The behavior of mucopolysaccharide in the pancreatic juice in chronic pancreatitis

Wakabayashi, Akira; Takeda, Yoshinobu

doi:10.1007/bf01071952

Cited by 19 publications

(6 citation statements)

References 7 publications

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“…These results suggest that PDH enhanced nonenzymatic proteins secretion, and such proteins were attributable to an increase in the protein concentration in PJ. Because nonenzymatic proteins have been shown to relate with the viscosity of PJ or formation of protein plugs (22,23,51), it is likely therefore that these proteins play some roles in the progression of pancreatic fibrosis in our model.…”

Section: Discussionmentioning

confidence: 98%

“…Sarles et al (39) previously reported that protein plugs are present in all small pancreatic ducts in the initial lesions of human CP. In addition, several studies have shown that the viscosity of pancreatic juice (PJ) is increased in patients with CP (22,51). Moreover, Bradley (6) demonstrated a significantly higher pancreatic ductal pressure in patients with CP compared with that in control subjects.…”

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confidence: 98%

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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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Section: Discussionmentioning

confidence: 98%

mentioning

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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“…Elevated pancreatic duct pressure has been demonstrated in patients with chronic pancreatitis 40 , which may be due to increased viscosity of pancreatic juice 41 , 42 . However, it was unclear whether chronic pancreatitis arises from or leads to increased pancreatic duct pressure until it was demonstrated experimentally that sustained elevation of pancreatic duct pressure in rats caused chronic pancreatitis 43 , 44 .…”

Section: Discussionmentioning

confidence: 99%

Piezo1 is a mechanically activated ion channel and mediates pressure induced pancreatitis

et al. 2018

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Merely touching the pancreas can lead to premature zymogen activation and pancreatitis but the mechanism is not completely understood. Here we demonstrate that pancreatic acinar cells express the mechanoreceptor Piezo1 and application of pressure within the gland produces pancreatitis. To determine if this effect is through Piezo1 activation, we induce pancreatitis by intrapancreatic duct instillation of the Piezo1 agonist Yoda1. Pancreatitis induced by pressure within the gland is prevented by a Piezo1 antagonist. In pancreatic acinar cells, Yoda1 stimulates calcium influx and induces calcium-dependent pancreatic injury. Finally, selective acinar cell-specific genetic deletion of Piezo1 protects mice against pressure-induced pancreatitis. Thus, activation of Piezo1 in pancreatic acinar cells is a mechanism for pancreatitis and may explain why pancreatitis develops following pressure on the gland as in abdominal trauma, pancreatic duct obstruction, pancreatography, or pancreatic surgery. Piezo1 blockade may prevent pancreatitis when manipulation of the gland is anticipated.

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“…In cases of alcoholic chronic pancreatitis, continuous drinking by the patient is considered to increase the protein concentration of the pancreatic juice (7,8) and thus its viscosity (9, 10), leading to formation of a protein plug in the pancreatic duct (11,12) and recurrent attacks of pancreatitis. Attempts have been made to treat such patients with secretin (13), and endoscopic removal of the pancreatic juice and protein plug (14), but it is difficult to achieve a permanent effect.…”

Section: Discussionmentioning

confidence: 99%

Mediastinal Pancreatic Pseudocyst Caused by Obstruction of the Pancreatic Duct Was Eliminated by Bromhexine Hydrochloride

et al. 2004

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A 49-year-old man, who had a 30-year history of drinking the equivalent of 80 g of ethanol per day, underwent a detailed medical examination for cough and dyspnea. Chest-abdominal computed tomography and endoscopic retrograde pancreatography led to the diagnosis of a mediastinal pancreatic pseudocyst resulting from obstruction of the pancreatic duct by a protein plug. The pseudocyst rapidly improved with conservative treatment with camostat mesilate, H2-receptor antagonist and digestive enzymes. Although the patient abstained from alcohol for approximately 6 months, he resumed drinking, leading to recurrent attacks of pancreatitis. Bromhexine hydrochloride was then administered for 6 months, with the expectation that it would have a mucolytic effect on the pancreatic juice, resulting in improvement in the clinical symptoms, pancreatic enzymes and pancreatic exocrine function, as well as elimination of the protein plug. Bromhexine hydrochloride may be a new therapy for pathological states, such as alcoholic chronic pancreatitis, in which there is increased viscosity of the pancreatic juice because of elevated protein concentration, leading to protein plug formation and temporary blockage of the pancreatic duct.

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The behavior of mucopolysaccharide in the pancreatic juice in chronic pancreatitis

Cited by 19 publications

References 7 publications

A new model of chronic pancreatitis in rats

A new model of chronic pancreatitis in rats

Piezo1 is a mechanically activated ion channel and mediates pressure induced pancreatitis

Mediastinal Pancreatic Pseudocyst Caused by Obstruction of the Pancreatic Duct Was Eliminated by Bromhexine Hydrochloride

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