International Journal of Pancreatology

, Volume 8, Issue 2, pp 133–139 | Cite as

A study of the time course of conversion of edematous to hemorrhagic pancreatitis

  • Nariman D. Karanjia
  • Surjait M. Singh
  • Vicki Porter- Fink
  • Adam L. Widdison
  • Howard A. Reber


We studied the conversion of acute edematous pancreatitis (AEP) to acute hemorrhagic pancreatitis (AHP) in an experimental model in cats. In the model, 16,16 dimethyl PgE2 effects this conversion by increasing microvascular permeability. First, we induced AEP in cats and then gave PgE2 at increasing intervalsafter the induction of AEP to see how long an interval would still allow conversion. In 6 groups of cats, PgE2 was administered for 2 h, starting at 2, 4, 6, 8, 10, or 12 h after the creation of AEP. Twelve h later, the cats were sacrificed and the pancreases were graded for inflammation and hemorrhage. Significant pancreatic hemorrhage did not occur when the PgE2 was administered at 12 h compared to 2 h. Next, we determined that PgE2 still retained its ability to increase pancreatic vascular permeability when administered 12 h after the creation of AEP. This was done by perfusing a marker molecule through the MPD (fluorescein iso-thiocyanate labeled dextran: FITC-D, mol wt 20,000) and then finding it in portal venous blood (PVB). The presence of FITC-D in PVB signified increased vascular permeability, since normally none was present. We concluded that conversion of AEP to AHP was possible during the first 12 h after induction of AEP. Lack of conversion at 12 h was not caused by a lack of vascular reactivity at that time.

Key Words

Acute pancreatitis edematous pancreatitis hemorrhagic pancreatitis prostaglandin 


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 1.
    Frey CF. Hemorrhagic pancreatitis. Am. J. Surg. 1979; 137: 616–623.PubMedCrossRefGoogle Scholar
  2. 2.
    Kivilaakso E, Fraki O, Nikki P, Lempinen M. Resection of the pancreas for acute fulminant pancreatitis. Surg. Gynecol. Obstet. 1981; 152: 493–498.PubMedGoogle Scholar
  3. 3.
    Beger HG, Bittner R, Block S, Buchler M. Bacterial contamination of pancreatic necrosis. A prospective clinical study. Gastroenterol. 1986; 91: 433–438.Google Scholar
  4. 4.
    Harvey MH, Wedgwood K, Reber HA. Vasoactive drugs, microvascular permeability and hemorrhagic pancreatitis in cats. Gastroenterol. 1987; 93: 1296–1300.Google Scholar
  5. 5.
    Wedgwood KR, Farmer RC, Reber HA. A model of hemorrhagic pancreatitis in catsthe role of 16,16-dimethyl prostaglandin E2. Gastroenterol. 1986; 90: 32–39.Google Scholar
  6. 6.
    Hallenbeck GA. Biliary and pancreatic intraductal pressures. Heidi W. eds, Handbook of Physiology, Alimentary Canal, Vol II, Secretion, Waverly Press, Baltimore, 1967; 1007–1025.Google Scholar
  7. 7.
    Harvey MH, Cates M, Reber HA. Possible mechanisms of acute pancreatitis induced by ethanol. Am. J. Surg. 1988; 155: 49–56.PubMedCrossRefGoogle Scholar
  8. 8.
    Glazer G, Bennett A, Dudley HAF. Elevation of prostaglandin like activity in the blood and peritoneal exudate of dogs with acute pancreatitis. Br. J. Surg. 1974; 6: 922–925.Google Scholar
  9. 9.
    Glazer G, Gilliland EL, Aldridge MA. The role of prostaglandins in acute pancreatitis. Nyhus LM. eds, Surgery Annual, Appleton and Lange, Connecticut, California, 1987; 175–203.Google Scholar
  10. 10.
    Hagen PO, Ofstad E, Amundson E. Experimental acute pancreatitis in dogs: Histamine release induced by pancreatic exudate. Scand. J. Gastro. 1969; 4: 75–96.CrossRefGoogle Scholar
  11. 11.
    Grega G, Svensjo E, Haddy FJ. Macromolecular permeability of the microvascular mem- brane: Physiological and pharmacological regulation. Microcirculation 1981; 325–41.Google Scholar
  12. 12.
    Majno G, Shea SM, Leventhal M. Endothelial contraction induced by histamine type mediators: An electron microscopic study. J. Cell. Biol. 1969; 42: 647–672.PubMedCrossRefGoogle Scholar
  13. 13.
    Geokas MC, Rinderknecht H. Free proteolytic enzymes in pancreatic juice of patients with acute pancreatitis. Dig. Dis. Sci. 1974; 19: 591–598.CrossRefGoogle Scholar
  14. 14.
    Troll W, Doubilet H. The determination of proteolytic enzymes and proenzymes in human pancreatic juice. Gastroenterol. 1951; 19: 326–330.Google Scholar
  15. 15.
    Singh SM, Porter-Fink V, Adham N, Reber HA. The migration of pancreatic enzymes from the main pancreatic duct into the portal venous blood. Pancreas 1988; 3: 618.Google Scholar
  16. 16.
    Balldin G, Ohlsson K. Demonstration of pancreatic protease-antiprotease complexes in the peritoneal fluid of patients with acute pancreatitis. Surgery 1979; 85: 451–456.PubMedGoogle Scholar
  17. 17.
    Harvey MH, Wedgwood KR, Reber HA. Treatment of acute pancreatitis with beta-adrenergic agonist drugs. Surgery 1987; 102: 229–234.PubMedGoogle Scholar
  18. 18.
    Karanjia ND, Lutrin FJ, Chang YB, Reber HA. Low dose dopamine protects against hemorrhagic pancreatitis in cats. J. Surg. Res. 1989; (In press).Google Scholar

Copyright information

©  The Humana Press Inc 1991

Authors and Affiliations

  • Nariman D. Karanjia
    • 1
  • Surjait M. Singh
    • 1
  • Vicki Porter- Fink
    • 1
  • Adam L. Widdison
    • 1
  • Howard A. Reber
    • 1
  1. 1.Departments of SurgeryVA Medical Center, Sepulveda, and UCLALos Angeles

Personalised recommendations