Basic Research
Copyright ©2005 Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jan 28, 2005; 11(4): 538-544
Published online Jan 28, 2005. doi: 10.3748/wjg.v11.i4.538
Pituitary adenylate cyclase activating-peptide and its receptor antagonists in development of acute pancreatitis in rats
You-Dai Chen, Zong-Guang Zhou, Zhao Wang, Hong-Kai Gao, Wen-Wei Yan, Cun Wang, Gao-Ping Zhao, Xiao-Hui Peng
You-Dai Chen, Zong-Guang Zhou, Zhao Wang, Hong-Kai Gao, Wen-Wei Yan, Cun Wang, Gao-Ping Zhao, Xiao-Hui Peng, Instistute of Digestive Surgery/Department of General Surgery, West China Hospital, Sichuan University, Chengdu 610041, Sichuan Province, China
Author contributions: All authors contributed equally to the work.
Supported by National Natural Science Foundation of China, No. 30271283
Correspondence to: Dr. Zong-Guang Zhou, Instistute of Digestive Surgery/ Department of General Surgery, West China Hospital, Sichuan University, Chengdu 610041, Sichuan Province, China. zhou767@21cn.com
Telephone: +86-28-85422525
Received: March 11, 2004
Revised: March 14, 2004
Accepted: April 5, 2004
Published online: January 28, 2005
Abstract

AIM: Pituitary adenylate cyclase activating-peptide (PACAP) is a late member of the secretin/glucagon/vasoactive intestinal peptide (VIP) family of brain-gut peptides. It is unknown whether PACAP takes part in the development of acute pancreatitis and whether PACAP or its antagonists can be used to suppress the progression of acute pancreatitis. We investigated the actions of PACAP and its receptor antagonists in acute pancreatitis on rats.

METHODS: Acute pancreatitis was induced in rats with caerulein or 3.5% sodium taurocholate. The rats were continuously infused with 5-30 μg/kg PACAP via jugular vein within the first 90 min, while 10-100 μg/kg PACAP6-27 and (4-Cl-D-Phe6, Leu17) VIP (PACAP receptor antagonists) were intravenously infused for 1 h. Biochemical and histopathological assessments were made at 4 h after infusion. Pancreatic and duodenal PACAP concentrations were determined by enzyme-linked immunosorbent assay (ELISA). Chinese ink-perfused pancreas was fixed, sectioned and cleared for counting the functional capillary density.

RESULTS: PACAP augmented caerulein-induced pancreatitis and failed to ameliorate sodium taurocholate-induced pancreatitis. ELISA revealed that relative concentrations of PACAP in pancreas and duodenum were significantly increased in both sodium taurocholate- and caerulein-induced pancreatitis compared with those in normal controls. Unexpectedly, PACAP6-27 and (4-Cl-D-Phe6, Leu17) VIP could induce mild acute pancreatitis and aggravate caerulein-induced pancreatitis with characteristic manifestations of acute hemorrhagic/necrotizing pancreatitis. Functional capillary density of pancreas was interpreted in the context of pancreatic edema, and calibrated functional capillary density (calibrated FCD), which combined measurement of functional capillary density with dry weight/wet weight ratio, was introduced. Hyperemia or congestion, rather than ischemia, characterized pancreatic microcirculatory changes in acute pancreatitis.

CONCLUSION: PACAP may take part in the pathogenesis of acute pancreatitis in rats. The two PACAP receptor antagonsits might act as partial agonists. Calibrated functional capillary density can reflect pancreatic microcirculatory changes in acute pancreatitis.

Keywords: Acute pancreatitis; PACAP; PACAP receptor antagonsits