced by endotoxins which have no direct cardiovascular action has been difficult to interpret. There has been debate on the indirect mechanisms1, such as endotoxin-epinephrine synergism or histamine release. However, none could explain the effectiveness of glucocorticoids in preventing the endotoxin shock2. Concerning endotoxin susceptibility after adrenalectomy in rabbits, Fukuda3,4 has pointed out that the diminution of hepatic glycogen which follows the accumulation of endotoxin in liver might have an intimate relation to the development of circulatory weakness. Prevention of the attendant hypoglycaemia and the lactacidaemic acidosis by infusions of a hypertonic glucose and sodium bicarbonate solution has been shown to be effective in the recovery of adrenalectomized rabbits even after intravenous administration of the lethal dose of endotoxin (200 µg/kg; LD100).
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