Role of induced histamine in tourniquet shock in mice

Abstract

Development of tourniquet shock in mice is accompanied by a progressive activation of histidine decarboxylase, the enzyme which produces histamine, in traumatized tissue and in all nontraumatized tissues tested except spleen. Involvement of absorbed endotoxins appears to be unimportant. In adrenalectomized mice, maintained on saline and hydrocortisone and given adrenergic blocking agents, a mild trauma is lethal; histidine decarboxylase activation occurs. Since the only apparent major defect of these mice is reduced ability to exert catecholamine actions, excessive vasoconstriction seems to be only an ancillary factor in delayed shock, not an essential one. The present findings, along with previously published evidence relating induced histamine synthesis to microcirculatory regulation, suggest that the fundamental process leading to shock after fluid loss is activation of histamine synthesis in or near cells of the capillaries to restore an adequate supply of blood to the tissues. Since induced histamine synthesis is controlled by local conditions, opening of the capillary beds proceeds independently of the over-all circulatory picture; finally, homeostasis can no longer be maintained.