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Biomedical subjects

P Layer

Publications and source records attributed to P Layer.

At least 127 records · Page 7Linked to original sources
PubMed1989

[Acute pancreatitis. 1: Principles of conservative therapy].

Any patient with suspected acute pancreatitis should be hospitalized in an intensive care unit. Since the course even of an apparently initially uncomplicated attack of pancreatitis can rapidly become severe and life-threatening, close clinical monitoring in accordance with the rules of critical care medicine is necessary. The major therapeutic measures comprise fasting, parenteral replacement of fluid, electrolytes and calories, and pain treatment. The care of patients with acute pancreatitis should be a joint effort on the part of the internist and the surgeon right from the start. At the present time, there is no specific treatment regimen for pancreatitis. Therapeutic concepts of hormonal inhibition of pancreatic secretion, or the inactivation of autodigestive enzymes, have not proved successful, or have not yet been adequately demonstrated to be effective. On resolution of the pancreatitis, an attempt must always be made to identify the cause of cause of the condition, since this forms the basis for further prophylactic and therapeutic consequences.

Acute Disease↗
PubMed1989

The effect of a new synthetic cholinergic compound (aclatonium napadisilate) on interdigestive motility and pancreatic function in humans.

To investigate the effect of aclatonium napadisilate (Ac), a synthetic cholinergic compound, on human interdigestive gastrointestinal function, six healthy volunteers underwent gastrointestinal intubation for measurement of duodeno-jejunal motor activity and pancreatic enzyme secretion. Each subject was studied twice on two separate days and received either aclatonium (300 mg) or placebo intraduodenally in randomized order. Aclatonium significantly increased the overall length of the cycle of interdigestive motor complex (IMC) by a mean of 34% (p less than 0.05) without stimulating the phases of increased motor activity. Aclatonium slightly, but significantly increased output of lipase during phase II of the IMC (p less than 0.05), whereas outputs during phase I and III were not significantly changed. We conclude that aclatonium in a dose of 300 mg has only weak cholinergic effects on motility and exocrine pancreatic secretion in healthy humans during the interdigestive state.

Acetylcholine↗
PubMed1989

Carbohydrate digestion and release of pancreatic polypeptide in health and diabetes mellitus.

The effects of meal volume and luminal digestion of carbohydrates on the release of pancreatic polypeptide (HPP) were investigated in eight healthy subjects and in six patients who had non-insulin dependent diabetes mellitus. On one occasion each subject ingested a placebo with 200 ml water and a starch (50 g) pudding meal (400 ml) 30 minutes later. On another occasion an amylase inhibitor that retards intraluminal starch digestion was given with the water and starch. In normal subjects, water caused a moderate rise in HPP plasma levels (16.9 (10.9) pg/ml; p less than 0.02) and ingestion of starch increased HPP in a double peaked pattern. The mean increments of the peaks were 45.0 (15.2) pg/ml (p less than 0.02) and 41.1 (17.3) pg/ml (p less than 0.05), respectively. In the diabetic subjects, the HPP concentrations did not increase in response to water. After ingestion of starch the diabetics had two peaks of HPP that were similar in magnitude, but the early postprandial peak was delayed significantly compared to normal subjects (37.5 (5.1) min v 23.4 (3.9) min; p less than 0.05). The amylase inhibitor (5 or 10 g) reduced the early postprandial HPP peak by 79% (p less than 0.05) in normal subjects and 4 g of the inhibitor reduced the early HPP peak by 58% (p less than 0.05) in the diabetics. In both groups ingestion of the amylase inhibitor abolished the late HPP peak (p less than 0.05). In conclusion, carbohydrate induced HPP release is dependent on undisturbed intraluminal starch digestion.

Adult↗
PubMed1989

[Recurrent gastroparesis following abdominal irradiation. Therapy with cisapride].

Following abdominal radiation a 16-year-old male patient developed nausea and vomiting secondary to gastric stasis, dilatation and impairment of antral motility. Symptoms improved after 2 months of treatment with a cholinergic agonist. Now, 7 years later, symptoms recurred. Cisapride, a newly developed agent which stimulates gastrointestinal motility probably evoked a prompt increase of antral motility and gastric emptying. We conclude that abdominal irradiation may cause gastrointestinal motility disturbances which may respond to medical therapy.

Adolescent↗
PubMed1988

Pancreatic and gastric responses to gastric versus jejunal beer in humans.

To investigate the influence of beer on gastric and pancreatic secretion, 14 fasted volunteers were studied on two different days. A multilumen intestinal tube allowed measurement of intraluminal pressures and collection of gastric and duodenal juices. Seven subjects received in random order 250 ml of either beer or glucose (5.6%, w/v) intragastrically; seven other subjects received these intrajejunally. After 15 min, 48 +/- 8% of beer and 47 +/- 6% of glucose were emptied into the duodenum. Intragastric beer induced a nearly sevenfold increase in gastric acid output as compared with glucose (16.3 +/- 2.9 mmol/h versus 2.5 +/- 0.6 mmol/h; p less than 0.05), intrajejunal beer induced a nearly threefold increase (5.1 +/- 0.8 mmol/h versus 1.7 +/- 0.3 mmol/h). The stimulated gastric acid output was threefold higher after intragastric than after intrajejunal beer. Trypsin output was slightly but significantly (p less than 0.05) stimulated by intragastric beer as compared with glucose (4,639 +/- 460 U/h versus 3,628 +/- 399 U/h) and nearly threefold by intrajejunal beer (2,579 +/- 455 U/h versus 849 +/- 181 U/h) (p less than 0.05). Trypsin response to intragastric beer was 1.8 times higher than after intrajejunal beer (p less than 0.05). Intragastric beer induced a nearly ninefold increase of the 1 h integrated plasma gastrin response as compared with glucose (998 +/- 347 pM min vs 115 +/- 70 pM min) (p less than 0.05). Intrajejunal beer and glucose did not release gastrin. We conclude that both intragastric and intrajejunal beer stimulate gastric acid and pancreatic enzyme secretion; intragastric beer being a more potent stimulant. Gastrin might partially mediate the responses to intragastric but not to intrajejunal beer.

Adult↗
PubMed1988

Effects of somatostatin-14 on gastric and pancreatic responses to hormonal and neural stimulation using an isolated perfused rat stomach and pancreas preparation.

To study the role of somatostatin in the regulation of pancreatic and gastric functions, a combined isolated rat stomach and pancreas preparation was developed. This model allowed simultaneous measurements of exocrine and endocrine secretion from the pancreas and gastrin secretion from the stomach. Somatostatin was applied either by a linear gradient or by constant infusion with one concentration in the presence of cerulein, secretin, electric vagal activity, or acetylcholine. Somatostatin did not influence exocrine pancreatic secretion irrespective of what substance was stimulated. In contrast, somatostatin significantly inhibited glucose-dependent insulin and gastrin secretion, either basal or stimulated by vagal activity or acetylcholine. Acetylcholine-induced gastrin secretion was more sensitive to inhibition by somatostatin than insulin. We conclude that in an isolated perfused organ system somatostatin has potent inhibitory effects on endocrine pancreas and stomach but has no effect on exocrine pancreatic volume and enzyme secretion.

Amylases↗
PubMed1988

Human pancreatic secretion during phase II antral motility of the interdigestive cycle.

We determined if changes in the irregular motor activity of phase II, the dominant motility phase in awake fasting humans, are associated with fluctuations in pancreatic secretion by intubating the upper gastrointestinal tract of 15 healthy humans and recording antral and duodenal motility and obtaining duodenal samples for one or two interdigestive motility cycles. Antral phase II activity was graded as having low, intermediate, or high frequency of contractions and related to duodenal trypsin output and plasma concentrations of motilin and human pancreatic polypeptide (HPP), a marker of vagal cholinergic tone. Low, intermediate, and high phase II motor activities were significantly associated with trypsin outputs (U/10 min; mean +/- SE) of 576 +/- 137, 1,441 +/- 225, and 3,621 +/- 521, respectively (P less than 0.001). Plasma motilin levels did not vary with the grades of phase II motility (P greater than 0.1), but levels of plasma HPP and the grades of phase II motility were positively correlated (P less than 0.001). The close correlation among motility, pancreatic secretion, and plasma HPP during phase II suggests that vagal cholinergic pathways are involved in the common regulatory mechanism controlling phase II interdigestive motility and pancreatic secretion.

Adolescent↗
PubMed1987

In vitro stimulation of pancreatic enzyme discharge by calcium.

The mechanism for acute hypercalcaemia increasing pancreatic enzyme secretion is unknown. To determine if raised extracellular calcium concentrations can directly stimulate pancreatic enzyme output, we measured discharges of pulse labelled protein and chymotrypsin from isolated cat pancreatic lobules in the presence of normal and raised calcium concentrations. Incubation in 5.0 mmol/l calcium increased discharges of pulse labelled protein (four fold), chymotrypsin (2.5 fold) and amylase (2.2 fold), compared with control experiments with 2.5 mmol/l calcium (p less than 0.001). This effect was similar to the maximal effect of carbachol or caerulein. Compared with 5.0 mmol/l calcium, incubation at the higher calcium concentration of 10.0 mmol/l induced similar discharges of chymotrypsin and amylase, whereas the increase in discharge of pulse labelled protein was smaller (p less than 0.01). The effects of raised calcium were not altered by atropine. Incubation in a high calcium medium did not impair pancreatic acinar response to subsequent stimulation with carbachol, but incubation in hypothermia abolished the effects of high calcium concentrations, suggesting that increased enzyme discharge is caused by stimulation of secretion not to cell damage. These data are consistent with a direct stimulatory effect of raised extracellular calcium concentrations on pancreatic acinar cell function.

Animals↗
PubMed1987

[Neural control of pancreatic secretion].

In humans and many laboratory animals, protein and fat digestion products are potent intestinal stimulants of pancreatic enzyme secretion. Both neural and hormonal pathways mediate the enzyme response to these intestinal stimulants. Enteropancreatic, cholinergic, vago-vagal reflexes are probably the most important mediators of the enzyme response to low loads of amino acids, fatty acids and HCl; hormones, such as cholecystokinin, seem to be the major mediators of the response to high loads of amino acids, fatty acids and HCl. Gastric acid is the major regulator of postprandial pancreatic bicarbonate secretion. Secretin released by HCl is probably the most important physiological hormonal mediator of postprandial pancreatic bicarbonate secretion; its effect being potentiated by extrinsic (vagal) and intrinsic (intrapancreatic) cholinergic nerves and release of other hormones, such as cholecystokinin. Under physiological conditions it is probably the interplay of neural and hormonal mechanisms which regulates the pancreatic response to intestinal stimulants. However, this interaction of nerves and hormones is greatly unknown.

Amylases↗
PubMed1987

[Regulation of gastric acid secretion: new aspects].

The purpose of this short review is to reveal new aspects of regulation of gastric acid secretion. The complex interactions between humoral, paracrine, neurocrine, neuroendocrine, vagal and sympathetic mechanisms will be emphasized. The finding that stimulation of the vagus nerves releases bombesin from peptidergic nerve fibers, which causes release of gastrin from endocrine cells in the stomach, demonstrates the complex interaction between nerves and hormones. The target organ, the parietal cell, has receptors for gastrin, acetylcholine and histamine, which potentiate each other regarding stimulation of acid secretion. New findings about the pathophysiology of acid secretion in duodenal ulcer patients are emphasized.

Animals↗
PubMed1987

[Interdigestive motility and secretion of the gastrointestinal tract].

In the fasting state, the digestive tract is not inactive but displays periodic motor and secretory activity. Each gastrointestinal motility cycle can be divided into specific phases of activity: a period of inactivity (phase I), followed by a longer period of irregular activity (phase II) and by a brief, conclusive period (phase III) of maximal, rhythmic contractions, the migrating motor complex (MMC), which migrates from the gastroduodenal region to the distal small bowel within one motility cycle. A short, inconstant transition segment between phases III and I is termed phase IV. Lower esophageal, gallbladder and sphincter of Oddi motilities are also linked to this functional cycle. In contrast, colonic motility follows independent patterns. Closely correlated to upper gastrointestinal motility are secretory activities: Output rates of gastric, pancreatic and bile secretions increase and decrease periodically, in concert with upper gastrointestinal motor activities. The physiologic role of periodic interdigestive activity is not fully understood. It is probably important for regular mechanical and enzymatic cleansing ot the gastrointestinal lumen and may serve to remove indigestible and/or foreign material, to prevent bacterial overgrowth or pathologic activation of pancreatic enzymes, and to revert duodeno-gastric and ceco-ileal refluxes. Control of the interdigestive cycle and mechanisms of motor/secretory coupling have been only partly uncovered; however, recent findings suggest that interactions between vagal and intrinsic cholinergic pathways and gastrointestinal hormones may play pivotal regulatory roles.

Digestion↗
PubMed1987

[Effect of circadian rhythm on gastrointestinal motility].

In western civilization, circadian rhythms of the gastrointestinal tract are dominated by a digestive-interdigestive rhythm: During the day interdigestive activity is rare because of frequent meal intakes prior to termination of preceding fed states: in contrast, nocturnal activity is largely interdigestive. Digestive and interdigestive functions are characterized by specific and interactive motor and secretory activity patterns. When exogenous influences via food intake are prevented, additional, underlying, endogenous, circadian rhythms are observed that modulate gastric and intestinal motility in a characteristic fashion, possibly with tight links to the central nervous system. It is likely that disturbances of physiologic circadian modulation of gastrointestinal function may have pathogenic importance.

Animals↗