The role of CGRP and afferent nerves in the modulation of pancreatic enzyme secretion in the rat

1997 ◽  
Vol 22 (2) ◽  
pp. 137-146
Author(s):  
Jolanta Jaworek ◽  
Stanisław J. Konturek ◽  
Aleksandra Szlachcic
1991 ◽  
Vol 260 (2) ◽  
pp. G197-G206 ◽  
Author(s):  
W. E. Schmidt ◽  
W. Creutzfeldt ◽  
A. Schleser ◽  
A. R. Choudhury ◽  
R. Nustede ◽  
...  

To evaluate the physiological role of cholecystokinin (CCK) in humans, we studied the influence of the specific CCK receptor antagonist loxiglumide (CR 1505) on gallbladder contraction, pancreatic enzyme output, plasma CCK concentrations, mouth-to-cecum transit time (MCTT), stool weight, and fecal fat excretion. Infusion of CCK-8, producing CCK plasma levels of 10-12 pmol/l, decreased gallbladder volume to 21% of the initial volume (P less than 0.01) and increased bilirubin output 8- to 10-fold and pancreatic enzyme secretion 2- to 4-fold. Infusion of loxiglumide (10 mg.kg-1.h-1 iv) abolished CCK-8-stimulated enzyme and bilirubin output. Basal gallbladder volume increased 68% during loxiglumide infusion (P less than 0.001) and 137% (P less than 0.001) after 7 days of oral loxiglumide treatment (3 x 1.6 g/day). Gallbladder contraction and bilirubin output in response to the intraduodenal instillation of a liquid meal (382 kcal) was completely inhibited by loxiglumide; gallbladder volume even increased 45% postprandially during loxiglumide infusion (P less than 0.02) and 145% after long-term loxiglumide treatment (P less than 0.001). Meal-stimulated pancreatic enzyme output was diminished 46-53% after acute and 25-29% after chronic administration of loxiglumide. Meal-stimulated integrated plasma CCK-immunoreactive (CCK-ir) concentrations, determined by RIA, were 3.2-fold higher during loxiglumide infusion (P less than 0.02); plateau CCK levels were markedly elevated (10.1 +/- 1.4 vs. 3.7 +/- 0.5 pM). Plasma CCK-like bioactivity, measured by a sensitive bioassay, was identical to CCK-ir levels in the absence of loxiglumide; in the presence of loxiglumide, no circulating CCK-like bioactivity was detectable, indicating complete inhibition of plasma CCK. MCTT was augmented 24% (P less than 0.05). Oral treatment with loxiglumide increased stool weight 72% (P less than 0.01) and fecal fat excretion 186% (P less than 0.001). In conclusion, 1) meal-induced gallbladder contraction and fasting tone are primarily controlled by CCK; 2) the contribution of CCK to the intestinal phase of postprandial pancreatic enzyme secretion is 40-50%; 3) GI motility and absorption are partially controlled by CCK; and 4) postprandial CCK secretion is substantially augmented by loxiglumide via an unknown mechanism.


1987 ◽  
Vol 92 (2) ◽  
pp. 449-458 ◽  
Author(s):  
Ulrich R. Fölsch ◽  
Per Cantor ◽  
Harald M. Wilms ◽  
Anton Schafmayer ◽  
Horst Dieter Becker ◽  
...  

1990 ◽  
Vol 25 (sup178) ◽  
pp. 99-105 ◽  
Author(s):  
A. J. L. De Jong ◽  
J. B. M. J. Jansen ◽  
C. B. H. W. Lamers

1991 ◽  
Vol 101 (2) ◽  
pp. 503-511 ◽  
Author(s):  
Michael Fried ◽  
Urs Erlacher ◽  
Werner Schwizer ◽  
Christine Löchner ◽  
Jacques Koerfer ◽  
...  

Pancreas ◽  
1990 ◽  
Vol 5 (2) ◽  
pp. 194-199 ◽  
Author(s):  
Alphons J. L. de Jong ◽  
Jan B. M. J. Jansen ◽  
Jan C. M. Hafkenscheid ◽  
Cornelis B. H. W. Lamers

2020 ◽  
Vol 1 (30) ◽  
pp. 30-36
Author(s):  
E. A. Krylova ◽  
D. V. Aleinik

The article presents the results of a study of the effectiveness of the use of an inhibitor of pancreatic enzyme secretion of octreotide (Octrade) for the prevention of pancreatitis after endoscopic retrograde cholangiopancreatography (ERCP). It was shown that the administration of Octrade at a dose of 0.3 mg in 500 ml of 0.9 % NaCl by continuous intravenous infusion for 7 hours and then 0.1 mg of Octrade subcutaneously at 6 and 12 hours after the end of intravenous infusion significantly reduced the frequency of pancreatitis (4.0 % and 22.2 %; p < 0.05) and hyperamylasemia (8.0 % and 25.9 %; p < 0.05) after ERCP. It is concluded that Octrade is effective in preventing the development of pancreatitis and hyperamilasemia after ERCP.


Sign in / Sign up

Export Citation Format

Share Document