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The role of the duodenum in the regulation of the lower esophageal sphincter pressure was studied in 3 anesthetized dogs with a duodenal fistula by relating the lower esophageal sphincter pressure with plasma gastrin and secretin level during intraduodenal acid infusion test. Instillation of hydrochloric acid into the duodenum produced an initial fall followed by a significant and sustained increase of the lower esophageal sphincter pressure. The initial fall of the lower esophageal sphincter pressure was found to correspond to a prompt but transient rise of plasma secretin concentration, while plasma gastrin did not change significantly throughout the experimental period. It is concluded that duodenum may be an important regulator of the lower esophageal sphincter pressure in the dog through secretin and other unknown factors.
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Eight Angus steers (290 +/- 8 kg), surgically prepared with pancreatic pouch-duodenal reentrant cannulas and abomasal infusion catheters were used in a replicated 4 x 4 Latin square experiment to investigate the effects of abomasal infusion of starch hydrolyzate (SH) and/or casein on pancreatic exocrine secretion and plasma concentration of hormones. Steers were fed a basal diet of alfalfa (1.2 x NEm) in 12 equal portions daily. Abomasal infusion treatments (6-L total volume infused per day) were water (control), SH [2.7 g/(kg BW x d)], casein [0.6 g/(kg BW x d)], and SH + casein. Periods were 3 d for adaptation and 8 d of full infusion. Pancreatic juice and jugular blood samples were collected over 30-min intervals for 6 h on d 11. Weight and pH of pancreatic samples were measured, and a 10% subsample was composited and frozen until analysis of total protein and pancreatic enzyme activities. The remaining sample was returned to the duodenum. Plasma was harvested and frozen until analyzed. Pancreatic juice (67 mL/h) and protein (1.8 g/h) secretion rates were not affected by nutrient infusion. There were SH x casein interactions for all pancreatic enzyme secretions (U/h; alpha-amylase, P < 0.03; trypsin, P < 0.08; and chymotrypsin, P < 0.03) and plasma insulin concentration (P < 0.10). Secretion of pancreatic enzymes was increased by SH (trypsin) and casein (alpha-amylase, trypsin, and chymotrypsin) but not when SH + casein were infused together. Glucose (P < 0.10) and cholecystokinin octapeptide concentrations (CCK-8; P < 0.05) were increased by SH, but glucagon was decreased (P < 0.10). Casein decreased (P < 0.10) plasma CCK-8 concentrations. These data indicate that positive effects of postruminal casein on enzyme secretion were inhibited by SH, emphasizing the complexity of the regulatory mechanisms involved in dietary adaptation of pancreatic exocrine secretion. Changes in hormone concentration may not relate directly to changes in enzyme secretion.
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We investigated the mechanism of humoral control of bile discharge into the duodenum. The actions of the GB, SO and duodenum were monitered by cinecholecystocholangiogrphy combined with manometry of the SO area using a hydraulic-capillary infusion system or MIKRO-TIP, and these were correlated with the plasma concentrations of GI hormones. We concluded that one of the most significant roles of the sphincter of Oddi is to limit bile flow. This postulation was favored by the observation of so-called 'spasm' of the SO where 8 to 10 contractions per min., in contrast to 'normal' contraction of 2 to 4 per min., were seen. On this special occasion, no discharge of the contrast material into the duodenum was noticed. Exogenous or endogenous CCK causes a coordinated action of the GB contraction, the SO relaxation and relaxation of the adjacent segment of the duodenum, resulting in an effective discharge of bile into the duodenum. The effect of Pancreozymin on bile discharge revealed by endoscopic cinematography was that Pancreozymin first made the orifice of the papilla of Vater widely open with a profuse bile flow and following this, caused a repeated shuttering action of the orifice with minimal discharge of bile. This observation opposes the opinion that active SO contractile activity is necessary to bile flow into the duodenum. Caerulein or CCK-33 caused no 'post-inhibition' enhancement of the SO activity that was seen in case of Pancreozymin administration. Motilin, calcium or other substances contained in Pancreozymin (Boots) might be causative for this enhancement.