Thermal bile duct and duodenal protection during pancreatic cryoablation

Aim

To examine whether thermo-perfusion of the bile duct and duodenum may protect these organs during cryoablation of adjacent pancreatic tissue.

Study design

Cryoablation of the pancreatic tissue, adjacent to the common bile duct and duodenum was performed in two groups of pigs. In the experimental group, the bile duct and duodenum were protected during the cryo-procedure by intraluminal perfusion of warm saline. In the control group, cryoablation was performed without thermo-protection.

Results

All three animals in the control group developed duodenal perforation and abscesses and died within a week. All the pigs in the experimental group survived and on re-operation 14 days after the first procedure were found to have normal duodenum and bile duct adjacent to the cryoablated pancreatic tissue. Histological examinations confirmed these results.

Conclusion

The present study confirms the feasibility and efficacy of thermo-protection of the duodenum and common bile duct during cryoablation of the head of the pancreas.     

Early observations of pancreatic ultrastructure during hemorrhagic necrosis in the rat with closed duodenal pouch]

Many problems are still unanswered in the pathogenesis of acute clinical and experimental pancreatic necrosis. A new technique which can be performed in the rat seems a suitable model for reflux pancreatic necrosis without artificial pressure changes in the ductal system. A closed duodenal loop is obtained with ligation proximal and distal to Vater's ampulla and a gastroenteroanastomosis is associated to avoid intestinal obstruction. All the rats die with hemorrhagic pancreatic necrosis in 36 hours. After 12 hours from the operation ductal and acinar lumina are enlarged. In the centroacinar and intercalated duct cells some lysosomes and mitochondria with clear matrix and reduced cristae are detected. Intercellular junctions in ducts and acini have normal morphology. In the basal cytoplasm of acinar cells some prominent autophagic vacuoles are detectable. After 24 hours in the acinar cells autophagic vacuoles are greatly increased and basal cytoplasmic degeneration often occurs, with plasmalemma and basal lamina interruptions. Intercellular junctions are apparently unaffected until cell necrosis sets in. In blood capillaries endothelial cells are swollen, fibrin thrombosis, hemorrhage and leucocyte infiltration are often detectable. As lysosomal activity occurs also in different kinds of experimental pancreatic necrosis, it could be a common pathogenetic factor, responsible for hydrolytic enzyme activation and for vascular damage in the early stages of hemorrhagic pancreatic necrosis.     

Increased serum pancreatic polypeptide and serum gastrin secretion in patients with functional dyspepsia: correlation to the shape of the duodenal loop

Simultaneous measurement of food-stimulated serum pancreatic polypeptide and serum gastrin was carried out in 18 patients with functional dyspepsia and correlated to the shape of the duodenal loop. Significantly higher serum concentrations of pancreatic polypeptide and gastrin were encountered in patients with an abnormal shape of the duodenal loop compared to patients with a normal shape. Although no cause could be given to the phenomenon it may be taken into account when evaluating hormone profiles in patients with functional dyspepsia.     

Effects of bile acids on dog pancreatic duct epithelial cell secretion and monolayer resistance

Pancreatic duct epithelial cells (PDEC) mediate the secretion of fluid and electrolytes and are exposed to refluxed bile. In nontransformed cultured dog PDEC, which express many ion transport pathways of PDEC, 1 mM taurodeoxycholic acid (TDCA) stimulated an (125)I(-) efflux inhibited by DIDS and 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB) and a (86)Rb(+) efflux inhibited by charybdotoxin. Inhibition by 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA)-AM suggests mediation via increased intracellular Ca(2+) concentration, whereas the absence of lactate dehydrogenase release excludes cellular toxicity. At 1 mM, TDCA stimulated a larger (125)I(-) efflux than glycodeoxycholate; two dihydroxy bile acids, taurochenodeoxycholate and TDCA, were similarly effective, whereas a trihydroxy bile acid, taurocholate, was ineffective. In Ussing chambers, 1 mM serosal or 2 mM luminal TDCA stimulated an I(sc) increase from confluent PDEC monolayers. TDCA also stimulated 1) a short-circuit current (I(sc)) increase from basolaterally permeabilized PDEC subject to a serosal-to-luminal Cl(-) gradient that was inhibited by BAPTA-AM, DIDS, and NPPB and 2) an I(sc) increase from apically permeabilized PDEC subject to a luminal-to-serosal K(+) gradient inhibited by BAPTA-AM and charybdotoxin. Along with the efflux studies, these findings suggest that TDCA interacts directly with PDEC to stimulate Ca(2+)-activated apical Cl(-) channels and basolateral K(+) channels. Monolayer transepithelial resistance was only minimally affected by 1 mM serosal and 2 mM luminal TDCA but decreased after exposure to higher TDCA concentrations (2 mM serosal and 4 mM luminal). A secretory role for bile acids should be considered in pancreatic diseases associated with bile reflux.