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Biomedical subjects

P Layer

Publications and source records attributed to P Layer.

At least 109 records · Page 6Linked to original sources
PubMed1992

[Intestinal regulation of pancreatic enzyme secretion: stimulatory and inhibitory mechanisms].

How exocrine pancreatic secretion is regulated is only partly known. It is assumed that interaction of several neural and hormonal mechanisms is involved. In man, the intestinal component of these control mechanisms is very important while extra-intestinal mechanisms (such as the cephalic and the gastric phase) play lesser roles. Regulation of pancreatic secretion by the intestine is composed of three main mechanisms. 1. The proximal intestinal (duodenal) phase of the secretory response to a meal is elicited by nutrients within the proximal intestinal lumen. It is mediated mainly by interactions between cholinergic reflexes and release of the peptide hormone cholecystokinin (CCK). Recent data suggest that part of the action of CCK is not exerted directly on the acinar cellular level, but rather by modulation of cholinergic inputs. 2. The distal intestinal (ileal) phase is elicited by contact of the distal intestinal mucosa with nutrients that pass through the ileal lumen due to physiological malabsorption. The ileum (in contrast to the duodenum) induces net-inhibition of pancreatic secretion. The mediation is unknown, candidate mediators are PYY and GLP-1. 3. Intestinal feedback-regulation of pancreatic secretion in humans is controlled by intraluminal protease activity; this mechanism is not covered in the present paper.

Animals↗
PubMed1991

[Influence of the ileum on the regulation of gastrointestinal motility].

Under normal conditions a "physiologic malabsorption" and thus nutrients in the lower small intestine in the late postprandial state can be observed in humans. To study the effects of "physiologic" quantities of nutrients in the distal small intestine on upper gastrointestinal motor functions, 9 healthy subjects were intubated with an oro-ileal multi-lumen tube. The continuous perfusion of the duodenum with essential amino acids induced a fed motility pattern. In 12 out of 14 cases additional ileal perfusion with carbohydrates (60 kcal), but not with saline, converted the fed motility pattern to a pattern characteristic of the interdigestive state. These findings suggest that the ileum takes part in the late postprandial regulation of proximal gastrointestinal motor functions in humans.

Amino Acids, Essential↗
PubMed1990

Human pancreatic secretion and intestinal motility: effects of ileal nutrient perfusion.

To study the effects of intraileal nutrients on human pancreatic secretion and gastrointestinal motility, nine healthy subjects were intubated with an oroileal multilumen tube for ileal perfusion, duodenal juice aspiration, and intestinal motility recording. The duodenum was perfused continuously with essential amino acids to induce submaximal stimulation of pancreatic enzyme secretion and fed motility pattern. Additional ileal perfusion with carbohydrate at quantities similar to those observed under physiological late postprandial conditions or fat at isocaloric loads significantly decreased pancreatic enzyme outputs by greater than 80% (P less than 0.001) compared with saline. Ileal carbohydrate or fat induced a duodenal motor activity front that migrated distally and was followed by reduced motility. In summary, ileal delivery of small quantities of nutrient markedly decreased endogenously stimulated pancreatic enzyme secretion in humans. This was associated with specific changes in fed intestinal motility that converted to patterns characteristic of the interdigestive state. Our findings suggest that the distal small intestine may participate in the late postprandial regulation of gastrointestinal function in humans.

Adult↗
PubMed1990

Feedback regulation of human pancreatic secretion. Effects of protease inhibition on duodenal delivery and small intestinal transit of pancreatic enzymes.

To determine the effects of luminal protease inhibition on duodenal delivery and the intraluminal fate of pancreatic enzymes, six healthy subjects were intubated with an oro-ileal multilumen tube assembly. By using nonabsorbable markers, cumulative trypsin, chymotrypsin, lipase, and amylase activities were measured as delivered to duodenum, midjejunum, and distal ileum, with or without simultaneous duodenal perfusion of the protease inhibitor camostat at graded doses. Compared with saline, camostat (a) inhibited trypsin activity in the entire small intestinal lumen by up to 99%, and significantly reduced chymotrypsin activity by up to 89%; (b) significantly increased duodenal deliveries of lipase activity, amylase activity and volume; (c) did not influence plasma cholecystokinin concentrations; and (d) significantly increased jejunal and ileal deliveries of lipase but not amylase activity. Small intestinal transit and motility were not affected by camostat. In additional in vitro studies, camostat significantly reduced the spontaneous decline in lipase activity in fresh human duodenal juice incubated at 37 degrees C. These findings demonstrate that duodenal deliveries of lipase and amylase activities increase when intraluminal protease activity is decreased; they suggest that this increase is not caused by slower proteolytic destruction of enzyme protein but by stimulation of pancreatic secretion. Thus, luminal protease-mediated feedback regulation of pancreatic secretion may be operative in humans. Because plasma cholecystokinin concentrations were not affected, these effects may in part be independent of cholecystokinin. The data further suggest that proteolytic digestion plays a major role in the rapid loss of luminal lipase activity on small intestinal transit.

Adult↗
PubMed1989

[Calcium homeostasis and exocrine pancreas: physiological ans pathological interrelations].

Calcium homeostasis and exocrine pancreas interact on several levels under both physiologic and pathophysiologic conditions. (1) Calcium ions are important intracellular mediators of cholinergic and hormonal stimulation of the pancreatic acinar cell, and thus play a central role in the stimulus-secretion coupling of ecbolic pancreatic function. (2) The calcium concentration in pancreatic juice is lower than in the interstitial fluid: pancreatic juice calcium is composed of two fractions, one of which is secreted together with enzyme proteins and the other diffuses along paracellular pathways dependent on serum calcium. Disturbed calcium secretion in pancreatic juice can be observed even following slight pancreatic alteration; conversely, disturbed calcium secretion may be of importance in the pathogenesis of chronic calcifying pancreatitis. (3) Hypocalcemia is an important symptom of acute pancreatitis whose pathogenesis has not been fully elucidated. (4) On the other hand, pancreatitis complicates chronic and acute hypercalcemic syndromes though the pathogenic mechanisms is uncertain. Experimental chronic hypercalcemia in animal models causes characteristic pancreatic secretory changes and disturbs the diffusion barrier for calcium. Experimental acute hypercalcemia causes stimulation of pancreatic enzyme secretion and cholecystokinin release. In addition, extracellular calcium has a direct stimulatory effect on pancreatic acinar cells in vitro.

Acute Disease↗
PubMed1989

[Acute pancreatitis. 2: Treatment of the complicated course].

Owing to its tendency to produce severe local and systemic complications, the hemorrhagic necrotic form of acute pancreatitis is still associated with a high mortality rate. Major local complications are pseudocystic space-consuming masses, arterial bleeding and abscess formation. The major systemic complications include circulatory shock, metabolic disorders, renal failure, respiratory insufficiency and sepsis. Of decisive importance for the prognosis is prophylaxis, early detection, and suitable treatment of these threatening complications, which is achieved on the basis of a combination of standardized basic treatment with problem- and symptom-oriented supplementary treatment. In the present paper, the current prophylactic, diagnostic and therapeutic concepts are described. In addition, a number of invasive measures and the indications for surgery are discussed.

Acute Disease↗