Histamine biosynthesis in shock.

The histidine decarboxylase activity of the lung and spleen was determined in rats made resistant to trauma either by prior sublethal exposure or by injection of extracts prepared from the spleens and plasma of trauma-resistant rats. The data describe the posttraumatic period in the normal animal as being associated with an increased histidine decarboxylase activity. In trauma-resistant animals, changes in the enzyme activity were prevented in the lung and were less pronounced in the spleen. The administration of extracts from trauma-resistant rats was similarly effective in impeding the changes in enzyme induction following trauma. It is suggested that an active humoral factor previously shown to be elaborated during conditioning and associated with the RES may act by inhibiting the activation of histidine decarboxylase.