SUMMARY A new approach in the diagnosis of exocrine pancreatic insufficiency has been evaluated in animals. The method involves the oral administration of a chymotrypsin-labile peptide which contains p-aminobenzoic acid (PABA) as a tracer group. In the small bowel in the presence of chymotrypsin, the PABA is split from the peptide and is rapidly absorbed. The amount of PABA (as total aromatic amines) recovered in the urine during the six hours after the dose is used as an index of exocrine pancreatic function. The procedure has been shown to be reliable in detecting surgically induced pancreatic insufficiency in rats, swine, and dogs.A new tubeless test for exocrine pancreatic insufficiency was suggested to us by Dr Norton J. Greenberger. Preliminary studies showed the test to be highly reliable in detecting pancreatic deficiency in animals (Imondi, Stradley, Wolgemuth, and Brown, 1971). In this procedure a synthetic peptide composed of an aromatic amino acid and a readily absorbable tracer group, p-aminobenzoic acid (PABA), is administered orally. In the presence of chymotrypsin, the peptide is split with the liberation of PABA which is absorbed from the gut, undergoes conjugation, and is excreted in the urine. The amount of PABA (aromatic amines) in the urine is used as a measure of exocrine pancreatic function. Methods ANIMALSExocrine pancreatic insufficiency was produced surgically in male and female Sprague-Dawley rats (200-400 g), mongrel dogs (5-10 kg), and West African Guinea swine (8-20 kg). The rats were anaesthetized with ether and the common bile duct was doubly ligated and sectioned near its attachment to the duodenum. These animals are referred to in this paper as B-PDL rats to denote the exclusion of both bile and pancreatic juice from the intestine.These rats, in which bile was excluded from the intestine, were prepared by ligating the bile duct just below the hilus of the liver (Grossman, 1958). An 18-hour recovery period was allowed before administering the peptide to the rats. Pancreatic Received for publication 2 June 1972. duct ligation and section (Pekas, Hays, and Thompson, 1964) was performed in the swine under halothane anaesthesia. These animals, referred to as PDL, were allowed a minimum of three postoperative recovery days before drug testing. Dogs were made exocrine pancreatic deficient by ligating the pancreatic ducts and separating the pancreas from the duodenum with omentum (Grossman, 1962). Studies in dogs were not begun until at least one week after surgery. The surgical procedures did not significantly affect the ability of the animals to absorb and excrete orally administered PABA. TEST PROCEDURE in vivo Animals to be tested were fasted overnight. The test peptide was administered orally as an aqueous solution of its sodium salt. After dosing the animals were confined individually to metabolism cages. Food was withheld, but water was allowed ad libitum. Urine collections were made at the times stated in each experiment. The total aromatic amine concentration of the urine...
The equine Paneth cell response to a shift in the microbial balance of the intestinal tract was studied by inducing an acute episode of alimentary laminitis in 6 mature ponies. The normal bacterial population of the gut was modified by administration of a carbohydrate-rich ration. During acute laminitis a dramatic degranulation of the Paneth cells occurred in the intestinal glands throughout the duodenum, jejunum, and ileum. Bacteriocidal lysozyme, which was immunohistochemically identified as a component of the Paneth cell secretory granule, was evident in the glandular lumina and in degranulated Paneth cells. These results indicate that lysozyme is secreted by the equine Paneth cell in an apparent attempt to regulate the changing microbial population induced by carbohydrate overload of the gut. From these observations, it is suggested that the Paneth cell plays a role in the mucosal defense system of the equine intestinal tract.
In order to evaluate the enteropancreatic hormone axis in dogs with pancreatic acinar atrophy, we measured the release of gastric inhibitory polypeptide and pancreatic polypeptide in response to a standard meal and a meal containing pancreatic enzymes in affected dogs and controls. Postprandial release of pancreatic polypeptide was normal in dogs with pancreatic atrophy and was not affected by addition of pancreatic enzymes to the food. Gastric inhibitory polypeptide was not released after a standard meal in affected dogs, but this blunted response was corrected by the addition of pancreatic enzymes to the food. Feeding the enzyme alone did not stimulate a gastric inhibitory polypeptide response. These results, in part, support similar observations previously reported in children with exocrine pancreatic insufficiency associated with cystic fibrosis. We conclude that dogs with idiopathic pancreatic acinar atrophy can be used as an animal model for future study of enteropancreatic hormonal abnormalities that occur in human beings with exocrine pancreatic insufficiency.
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