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Influence of anoxia, reoxygenation, and uncoupling on survival, respiration, and Trypsin-Inhibiting capacity of isolated pancreatic acinar cells

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Summary

In the pathogenesis of acute pancreatitis, the events and mechanisms increasing the digestibility of the pancreatic acinar cells are widely unknown. Therefore, the possible contribution of a disturbed energy supply (provoked by anoxia or partial uncoupling) to the induction of autodigestion was studied in experiments on acinar cells isolated from the pancreas. During incubation viability, respiration under normal and maximally stimulated conditions, and trypsin-inhibiting capacity (TIC) of these cells were determined.

With increasing duration of anoxia, the portion of surviving cells was strongly diminished, and the number of cells with blebs and vesicularly transformed endoplasmic reticulum was increased. Although the endogenous respiration was not influenced up to 1.5 h of anoxia, 30 min of anoxia substantially decreased the capacity of oxidative energy production.

The survival curves were characterized by a self-accelerating course of cell destruction. The alteration of the cellular energy metabolism found its reflection in the decreased TIC of the cells.

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References

  1. Steer ML, Meldolesi J. The cell biology of experimental pancreatitis. N. Engl. J. Med. 1987; 316: 144–150.

    PubMed  CAS  Google Scholar 

  2. Lüthen R, Niederau C. Pathophysiologie der akuten Pankreatitis. Z. Gastroenterol. 1990; 28: 211–221.

    PubMed  Google Scholar 

  3. Rinderknecht H. Activation of pancreatic zymogens. Normal activation, protective mechanism against inappropriate activation. Dig. Dis. Sci. 1986; 31: 314–321.

    Article  PubMed  CAS  Google Scholar 

  4. Grant DAW. Acute necrotising pancreatitis—a role for enterokinase. Int. J. Pancreatol. 1986; 1: 167–183.

    PubMed  CAS  Google Scholar 

  5. Kaplan MH. Stress, pancreatic perfusion and acute pancreatitis. Mt. Sin. J. Med. 1985; 52: 326–330.

    CAS  Google Scholar 

  6. Warshaw AL, O’Hara PJ. Susceptibility of the pancreas to ischemic injury in shock. Ann. Surg. 1978; 188: 197–201.

    PubMed  CAS  Google Scholar 

  7. Spormann H, Sokolowski A, Letko G. Effects of temporary ischemia upon development and histological patterns of acute pancreatitis in the rat. Path. Res. Pract. 1989; 184: 507–513.

    PubMed  CAS  Google Scholar 

  8. Letko G, Spormann H, Sokolowski A, Schulz HU. Pancreatic acinar cells: isolation, characterization and application in physiologic studies, with special reference to acute pancreatitis. Exp. Pathol. 1988; 34: 10–22.

    Google Scholar 

  9. Merisko EM, Fletcher M, Palade GE. The reorganization of the Golgi Complex in anoxic pancreatic acinar cells. Pancreas 1986; 1: 95–109.

    Article  PubMed  CAS  Google Scholar 

  10. Mitchell P. Vectorial chemistry and the molecular mechanics of chemi-osmotic coupling: power transmission by protocity. Biochem. Soc. Trans. 1976; 4: 399–430.

    PubMed  CAS  Google Scholar 

  11. Langner J, Wakil A, Zimmermann M, Ansorge S, Bohley P, Kirschke H, Wiederanders B. Aktivitätsbestimmung proteolytischer Enzyme mit Azokasein als Substrat. Acta Biol. Med. Germ. 1973; 31: 1–18.

    PubMed  CAS  Google Scholar 

  12. Amsterdam A, Jamieson JD. Studies on dispersed pancreatic exocrine cells. I. Dissociation technique and morphologic characteristics of separated cells. J. Cell. Biol. 1974; 63: 1037–1056.

    Article  PubMed  CAS  Google Scholar 

  13. Sanfey H, Bulkley GB, Cameron JL. The role of oxygen-derived free radicals in the pathogenesis of acute pancreatitis. Ann. Surg. 1984; 200: 405–413.

    Article  PubMed  CAS  Google Scholar 

  14. Florack G, Sutherland DER, Ascherl R, Heil J, Erhardt W, Najarian JS. Definition of normothermic ischemia limits for kidney and pancreas grafts. J. Surg. Res. 1986; 40: 550–563.

    Article  PubMed  CAS  Google Scholar 

  15. Jewell SA, Bellomo G, Thor H, Orrenius S, Martyn TS. Bleb formation in hepatocytes during drug metabolism is caused by disturbances in thiol and calcium ion homeostasis. Science 1982; 217: 1257–1259.

    Article  PubMed  CAS  Google Scholar 

  16. Donohoe MJ, Rush BF, Machiedo GW, Barillo DJ, Murphy TF. Biochemical and morphologic changes in hepatoGytes from the shock injured liver. Surg. Gynecol. Obstet. 1986; 162: 323–333.

    PubMed  CAS  Google Scholar 

  17. Myagkaya G, van Veen H, James J. Ultrastructural changes in rat liver sinusoids during prolonged normothermic and hypothermic ischemia in vitro. Virchows Arch. (B) 1984; 47: 361–373.

    Article  CAS  Google Scholar 

  18. Ishiharajima S, Aids T, Nakagawa R, Kameyama K, Sugano K, Oguro T, Asano G. Early membrane damage during ischemia in rat heart. Exp. Mol. Pathol. 1986; 44: 1–6.

    Article  PubMed  CAS  Google Scholar 

  19. Schulz HU, Letko G, Hass HJ, Spormann H, Kemnitz P, Burger P, Wendt U. Effects of pancreatic acinar cell surface antibodies and complement on isolated rat acinar cells in vitro. Virchows Arch. (B) 1988; 55: 101–106.

    CAS  Google Scholar 

  20. Letko G, Falkenberg B, Boschmann M. Differences in time course of hepatocyte and pancreatocyte damage after incubation with trypsin, chymotrypsin and 2,4-dinitrophenol. Exp. Pathol. 1990; 40: 105–109.

    PubMed  CAS  Google Scholar 

  21. Leaf A, Cheung JY, Mills JW, Bonventre JV. Nature of the cellular insult in acute renal failure. In:Acute Renal Failure. Brenner BM, Lazarus JM, eds., Philadelphia, Saunders, 1983; pp. 2–20.

    Google Scholar 

  22. Lucas M, Schmid G, Kromas R, Lüffler G. Calcium metabolism and enzyme secretion in guinea pig pancreas. Uptake, storage and release of calcium in whole cells and mitochondrial and microsornal fractions. Eur. J. Biochem. 1978; 85: 609–619.

    Article  PubMed  CAS  Google Scholar 

  23. Ohlsson K, Balldin G, Lasson A. Trypsin-induced release of bradykinin and of C3 fragments in man: clinical and experimental studies on the protective role of alpha 2 macroglobulin and aprotinin. Adv. Exp. Med. Biol. 1983; 156 B: 1083–1090.

    PubMed  Google Scholar 

  24. Ohshio G, Saluja AK, Leli U, Sengupta A, Steer ML. Esterase inhibitors prevent lysosomal enzyme redistribution in two noninvasive models of experimental pancreatitis. Gastroenterology 1989; 96: 853–859.

    PubMed  CAS  Google Scholar 

  25. Saluja A, Hashimoto S, Saluja M, Powers RE, Meldolesi J, Steer ML. Subcellular redistribution of lysosomal enzymes during cerulein-induced pancreatitis. Am, J. Physiol. 1987; 253: G5O8-G516.

    Google Scholar 

  26. Saluja A, Saluja M, Villa A, Leli U, Rutledge P, Meldolesi J, Steer ML. Pancreatic duct obstruction in rabits causes digestive zymogen and lysosomal enzyme colocalization. J. Clin. Invest. 1989; 84: 1260–1266.

    Article  PubMed  CAS  Google Scholar 

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Hass, H.J., Wilhelm, W., Kemnitz, P. et al. Influence of anoxia, reoxygenation, and uncoupling on survival, respiration, and Trypsin-Inhibiting capacity of isolated pancreatic acinar cells. Int J Pancreatol 10, 39–49 (1991). https://doi.org/10.1007/BF02924252

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  • DOI: https://doi.org/10.1007/BF02924252

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