[Study on acute pancreatitis-associated lung injury induced by L-arginine in mice]

To establish the model of acute pancreatitis (AP)-associated lung injury induced by L-arginine and study the role of TNF-alpha and ICAM-1 in the model mice.

For the establishment of the AP model, the mice were given the first injection (2 g/kg) of L-arginine intraperitoneally and then the second injection in the same way an hour later. At 12 h after the second injection, the animals' serum amylase activities were assayed by colorimetry, and the tumor necrosis factor-alpha (TNF-alpha) contents of their pancreatic tissue were determined by radioimmunoassay. At 24 h after the second injection, the histopathological changes in the animals' pancreatic and pulmonary tissues were observed. The pulmonary expression and cellular localization of intercellular adhesion molecule-1 (ICAM-1) were characterized by immunohistochemistry.

The serum amylase activities, TNF-alpha content and ICAM-1 expression in lung tissue significantly increased in the AP group as compared with those in the control group. Histopathological examinations revealed that the acinar architecture was partially destroyed with necrosis, interstitial edema and inflammatory infiltration at 24 h after the second injection.

TNF-alpha and ICAM-1 may play important roles in the mice with acute pancreatitis-associated lung injury.