Histidine decarboxylase activity in trauma-resistant rats.

Studies have been carried out to determine the possible role of nascent histamine in the development of traumatic shock. This was done by examining histidine decarboxylase (HD) activity of the lung, spleen, and plasma following exposure to trauma in normal and trauma-resistant rats. In normal rats, there was a significant increase in lung HD activity at 15 min and 4 h; and in the spleen the HD activity increased significantly at 4 h. In trauma-resistant rats exposed to trauma, there were no changes in enzyme activity in the lung and less pronounced changes in the spleen. The plasma HD activity remained stable in normal and resistant rats following episodes of trauma. Changes in total erythrocyte hemoglobin were observed in both normal and trauma-adapted rats following exposure to this stress, increasing significantly in normal rats, but decreasing in trauma-resistant rats. Blood volume decreased significantly at 4 h after trauma in normal animals; whereas only a slight decrease was noted in resistant animals. The data support the concept that newly formed histamine contributes to the pathogenesis of shock. It is also proposed that the increased resistance, characteristic of trauma-adapted rats, could be partly due to an inhibition of enzyme activation following trauma.