Alpha 1-acid glycoprotein and peripheral nerve injury, studied with a wound chamber.
BACKGROUND
The aim of the present study is to demonstrate the distribution and quantitative changes of alpha 1-acid glycoprotein (AGP) in rat sciatic nerve subsequent to mechanical injury. AGP is a serum protein, whose level rises after injury; hence the term "acute phase reactant." AGP is synthesized mainly by hepatocytes and the production is stimulated by cytokines released by inflammatory cells. The biologic role of AGP is not known except that it has in vitro nerve growth promoting property.


METHODS
Impermeable silicone tubes, 10 mm long and 1.4 mm in internal diameter, were sutured to the ends of transected rat sciatic nerve. On the 1st to 21st postoperative days, the wound fluid in the tube and the rat sera were collected for protein analysis and quantitative determination of AGP. The sciatic nerves were removed and immunostained with a monoclonal antibody against rat AGP.


RESULTS
The protein content in the wound fluid was 1/5 that of the serum, the proteins of the wound fluid and the serum had similar electrophoretic patterns on sodium dodecyl sulfate-polyacrylamide gel electrophoresis. There was a parallel rise of AGP levels in serum and in wound fluid beginning 1 day after the operation reaching the highest level on the 5th day. Immunohistochemical study showed deposits of extravasated AGP in fibrin cable connecting the ends of the transected nerve, in endoneurium, perineurium, perivascular mononuclear, and mesenchymal cells of epineurium at the wound and diffusely in the entire distal nerve segment.


CONCLUSIONS
Increased vascular permeability with exudation of leukocytes and plasma proteins are basic pathophysiologic reactions to injury. The wound chamber method employed in the present study may provide a useful model for investigations dealing with the roles of circulating plasma proteins and other molecules as well as local cellular products involved in wound healing and nerve regeneration.
Liu
H M
HM
Department of Pathology, National Cheng Kung University, Medical College, Tainan, Taiwan, Republic of China.
Lei
H Y
HY
Schmid
K
K
D000209:Acute-Phase Proteins / Q000032:analysis / Q000378:metabolism; D000210:Acute-Phase Reaction / Q000378:metabolism / Q000503:physiopathology; D000818:Animals; D000911:Antibodies, Monoclonal; D001798:Blood Proteins / Q000032:analysis / Q000502:physiology; D002199:Capillary Permeability / Q000502:physiology; D004591:Electrophoresis, Polyacrylamide Gel; D015151:Immunoblotting; D007150:Immunohistochemistry; D009414:Nerve Growth Factors / Q000032:analysis / Q000378:metabolism / Q000502:physiology; D009961:Orosomucoid / Q000032:analysis* / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012584:Sciatic Nerve / Q000737:chemistry* / Q000293:injuries* / Q000502:physiology; D013314:Stress, Mechanical; D014947:Wounds and Injuries / Q000097:blood / Q000378:metabolism / Q000503:physiopathology*
D000209:Acute-Phase Proteins; D000911:Antibodies, Monoclonal; D001798:Blood Proteins; D009414:Nerve Growth Factors; D009961:Orosomucoid