1985 Volume 82 Issue 8 Pages 1924-1931
To determine the significance of manometric pressure of the pancreatic duct, duodenoscopic measurements of the papillary sphincter zone and pancreatic main duct in control subjects (n=20) and patients with chronic pancreatitis (n=20), and the effects of exogenous glucagon or secretin were studied. There was not any significant difference between control subjects and patients with chronic pancreatitis without papillitis in the motility of the sphincter of Oddi. The pancreatic main ductal pressure in patients with chronic pancreatitis (54.5±29.9mmHg) was significantly higher than that in control subjects (16.2±8.7mmHg). In patients (n=6) with minimal-change chronic pancreatitis (MIP) without dilatation of pancreatic main duct, patients (n=10) with moderate-change chronic pancreatitis (MOP) and patients (n=4) with advanced-change chronic pancreatitis (ADP), the pancreatic main ductal pressure showed 51.8mmHg, 62.8mmHg and 37.8mmHg on average, respectively. The viscosity of pure pancreatic juice, which appeared to be one of constituents of resistance to secretion of pancreatic juice, in patients with chronic pancreatitis (5.8 centi-Poise: cP) in the basal secretory phase was significantly higher than that in control subjects (1.61 cP). But there was not any relationship between pancreatic main ductal pressure and viscosity of pure pancreatic juice. These data lead to the hypothesis that increased pancreatic ductal pressure in patients with chronic pancreatitis without papillitis appeared not to be due to papillary dysfunction, but to increased viscosity or other unknown factors; for example, basal secretory pressure, and then initially increased pancreatic ductal pressure may induced dilatation of the pancreatic main duct. Moreover, glucagon or secretin has a reducing effect on pancreatic ductal pressure in patients with chronic pancreatitis.
Nippon Shokakibyo Gakkai Zasshi
Nippon Shokakibyo Gakkai Zasshi Kou
