COMPOSITION OF GASTRIC JUICE AND BILE IN RATS AT THE EXPERIMENTAL CHRONIC PANCREATITIS
Z.А. Gorenko, О.А. Grinchenko, S.P. Veselsky, V.M. Baban
Peter Bogach Institute of Physiology Educational and
Scientific Centre “Institute of Biology” National Taras
Shevchenko University of Kyiv
DOI: https://doi.org/10.15407/fz61.06.086

Abstract
Chronic pancreatitis is an inflammatory disease of the
pancreas, which is characterized by destruction of pancreatic
secretory parenchyma and progressing exocrine and endocrine
insufficiency. Usually these patients have complications as
cardiovascular, renal, respiratory and liver failure, and various
gastric dysfunctions. The data of clinical observations do
not reveal fully the functional state of the stomach and liver
in chronic pancreatitis also remains an open question about
the quality of the gastric juices and bile by this pathology.
Therefore our aim was to investigate the secretory functions
of the stomach and liver features in rats at the experimental
chronic pancreatitis. This pathology modeled using L-arginine.
Basal gastric secretion was investigated in chronic experiment
by aspiration method for 10th and 63rd days, and pancreas
and liver – in acute experiments at 13th and 68th days after
the last administration of L-arginine. It was established that
the character of the secretory response of the digestive tract
depends on the duration of the pathology course. On the
10th day the functional state of the gastric secretory glands
in rats with chronic pancreatitis characterized by twice
increase of gastric acid production but decrease the level of
hexosamines on 23,8% (P<0,001) that indicate a increase of
gastric content aggressiveness and mucus producing cells
secretory insufficiency. In these animals the rate of total protein
decreased on 61,7 % (Р<0,05). On the 13th day observed
the increase of pancreatic juice on 332% (Р<0,01), hepatic
secret volume on 74,9% (Р<0,001) and redistribution in the
cholates spectrum: glycocholates level increased but tauro-,
free and total dehydroxylated bile acids decreased. These
changes suggest deterioration of bile detergent properties,
inhibition of acidic pathway of bile acids biosynthesis and
conjugation of cholates with taurine. In two months total
deficit of amino acids in gastric juice correlated with exocrine
pancreatic insufficiency. Herein the acidity of gastric content
partially restored, while the level of protein and mucus
secretion proceed to decline. Consequently gastric mucosa
is more vulnerable. In these rats the rates of free bile acids
greatly increased while tauro- and glycocholates significantly
decreased. Thus the processes of hydroxylation and
conjugation of bile acids with amino acids inhibited suggesting
interruption of synthetic and detoxification functions of the
liver. The present work is important for comprehension the
pathophysiological aspects of chronic pancreatitis particularly
the digestive system functioning features at this pathology.
These data could be considered in the appointment of treatment
to avoid complications.
Keywords:
chronic pancreatitis; gastric secretion; hydrochloric acid; bile formation; bile acids.
References
- Stepanov YuM, Krylova OO, Rudenko AI, Tropko LV, Seitl TM The peculiarities of secretory function and character of microbial contamination of the stomach in various forms of chronic pancreatitis. Modern Gastroenterol. 2013; 3(71):33-9. [Ukrainian].
- Cao M, Li J, Xu J, Feng Y, Lin X, Han T, Chen C. Cannabinoid HU210 protect isolated rat stomach against impairment caused by serum of rats with experimental acute pancreatitis. PLoS ONE. 2012; 7(12): e52921.
- Kong L, Santiago N, Han TQ, Zhang SD. Clinical characteristics and prognostic factors of severe acute pancreatitis.World J Gastroenterol. 2004;10(22):3336-8.
CrossRef
PubMed PubMedCentral
- Browne GW, Pitchumoni CS. Pathophysiology of pulmonary complications of acute pancreatitis. World J Gastroenterol. 2006; 12(44):7078-96.
- Murr MM, Yang J, Fier A, Kaylor P, Mastorides S, Norman JG. Pancreatic elastase induces liver injury by activating cytokine production within Kupffer cells via nuclear factor-Kappa B. J Gastrointest Surg. 2002; 6:474-80.
CrossRef
- Mayev IV, Kucheryavy YuA. Gastric acid production and chronic pancreatitis: how strong is the mutual relationship? RJGHC. 2008; 3:4-14. [Russian].
- Hegyi P, Raconzay Z, Sari R, God C, Lonovics J, Takacs T, Czako L. L-arginine-induced experimental pancreatitis. World J Gastroenterol. 2004; 10(14):2003-9.
CrossRef
PubMed PubMedCentral
- Cuthbertson CM, Christophi C. Disturbances of the microcirculation in acute pancreatitis. Br J Surg. 2006; 93(5):518-30.
CrossRef
PubMed
- Folch-Puy E. Importance of the liver in systemic complications associated with acute pancreatitis: the role of Kupffer cells. J Pathol. 2007; 211(4):383-8.
CrossRef
PubMed
- Aghdassi AA, Mayerle J, Christochowitz S, Weiss FU, Sendler M, Lerch MM. Animal model for investigating chronic pancreatitis. Fibrogenesis & tissue repair. 2011; 4(1):26.
CrossRef
PubMed PubMedCentral
- Delaney CP, McGeeney KF, Dervan P, Fitzpatrick JM. Pancreatic atrophy: a new model using serial intraperitoneal injections of L-arginine. Scand J Gastroenterol. 1993; 28(12):1086-90.
CrossRef
PubMed
- Czako L, Takacs T, Varga IS, Tiszlavicz L, Hai DQ, Hegui P, Matkovics B, Lonovics J. Oxidative stress in distant organs and the effects of allopurinol during experimental acute pancreatitis. Int J Pancreatol. 2000; 27(3):209-16.
CrossRef
- Takacs T, Czako L, Morschl E, Laszlo F, Tiszlavicz L, Rakonczay ZJr, Lonovics J. The role of nitric oxide in edema formation in L-arginine-induced acute pancreatitis. Pancreas. 2002; 25(3):277-82.
CrossRef
PubMed
- Makhija R, Kingsnorth AN. Cytokine storm in acute pancreatitis. J Hepatobiliary Pancreat Surg. 2002; 9(4):401-10.
CrossRef
PubMed
- Elfar M, Gaber LW, Sabek O, Fisher CP, Gaber AO. The inflammatory cascade in acute pancreatitis: relevance to clinical disease. Surg Clin North Am. 2007; 87(6):1325-40.
CrossRef
PubMed
- Tashiro M, Schäfer C, Yao H, Ernst SA, Williams LA. Arginine induced acute pancreatitis alters the actin cytoskeleton and increases heat shock protein expression in rat pancreatic acinar cells. Gut. 2001; 49:241-50.
CrossRef
PubMed PubMedCentral
- Yamaguchi T, Kihara Y, Taguchi M, Nagashiro Y, Tashiro M, Nakamura H, Otsuki M. Persistent destruction of the basement membrane of the pancreatic duct contrinutes to progressive acinar atrophy in rats with experimentally induced pancreatitis. Pancreas 2005; 31(4):365-72.
CrossRef
PubMed
- Campbell CA, Gaskin PJ, Darton J, Chiu P, Lee K, McLean PG. Validation of a conscious rat model for the discovery of novel agents that inhibit gastric acid secretion. Eur J Pharmacol. 2008; 589(1-3):260-3.
- Kochetov GA. A practical guide to enzymology. Severin S.E., editor. Moskow: Graduate school: 1980. [Russian].
- Korobeinikova EM, Mescheryakova GV. Determination of free amino acids in the serum and urine of healthy children. Laboratory case. 1981; 4:221-4. [Russian].
- SU 1624322 A1 copyright certificate description No. 4411066/14 IPC G 01 N 33/50. A method for determination of bile acids in biological liquid. Veselsky SP, Lyashchenko PS, Lukyanenko IA. [Russian].
- Hrinchenko OA, Ianchuk PI. The pathways of taurine influences on gastric secretion. Fiziol Zh. 2010; 56(4):111-20. [Ukrainian].
- Girish BN, Rajesh G, Vaidyanathan K, Balakrishnan V. Alterations in plazma amino acid levels in chronic pancreatitis. JOP J Pancreas. 2011; 12(1):11-8.
- Singh J, Salido GM, Camello PJ, Lennard R, Render C, Wisdom D, Pozo MJ, Pariente JA. Interactions between cholecistokinin-octapeptide and secretin in the rat pancreas in vivo and in vitro. Exp Physiol. 1992; 77(1):191-204.
CrossRef
PubMed
- Gielkens HA, Eddes EH, Vecht J, van Oostayen JA, Lamers CB, Maslee AA. Gallbladder motility and cholecystokinin secretion in chronic pancreatitis: relationship with exocrine pancreatic function. J Hepatol. 1997; 27(2):306-12.
CrossRef
- Otsuki M. Pathophysiological role of cholecystokinin in humans. J Gastroenterol Hepatol. 2000; 15 Suppl: D71-83.
- Guerrier M, Attili F, Alpini G, Glaser S. Prolonged administration of secretin to normal rats increases biliary proliferation and secretin-induced ductal secretory activity. Hepatobiliary Surg Nutr. 2014; 3 (3): 118-25.
- Reeve JRJr, Wu V, Keire D, Faull K, Chew P, Solomon TE, Green GM, Coskun T. Differential bile-pancreatic secretory effects of CCK-58 and CCK-8. Am J Physiol Gastrointest Liver Physiol. 2004; 286(3):G395-G402.
- Ding WG, Tooyama I, Kimura H, Kuriyama K. Immunohistochemical localization of taurine-conjugated bile acids in the liver of mouse, rat, monkey and human. Adv Exp Med Biol. 1994; 359:91-8.
CrossRef
PubMed
- Ikeda S, Tachikawa M, Akanuma S, Fujinawa J, Hosoya K. Involvement of γ-aminobutiric acid transporter 2 in the hepatic uptake of taurine in rats. Am J Physiol Gastrointest Liver Physiol. 2012; 303(3):G291-G297.
- Vasheka IP, Vesel'skyĭ SP, Horenko ZA, Hrinchenko OA, Karbovs'ka LS, Makarchuk MIu. The influence of amylin on the bile acid spectrum in rats. Fiziol Zh. 2014; 60(3):46-53. [Ukrainian].
- Furutani M, Arii S, Higashitsuji H, Mise M, Fukumoto M, Nakano S, Nakayama H, Immamura M, Fujita J. Reduced expression of kan-1 (encoding putative bile acids-CoAamino acid N-acyltransferase) mRNA in livers of rats after partial hepatectomy and during sepsis. Biochem J. 1995; 311(1):203-8.
CrossRef
PubMed PubMedCentral
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