The Effect of Antecedent Acute Ethanol Ingestion on the Pancreas Ultrastructure in Taurocholate Pancreatitis in Rats

Andrzejewska, Anna; Długosz, Jan; Jurkowska, Grażyna

doi:10.1006/exmp.1998.2226

Cited by 13 publications

(13 citation statements)

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“…Therefore, the possible effect of chronic ethanol intake did not produce the characteristic signs of chronic pancreatitis. However, APTE et al (4) observed an increase in the synthesis of the lysosomal enzyme cathepsin B after chronic ethanol, which may be relevant to the pathogenesis of alcoholic pancreatitis and coincides with ours and other authors' results concerning the increased damage of the pancreas observed after experimentally-induced acute pancreatitis (3,7).…”

Section: Discussionsupporting

confidence: 71%

“…Though it has been reported that the pancreas of ethanol-fed rats is more susceptible to damage after experimentallyinduced pancreatitis (3,7) than that of control rats, we could not find any increase in plasmatic amylase levels in ethanol-fed rats. Moreover, the histologic evaluation of pancreatic tissue from alcoholized animals did not show any apparent difference (results not shown).…”

Section: Discussioncontrasting

confidence: 51%

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Influence of chronic ethanol consumption on the muscarinic cholinergic control of rat pancreatic acinar cells

Acosta

Román

López

et al. 2000

J. Physiol. Biochem.

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There are a number of hypothetical explanations for the actions of ethanol on the exocrine pancreas; among them, the cholinergic hypothesis has received special attention. According to this hypothesis, chronic alcohol consumption induces alterations in the control of exocrine pancreatic function resulting in cholinergic hyperstimulation of pancreatic acinar cells and their muscarinic receptors. Our aim was to investigate the cholinergic control of pancreatic enzyme secretion and the number and affinity of muscarinic receptors in the pancreatic acinar cells of rats subjected to chronic ethanol ingestion. We also investigated whether a high-fibre diet modifies the actions of ethanol on these aspects of the exocrine pancreatic function. Four groups of rats received either a standard or a high fibre diet, and either water or 20% (v/v) ethanol. After 6 months of treatment, isolated pancreatic acini were used for the determination of carbachol-stimulated amylase secretion and for the analysis of muscarinic receptors, using 1-[N-methyl-3H]scopolamine as a radioligand. Neither chronic ethanol intake nor a high fibre diet caused any apparent alteration in pancreatic histology, neither did them modify plasmatic amylase levels. Chronic alcoholization resulted in a significant increase in the amylase released from pancreatic acini in response to carbachol stimulation, but it did not affect either the number or the affinity of pancreatic acinar muscarinic receptors. The actions of ethanol are not significantly modified by the simultaneous consumption of a high fibre diet.

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Section: Discussionsupporting

confidence: 71%

Section: Discussioncontrasting

confidence: 51%

Influence of chronic ethanol consumption on the muscarinic cholinergic control of rat pancreatic acinar cells

Acosta

Román

López

et al. 2000

J. Physiol. Biochem.

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“…Long-term ethanol feeding alone has failed to induce acute or chronic pancreatitis in animals (1,9,43,44). In addition, CP occurs in only a limited number of heavy drinkers (20,37).…”

Section: Discussionmentioning

confidence: 98%

A new model of chronic pancreatitis in rats

Yamamoto

Otani²,

Ōtsuki³

2006

American Journal of Physiology-Gastrointestinal and Liver Physi

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This study was designed to examine whether continuous pancreatic ductal hypertension (PDH) plays an important role in the onset and development of chronic pancreatitis (CP). Pancreatic, biliary, and duodenal cannulas were implanted in male Wistar rats. PDH was induced by vertically raising the free end of the pancreatic duct cannula to exert a hydrostatic pressure and maintained for 2 wk. PDH was gradually increased, but when the pancreatic juice (PJ) flow was interrupted, PDH was decreased to restore PJ flow. The induction of PDH resulted in a marked reduction of amylase activity in PJ and an increase in serum amylase activity. At 2 wk after persistent PDH, pancreatic exocrine function was markedly decreased in response to a bolus injection of secretin (100 pmol/kg) compared with the control group. Histological examination revealed interlobular as well as intralobular fibrosis in the form of nodular pancreatitis at 2 wk after the induction of PDH. Immunohistochemistry revealed the expression of fibronectin and collagen types I and III. Quantitative real-time RT-PCR showed an increase in transforming growth factor-beta(1) mRNA expression in the pancreas during PDH. The present results suggest that PDH plays an important role in the onset and development of CP. Furthermore, our animal model seems useful for investigating the mechanisms of CP in rats.

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“…However, no animal model has been developed in which acute experimental pancreatitis is induced by acute ethanol application alone [12][13][14]. Animal models with direct installation of ethanol into the pancreatic duct are of no relevance in the setting of human disease as installation of any substance corresponding to concentration and pressure leads to pancreatic damage.…”

Section: Animal Models Of Acute Ethanol Administrationmentioning

confidence: 99%