Abstract
Experimental interference with the circulation in a circumscribed tissue area, too slight to produce any manifest disturbance in itself, can strikingly alter topical reactivity to irritants and to the antiphlogistic effect of hydrocortisone. Thus, certain vascular territories can be "selectively conditioned" to the anti-inflammatory actions of blood-borne corticoids. Conversely, when tissue damage is severe, such "selective conditioning" may induce a seemingly paradoxic reversal of the hydrocortisone effect, so that the hormone enhances inflammation. Here, impairment of circulation and hydrocortisone facilitate the production by irritants of necrosis, more than of inflammation. The resulting wide-spread necrosis induces an even greater inflammatory response, despite hydrocortisone, than would have been observed without hormone treatment.

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