Trauma induced histamine synthesis and RES activity.
The histidine decarboxylase activity of the lung and spleen was determined in animals made resistant to tumbling 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 post-traumatic period in the normal animal as being associated with an increased histidine decarboxylase activity. In addition, the increased histidine decarboxylase activity was paralleled by an increased phagocytic activity of the reticuloendothelial elements of the spleen. In trauma resistant animals, changes in the enzyme activity and phagocytic capability were prevented or curtailed. The administration of spleen and plasma protective extracts were similarly effective in impeding these changes following trauma. It is suggested that the active humoral factor elaborated during conditioning and associated with the RES may act by inhibiting the activation of histidine decarboxylase.
D000818:Animals; D001692:Biological Transport; D001803:Blood Transfusion; D003102:Colloids; D005260:Female; D006632:Histamine / Q000096:biosynthesis*; D006640:Histidine Decarboxylase / Q000378:metabolism; D008168:Lung / Q000201:enzymology; D012157:Mononuclear Phagocyte System / Q000503:physiopathology*; D010587:Phagocytosis; D051381:Rats; D012399:Rotation; D013154:Spleen / Q000378:metabolism / Q000503:physiopathology; D013910:Thorium / Q000378:metabolism; D014947:Wounds and Injuries / Q000378:metabolism*
D003102:Colloids; D013910:Thorium; D006632:Histamine; D006640:Histidine Decarboxylase