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IT has been reported from this laboratory that the extreme susceptibility of adrenalectomized dogs to endotoxin is mainly a result of the development of an endogenous factor which produces

marked hepatic engorgement of the shocked animals1,2. This factor seemed to be formed in the liver when its glycogen becomes depleted in the absence of glucocorticoids. The appearance of

this factor in the circulating blood could be detected by injecting the shock serum into a normal recipient dog under pentobarbitone sodium anaesthesia when a delayed depressor response

caused by induction of hepatic engorgement could be observed. This “shock-factor” in the serum was found to be non-dialysable, heat-unstable (inactivated by heating at 56° C for 30 min) and

contained in the serum protein fraction precipitable by 20 per cent to 34 per cent saturation with ammonium sulphate. Further experiments, shortly to be published, showed that there was no

appreciable release of histamine from the liver of endotoxin-shocked adrenalectomized dogs and that the “shock-factor” does not act as a histamine-releaser. The “shock-factor” and the

hepatic engorgement were examined, therefore, in relation to an induction of histamine formation in the liver. Dogs are known to have no detectable histamine forming capacity in their

tissues3, and so the possibility that histamine forming activity was induced in the liver of endotoxin-shocked adrenalectomized dogs was therefore examined, using the method of Waton3 to

determine this capacity.

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