Extrapancreatic organ impairment in caerulein induced pancreatitis

Citation
Zj. He et al., Extrapancreatic organ impairment in caerulein induced pancreatitis, ANN CHIR GY, 88(2), 1999, pp. 112-117
Citations number
20
Categorie Soggetti
Reproductive Medicine
Journal title
ANNALES CHIRURGIAE ET GYNAECOLOGIAE
ISSN journal
03559521 → ACNP
Volume
88
Issue
2
Year of publication
1999
Pages
112 - 117
Database
ISI
SICI code
0355-9521(1999)88:2<112:EOIICI>2.0.ZU;2-2
Abstract
Background and Aims: Multiorgan function failures are the major fatal compl ications in acute pancreatitis. In this experiment, we studied 1) the manif estation and time course of extrapancreatic organ damage in an acute pancre atitis model and 2) whether the obstructive liver damage in this model is c aused by the obstruction of common biliopancreatic duct compressed by oedem atous pancreas. Material and Methods: 80 male Wistar rats were divided into two groups: con trol and caerulein groups (five subgroups in each group). In the caerulein group, the acute pancreatitis was induced by caerulein intraperitoneal inje ctions. In the controls equal volume of saline was injected. Two subgroups, one in caerulein and one in control groups, had an intrapancreatic bile du ct stent inserted transduodenally before the injections. The pancreas, live r, lung and kidney tissues and blood samples were obtained for the measurem ent or analysis of interstitial oedema, plasma amylase, alanine aminotransf erase, bilirubin, urea, creatinine, alkaline phosphatase, lactate dehydroge nase, blood gas and electron microscopy at 1, 6, 12 and 24 hours after the last injection in unstented animals, and at 6 hours in stented animals. Results: Lungs and kidney remained unchanged. Liver damage was found during the first 6-12 hours, manifest as increased plasma alanine aminotransferas e and bilirubin and dilatation of bile canaliculi and hepatocyte damage in electron microscopy. The intrapancreatic bile duct stent did not resolve th ese changes. Conclusions: The liver may be the first evolved extrapancreatic organ in th e early stage in this mild oedematous pancreatitis model and the hepatocyte damage is not caused by the obstruction of common biliopancreatic duct com pressed by the oedematous pancreas.