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Trauma induced histamine synthesis and RES activity
Advances in Experimental Medicine and Biology
|January 1, 1976
Summary
Trauma resistance in animals prevents increased histidine decarboxylase and phagocytic activity post-injury. A humoral factor from resistant animals may inhibit this enzyme activation, offering a protective mechanism.
Area of Science:
- Biochemistry
- Immunology
- Physiology
Background:
- Tumbling trauma induces significant physiological stress.
- Histidine decarboxylase (HDC) activity and phagocytic function are altered post-trauma.
Purpose of the Study:
- To investigate the role of histidine decarboxylase activity in trauma response.
- To explore the protective mechanisms in trauma-resistant animals.
Main Methods:
- Assessing lung and spleen histidine decarboxylase activity in normal and trauma-resistant rats.
- Measuring phagocytic activity of reticuloendothelial system (RES) elements.
- Administering spleen and plasma extracts from trauma-resistant rats.
Main Results:
- Normal animals showed increased HDC and phagocytic activity after trauma.
- Trauma-resistant animals exhibited attenuated changes in HDC and phagocytic activity.
- Extracts from trauma-resistant animals prevented or reduced post-traumatic changes.
Conclusions:
- Trauma resistance is associated with modulated HDC and phagocytic responses.
- A humoral factor, possibly linked to the RES, may inhibit HDC activation.
- This factor appears to play a role in the protective effects observed in trauma-resistant states.