title: Stenting does not decompress the pancreatic duct as effectively as surgery in experimental chronic pancreatitis.
abstract: BACKGROUND
  In humans with chronic pancreatitis (CP), pancreatic interstitial pressure (IP) is elevated and pancreatic blood flow (PBF) is reduced. The efficacy of surgical decompression (SD) of the pancreatic duct (ie, pancreaticojejunostomy) is believed to be due to its ability to decrease IP and pancreatic vascular resistance (Rp), which increases PBF. Pancreatic duct stenting (STE) also probably reduces IP and Rp, which may explain its efficacy. The purpose of this study was to compare the efficacy of SD with STE.
  
  
  METHODS
  CP in cats was created by narrowing the main pancreatic duct. Six weeks later, CP and normal pancreata were isolated and perfused ex vivo under basal conditions and after secretin stimulation. In normal and CP glands, IP and perfusion pressure were measured and Rp (U) was calculated. In two additional groups, the pancreatic duct was decompressed, either by stenting or by complete transection of the duct with a longitudinal capsulotomy.
  
  
  RESULTS
  In CP glands, IP and Rp were increased and secretory output was markedly reduced compared with the normal (0.65 +/- 0.30 mm Hg and 0.46 +/- 0.04 U vs 3.90 +/- 0.80 mm Hg and 1.68 +/- 0.05 U; P < .05). Secretin administration (2 units) increased IP and Rp in CP glands (6.60 +/- 1.10 mm Hg and 2.87 +/- 0.07 U; P < .05), but these values did not chang in normal glands (0.81 +/- 0.20 and 0.53 +/- 0.03 U; NS). STE and SD decreased IP and Rp in CP glands (2.20 +/- 0.20 to 1.0 +/- 0.40 mm Hg and 1.20 +/- 0.015 to 0.90 +/- 0.01 U, respectively; P < .05). Both methods prevented an increase of IP and Rp after secretin administration. IP and Rp decreased to a greater degree following SD, compared with STE (P < .05).
  
  
  CONCLUSIONS
  Both STE and SD decreased IP and Rp in this experimental model of CP. However, SD was significantly more effective than STE.
authors.affiliation: Department of General Surgery, UCLA School of Medicine, USA.
authors.forename: P U
authors.initials: PU
authors.lastname: Reber
authors.forename: A G
authors.initials: AG
authors.lastname: Patel
authors.forename: M P
authors.initials: MP
authors.lastname: Lewis
authors.forename: S W
authors.initials: SW
authors.lastname: Ashley
authors.forename: H A
authors.initials: HA
authors.lastname: Reber
mesh_terms: D000818:Animals; D002415:Cats; D002908:Chronic Disease; D004195:Disease Models, Animal; D005260:Female; D008297:Male; D010179:Pancreas / Q000098:blood supply* / Q000378:metabolism / Q000601:surgery; D010183:Pancreatic Ducts / Q000601:surgery*; D010195:Pancreatitis / Q000601:surgery*; D012039:Regional Blood Flow; D015607:Stents; D013514:Surgical Procedures, Operative; D014655:Vascular Resistance