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PubMedDate not supplied

Physiological mechanisms for cardiac control by nutritional intake after early maternal separation in the young rat.

Series of analytic experiments are presented that explore possible physiological mechanisms for the control of cardiac rate by nutritional intake in the pre-weanling rat. The essential properties of the nutrient and the first site of action were studied by using fluids of different pH, osmolality and chemical composition administered intravenously as well as intragastrically. Several probable effector pathways were explored: neuroendocrine (adrenal medullary and adrenocortical, thyroid), cholinergic and adrenergic. Pharmacological blocking agents, surgical removal of glands, replacement hormones and spinal cord trasaction were utilized. Afferent pathways such as vagus and splanchnic systems were approached surgically and the gastrointestinal hormones, histamine, insulin and glucagon, were studied by administration and pharmacological blockade. The evidence tended to rule out a number of possible mechanisms and pathways and to make it appear likely that nutrient acts initially at the gut wall, that the CNS then responds by increasing tone in the classical spinal cardioacceleratory pathways to the beta-adrenergic synapses of myocardium.

Adrenal Cortex Hormones↗
PubMed1994

Detection of gastrin mRNA in paraffin-embedded samples of normal antral mucosae using polymerase chain reaction technique.

Gastrin, a peptide hormone produced by the G cells of the gastric antrum, plays a major role in the regulation of digestive mucosal growth. Although some light has been shed on the peptidic aspects of this hormone's mode of action and the co-regulatory activity in which it is involved along with the other gastrointestinal hormones, little is known at present about the modes of expression of its mRNA at the tissue level. A few attempts have been made so far to detect the transcript, mostly using molecular hybridization techniques. Here it was proposed to detect gastrin mRNA using a RT-PCR technique on a series of paraffin-embedded samples of normal human antrum processed with various fixatives commonly used in histology. The transcript was detectable in all the 7-microns sections of the samples treated with either formalin or Carnoy's solution, whereas Bouin's solution, which is also used as a fixative in histology, was found to have inhibitory effects on the method described here.

Acetates↗
PubMed1982

Infantile hypertrophic pyloric stenosis: a review.

Infantile hypertrophic pyloric stenosis is a relatively common condition and there is some recent evidence that the incidence is increasing in this country. Gastric outlet obstruction is caused by hypertrophy of the pyloric smooth muscle and the clinical presentation is with non-bilious vomiting starting at the age of 3-4 weeks. The diagnosis can usually be made by palpation of the hypertrophied pylorus. Operation has now superseded medical treatment as the treatment of choice but meticulous assessment and correction of fluid and electrolyte imbalance is essential preoperatively. The operation of pyloromyotomy as described by Ramstedt in 1912 is simple and effective, but attention to detail is necessary if minimal morbidity and zero mortality are to be achieved. Untreated, the mortality is high but, after successful treatment, these babies are healthy and normal, so that treatment is both worth while and gratifying. The aetiology is obscure; a polygenic pattern of inheritance has been shown to be a predisposing factor, but the postnatal precipitating factors are less defined. Early hopes that the hormone gastrin might prove to be the key have not been sustained by more recent research, but the role of other gastrointestinal hormones awaits clarification.

Female↗
PubMed1978

Neurohormonal control of pancreatic secretion. A review.

This is a review of current information concerning the role of hormones and the autonomic nervous system in the control of exocrine secretions of the pancreas. A greater emphasis has been placed on the role of hormones because of information accumulated during the last several years. With the development of radioimmunoassay techniques, it is now possible to correlate circulating hormone concentrations with biological function. The role of hormones has been discussed with the framework of the secretin-glucagon family, the cholecystokinin-gastrin family, and other proposed gastrointestinal hormones and related peptides. Gastrin, secretin and cholecystokinin-pancreozymin are three prime gut hormones that regulate pancreatic secretion. Other hormones that may have a role in pancreatic secretion include glucagon, vasoactive intestinal polypeptide, chymodenin, somatostatin, pancreatic polypeptide, motilin, and bombesin. Neural mechanisms play an important although not so succinct a role in the over-all control of exocrine secretion. A complex relationship exists between the parasympathetic nervous system and the release of the hormones and their effect on pancreatic acinar and duct cells.

Animals↗
PubMed1998

Somatostatin and the gastrointestinal tract.

Somatostatin has various significant effects on the gastrointestinal tract: it inhibits the release of several gastrointestinal hormones, blocks the exocrine function of the stomach and the pancreas, and decreases the motility of both the stomach and the gut. Its physiological effects make it potentially useful in the therapy of various gastrointestinal diseases and disorders. Somatostatin is effective in the management of active variceal bleeding and increases the effectiveness of sclerotherapy. Previous studies show controversial data about the efficacy of somatostatin in preventing complications following endoscopic retrograde cholangiopancreatography. The use of this compound may be indicated only in high-risk patients in whom endoscopic sphincterotomy may also become necessary. The perioperative use of somatostatin decreases the risk of pancreatic surgery and its application is effective in promoting the closure of pancreatic fistulae. The somatostatin analogue octreotide has a definitive role in the medical management of hormone-secreting neuroendocrine tumours of the gut.

Digestive System↗
PubMedDate not supplied

Tryptophan as a link between psychopathology and somatic states.

OBJECTIVE: Several somatic illnesses are associated with psychiatric comorbidity. Evidence is provided that availability of the essential amino acid tryptophan, which is the precursor of serotonin, may cause this phenomenon. METHODS: We performed a database search to find relevant articles published between 1966 and 2002. For our search strategy, we combined several diseases from the categories hormonal, gastrointestinal, and inflammatory with the search terms "tryptophan" and "serotonin." RESULTS: The catabolism of tryptophan is stimulated under the influence of stress, hormones and inflammation by the induction of the enzymes tryptophan pyrrolase (in the liver) and IDO (ubiquitous). Because of the reduction in blood levels of tryptophan under these circumstances the formation of cerebral serotonin is decreased. CONCLUSIONS: It is argued that the coupling of peripheral tryptophan levels and cerebral serotonin levels has physiological significance. The clinical implications and therapeutic consequences of changes in tryptophan and consequently serotonin metabolism are discussed.

Animals↗
PubMed1995

Cholecystokinin is a potent protective agent against alcohol-induced gastric injury in the rat. Role of endogenous prostaglandins.

Cholecystokinin is a gastrointestinal hormone known to physiologically regulate pancreatic protein secretion and gallbladder contractility. Some evidence suggests that cholecystokinin is also involved in the maintenance of gastrointestinal mucosal integrity. This study was undertaken to ascertain whether cholecystokinin could prevent the gastric mucosal injury induced by acidified ethanol and what role prostaglandins, and type A and type B cholecystokinin receptors might play in this process. Conscious, fasted rats were given subcutaneous saline or cholecystokinin octapeptide (10-100 micrograms/kg) 30 min before a 1-ml oral gastric bolus of acidified ethanol (150 mM HCl/50% ethanol). Five minutes later, rats were sacrificed and the total area of macroscopic injury quantitated (square millimeters). In additional experiments using a similar protocol, 1 ml of either the cyclooxygenase inhibitor, indomethacin (5 mg/kg), a type A cholecystokinin receptor antagonist, L-364,718 (0.01-1 mg/kg), or the type B cholecystokinin receptor antagonist, L-365,260 (12.5-25 mg/kg) was given intraperitoneally 30 min prior to pretreatment with cholecystokinin octapeptide. Cholecystokinin octapeptide dose-dependently prevented mucosal injury from acidified ethanol (corroborated by histology). The protective effect of cholecystokinin octapeptide was completely negated by L-364,718 and partially reversed by indomethacin, while L-365,260 had no discernible effect in this process. In a further study, cholecystokinin was unable to prevent the damaging effects of aspirin and the inhibition of endogenous prostaglandins. This, it appears that cholecystokinin is able to maintain mucosal integrity in the face of a damaging insult by activation of type A cholecystokinin receptors, an effect mediated, at least in part, through the release of endogenous prostaglandins.

Animals↗
PubMed1977

Extrinsic neural influences on gastrointestinal motility.

The gastrointestinal tract is capable of carrying on all its major functions after all extrinsic nerves have been cut. This automaticity is due to the local nervous mechanisms in the walls of the gastrointestinal tract and the inherent properties of the smooth muscles in its walls, and gastrointestinal hormones. All levels of the central nervous system have been shown, by stimulation and ablation studies, to influence the motility of the entire gastrointestinal tract. Throughout many cerebral areas there are loci which, on stimulation, exert both inhibitory, and less often, excitatory influence on gastrointestinal motility. These influences are mediated by sympathetic and parasympathetic visceral efferent nerves, as well as humoral agents from the neurohypophysis. Thus, they impose an influence of higher control on the automatically efficient intrinsic motility. They are guided by information received from visceral, cranial, and somatic afferents, as well as intracerebral, or psychic inputs. Under normal circumstances they only influence gastrointestinal activity as will best afford the optimal functioning of a performance done automatically with efficiency and finesse.

Afferent Pathways↗
PubMed1986

Effect of pentagastrin, secretin and cholecystokinin on growth and differentiation in organ cultured rabbit small intestine.

The effect of pentagastrin, secretin and cholecystokinin on biochemical parameters of mucosal growth and differentiation was studied in organ cultured rabbit jejunum and ileum. Pentagastrin at 0.05-5.0 microgram/ml did not affect DNA content of the biopsy, but led to a significant decrease of sucrase and alkaline phosphatase activity in the ileum. Secretin prompted a significant decrease of DNA and protein in the ileum at a level of 10(-7) and 10(-5) M, but had no effect in the jejunum. Of the brush border enzymes, sucrase and alkaline phosphatase were suppressed in both parts of the intestine both with respect to specific activity and total biopsy content. Cholecystokinin, like pentagastrin, did not influence DNA or protein content, but reduced sucrase, maltase and alkaline phosphatase activity. HMG-CoA reductase, the key enzyme of cholesterol synthesis, was not significantly affected by any of the three hormones tested. When brush border enzymes or DNA from desquamated cells were measured in the post-culture medium, no consistent effect of any gastrointestinal hormone was apparent. The present study demonstrates a direct "antitrophic" effect of secretin in cultured mucosa. Pentagastrin and cholecystokinin did not influence mucosal DNA content in vitro but apparently inhibited villus cell differentiation.

Animals↗
PubMed2006

The sympathoinhibitory effects of systemic cholecystokinin are dependent on neurons in the caudal ventrolateral medulla in the rat.

The gastrointestinal hormone CCK inhibits a subset of presympathetic neurons in the rostroventrolateral medulla (RVLM) that may be responsible for driving the sympathetic vasomotor outflow to the gastrointestinal circulation. We tested the hypothesis that the central neurocircuitry of this novel sympathoinhibitory reflex involves a relay in the caudal ventrolateral medullary (CVLM) depressor area. Blood pressure and greater splanchnic sympathetic nerve discharge (SSND) or lumbar sympathetic nerve discharge (LSND) were monitored in anesthetised, paralyzed male Sprague-Dawley rats. The effects of phenylephrine (PE, 10 microg/kg iv; baroreflex activation), phenylbiguanide (PBG, 10 microg/kg iv; von Bezold-Jarisch reflex) and CCK (4 or 8 microg/kg iv) on SSND or LSND, were tested before and after bilateral injection of 50-100 nl of the GABAA agonist muscimol (1.75 mM; n=6, SSND; n=7, LSND) or the excitatory amino acid antagonist kynurenate (55 mM; n=7, SSND) into the CVLM. PE and PBG elicited splanchnic and lumbar sympathoinhibitory responses that were abolished by bilateral muscimol or kynurenate injection into the CVLM. Similarly, the inhibitory effect of CCK on SSND was abolished after neuronal inhibition within the CVLM. In contrast, CCK-evoked lumbar sympathoexcitation was accentuated following bilateral CVLM inhibition. In control experiments (n=7), these agents were injected outside the CVLM and had no effect on splanchnic sympathoinhibitory responses to PE, PBG, and CCK. In conclusion, neurons in the CVLM are necessary for the splanchnic but not lumbar sympathetic vasomotor reflex response to CCK. This strengthens the view that subpopulations of RVLM neurons supply sympathetic vasomotor outflow to specific vascular territories.

Adrenergic alpha-Agonists↗
PubMed1972

Hormone-elicited enzyme release by the small intestinal wall.

Three enzymes of intestinal origin-enterokinase, alkaline phosphatase, and sucrase-were released into the perfused small intestinal lumen of the rat upon intravenous injection of the gastrointestinal hormone cholecystokinin-pancreozymin (CCK-PZ). The presence of bile in the perfusion fluid greatly augmented this release. The results suggest that a combined mechanism of enzyme liberation due to direct hormonal stimulation of the gut wall and further solubilization of released intestinal enzymes by bile may be responsible for the appearance of these enzymes in the gut lumen.

Alkaline Phosphatase↗
PubMed1989

Effect of duodenectomy on interdigestive pancreatic secretion, gastrointestinal motility, and hormones in dogs.

We tested the hypothesis that the duodenum is necessary to coordinate interdigestive pancreatic trypsin secretion with gastrointestinal motility and determined whether duodenectomy altered interdigestive cycles of plasma motilin and pancreatic polypeptide and their relationship to trypsin secretion and motility. Consequently, in normal and duodenectomized dogs, we measured trypsin secretion, gastrointestinal motility, and plasma concentrations of motilin and pancreatic polypeptide during the interdigestive period. After duodenectomy, peaks of trypsin secretion continued to cycle at normal intervals (102 +/- 15 min), but the amounts of trypsin were reduced during peaks of secretion (P = 0.02) and throughout the entire cycle (P = 0.02). Trypsin secretory cycles after duodenectomy, however, were not coordinated with cycles of interdigestive motility, and the plasma concentrations of motilin (P = 0.02) and pancreatic polypeptide (P = 0.05) were reduced and had no cyclic pattern. In addition, we confirmed that duodenectomy alters canine interdigestive antral motility, interrupts coordination between antral and intestinal motility, and shortens the period of jejunal migrating motor complexes. We conclude that duodenectomy disrupts the relationship between the cycles of interdigestive gastrointestinal motility and trypsin secretion and reduces the amount of interdigestive trypsin secretion. These effects of duodenectomy may be due to interruption of the duodenopancreatic neural connections or the hormonal abnormalities we have described. The loss of the cyclic pattern of plasma pancreatic polypeptide after duodenectomy suggests that the duodenum controls the release of pancreatic polypeptide by either a neural or hormonal mechanism.

Animals↗
PubMed2000

Prostaglandin E2 stimulates motilin release via a cholinergic muscarinic pathway in the dog.

Prostaglandins are well known to be widely distributed in mammalian gastrointestinal tissues and to play a role in the regulation of gastrointestinal hormones and contractions. The present study was undertaken to determine whether prostaglandins have an effect on the endogenous release of motilin in the dog. In six conscious dogs, gastrointestinal contractions were monitored by means of chronically implanted force transducers. Prostaglandin E2 (PGE2; 3, 10, 30 microgram kg-1) was given intravenously during the interdigestive phase I period with or without a muscarinic or nicotinic receptor antagonist. Blood samples were collected from 10 min before, to 30 min after, prostaglandin injection. Indomethacin (5 mg kg-1) was given intravenously to investigate the effect of endogenous prostaglandins on motilin release. PGE2 significantly stimulated motilin release but not gastric contractions. Atropine, but not hexamethonium, blocked PGE2-induced motilin release. Motilin release in response to PGE2 was significantly increased by pretreatment with hexamethonium. Indomethacin inhibited the cyclic release of motilin and gastric phase III contractions. We conclude that PGE2 appears to stimulate motilin release via cholinergic muscarinic pathways, and nicotinic receptors modulate this reaction. PGE2 may be involved in part in the regulation of the cyclic release of motilin and the occurrence of gastric phase III.

Animals↗
PubMed1984

[Neurotensin--what is known about its role as a hormone in the gastrointestinal tract?].

Neurotensin is a tridecapeptide originally isolated and characterized from bovine hypothalamus and later, in identical form, from bovine and human intestine. In the rat about 85% of immunoreactive neurotensin is found in the gut and about 10% in the brain. When an antibody specific for the amino terminal region of neurotensin was used the highest concentrations were found in the mucosa of the ileum, while an antibody specific for the biologically active region, the carboxyl terminus, also detected large amounts in the mucosa of the upper gastrointestinal tract. After a meal neurotensin - as measured by carboxyl terminal antibodies - rises after 5 min, a time in which the chymus has not yet reached the ileum, the main source of whole neurotensin. It is therefore possible that the carboxyl terminal molecules of neurotensin, found in the upper gastrointestinal tract, play an important physiological role. In plasma, neurotensin is rapidly degraded into smaller amino terminal and therefore biologically inactive molecules. Increases of carboxyl terminal neurotensin have been found in plasma in only a very few studies. The nature of this immunoreactive material has not yet been established. Therefore, the physiological role of neurotensin as a circulating hormone is unknown. Potential actions of neurotensin include thermoregulation, regulation of hormone release from brain (pituitary hormones) and gut (glucagon, insulin, somatostatin, pancreatic polypeptide), increase of vascular permeability, vasodilatation, inhibition of gastric acid secretion, stimulation of pancreatic secretion and changes of gut motility from the fasting to the fed type.

Animals↗
PubMed1995

[Study on essence of liver-qi stagnation in ulcerative colitis].

The links between stagnation of the Liver-Qi in the pathogenesis and ulcerative colitis (UC) were clinically and experimentally studied using the principle of nourishing the Liver in treated group and the principle of invigorating the Spleen in control group. The results showed that the effective rate was 96% in treated group and 82% in control group, and the difference was significant (P < 0.05); the formation rate of E rosettes and the transformation rate of lymphocytes were significantly raised in the two groups compared with the pre-treatment period, treated group was evidently superior to control group in the rate of dysfunction of autonomous nerve system (P < 0.01). The level of intestinal styrenated phenol (SP) and vasoactive intestinal polypeptide (VIP) of UC model were determined in rats. The results showed that the level of SP and VIP significantly increased in UC model group. They markedly lowered in treated group compared with model group (P < 0.01) and there was significant difference in comparing with control group (P < 0.01). It revealed that Wei Chang Ning, a drug to nourishing the Liver, had the action of regulating neurological -endocrinological (gastrointestinal hormone)-immunological system.

Adult↗
PubMed1983

Gastrointestinal drug receptors.

Drug receptors consist of recognition sites coupled to transducer and cellular amplifier mechanisms. Slight differences in receptor recognition sites can be exploited pharmacologically to provide drugs with a high degree of selectivity for activating or blocking individual receptor subtypes. For example, it may now be possible to block, selectively, subtypes of muscarinic cholinergic receptors in the gastrointestinal tract with pirenzepine and other drugs that discriminate between subtypes of muscarinic cholinergic receptors. The recognition of subtypes of adrenergic receptors may allow highly selective pharmacological activation and blockage of gastrointestinal neural and smooth muscle receptors. The development of nonpeptide receptor antagonists of gastrointestinal hormones and peptide neurotransmitters also offers promise for improved therapy of digestive diseases. Tremendous progress has occurred in recent years in defining multiple types of opioid receptors that alter gastrointestinal secretory, absorptive and motility functions. These receptors are located in the mucosa, nerves and muscle of the intestine and in the brain and spinal cord.

Animals↗
PubMed1999

New horizons in the treatment of irritable bowel syndrome.

Irritable bowel syndrome is one of the most common diseases in gastroenterology clinics. Bowel movement is controlled by many factors such as gastrointestinal hormones and gut brain system, which are too complicated to evaluate by clinical investigation. Therefore, IBS is diagnosed on the basis of the Rome diagnostic criteria, after excluding organic gastrointestinal diseases. The basic principle in the therapy of IBS is to centrally stabilize the mental state and locally normalize intestinal function, in addition to regular daily life and dietary guidance.

Journal Article↗