Changes of inflammation and apoptosis in adrenal gland after experimental injury in rats with acute necrotizing pancreatitis.

We hypothesize that adrenal insufficiency in acute necrotizing pancreatitis (ANP) is attributable to hemorrhagic inflammation, necrosis, and apoptosis of the adrenal cortex. Arguments to support this view are presented in the study that investigated morphological and functional changes of adrenal and the distinct roles of inflammatory mediator secretory phospholipase A(2) (sPLA(2)) and apoptosis-related genes Bax and Bcl-2 played in acute adrenal injury in ANP. After ANP model was induced, pancreatic histology, serum amylase, sPLA(2), and corticosterone were analyzed. The adrenal morphology, apoptotic cells by TUNEL assay, and ultrastructures were observed. sPLA(2)-IIA and Bcl-2 and Bax expressions were detected by immunohistochemistry. Histopathologic grading of adrenal was higher in ANP group than in controls. Serum corticosterone was stimulated to maximal level at 3 h, then dropped to the bottom at 24 h (P<0.05). Apoptotic index, sPLA2-IIA, and Bax expression were increased steeply after pancreatitis, and the Bax/Bcl-2 ratio was elevated gradually (P<0.05). Sustained decrease in serum corticosterone level following adrenal injury during ANP appears to be, in part, due to the crucial roles of inflammation and apoptosis in adrenal cortex. These findings could suggest that sPLA2, Bax, and Bcl-2 may be involved in the course of adrenal injury after ANP.