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.
Acinar cells isolated anoxia cellular respiration rat trypsininhibiting capacity uncoupling
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Steer ML, Meldolesi J. The cell biology of experimental pancreatitis. N. Engl. J. Med. 1987; 316: 144–150.PubMedGoogle Scholar
Lüthen R, Niederau C. Pathophysiologie der akuten Pankreatitis. Z. Gastroenterol. 1990; 28: 211–221.PubMedGoogle Scholar
Rinderknecht H. Activation of pancreatic zymogens. Normal activation, protective mechanism against inappropriate activation. Dig. Dis. Sci. 1986; 31: 314–321.PubMedCrossRefGoogle Scholar
Grant DAW. Acute necrotising pancreatitis—a role for enterokinase. Int. J. Pancreatol. 1986; 1: 167–183.PubMedGoogle Scholar
Kaplan MH. Stress, pancreatic perfusion and acute pancreatitis. Mt. Sin. J. Med. 1985; 52: 326–330.Google Scholar
Warshaw AL, O’Hara PJ. Susceptibility of the pancreas to ischemic injury in shock. Ann. Surg. 1978; 188: 197–201.PubMedGoogle Scholar
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.PubMedGoogle Scholar
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
Merisko EM, Fletcher M, Palade GE. The reorganization of the Golgi Complex in anoxic pancreatic acinar cells. Pancreas 1986; 1: 95–109.PubMedCrossRefGoogle Scholar
Mitchell P. Vectorial chemistry and the molecular mechanics of chemi-osmotic coupling: power transmission by protocity. Biochem. Soc. Trans. 1976; 4: 399–430.PubMedGoogle Scholar
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.PubMedGoogle Scholar
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.PubMedCrossRefGoogle Scholar
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.PubMedCrossRefGoogle Scholar
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.PubMedCrossRefGoogle Scholar
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.PubMedCrossRefGoogle Scholar
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.PubMedGoogle Scholar
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.CrossRefGoogle Scholar
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.PubMedCrossRefGoogle Scholar
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.Google Scholar
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.PubMedGoogle Scholar
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
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.PubMedCrossRefGoogle Scholar
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.PubMedGoogle Scholar
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.PubMedGoogle Scholar
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
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.PubMedCrossRefGoogle Scholar