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At least 469 records · Page 26Linked to original sources
PubMed1985

Gastrointestinal motility disturbances in patients with orthostatic hypotension.

Orthostatic hypotension syndromes may be associated with visceral denervation, resulting in disturbances of the gastrointestinal and urinary systems. This report analyzes the findings in 9 patients with neurogenic orthostatic hypotension and gastrointestinal symptoms. Antral and proximal small intestinal motor dysfunction was demonstrated in all patients: a significant reduction (p = 0.007) in the number of interdigestive motor complexes during 3 h of fasting (mean 0.4 vs. 1.3 controls); absence of gastric component in interdigestive motor complexes observed; incoordination of fasting and fed antral activity; and development of nonpropagating bursts of phase III-like activity in the intestine that were of at least 2-min duration, high amplitude and frequency, and associated with tonic elevations in baseline pressure. These motor abnormalities may provide a potential means for the diagnosis of impaired autonomic supply to the upper gut.

Adult↗
PubMed1997

Action of FMRFamide-like peptides on porcine gastrointestinal motility in vitro.

Mechanical activity was recorded in circular and longitudinal smooth muscle preparations isolated from extensive regions of the porcine gastrointestinal tract in response to the FMRFamide-like neuropeptides F8Famide and A18Famide. In all preparations, the peptides were about equipotent in producing phasic contractions or enhancing spontaneous activity. The most prominent responses were observed in jejunal longitudinal strips which were on the average 91% (+/- 4% SEM, n = 15; 10(-6) M) of the histamine (10(-5) M) responses. The peptide-induced phasic activity was completely abolished by nifedipine but was unaffected by tetrodotoxin, atropine, phentolamine, yohimbine, phenoxybenzamine, propranolol, methysergide, cimetidine, indomethacin, levallorphane or naloxone. Both peptides enhanced acetylcholine-induced contractions. However, bovine ileum and guinea-pig taenia coli was not affected by these peptides. The results indicate that F8F- and A18F-amide contract porcine gastrointestinal smooth muscle by acting directly via non-opioid receptors on L-type calcium channels. In addition an increase of the sensitivity to cholinergic stimulation occurs.

Animals↗
PubMedDate not supplied

Influence of vagal pyloric branches on gastric acid secretion and gastrointestinal motility in patients following a pylorus preserving pancreatoduodenectomy.

BACKGROUND/AIMS: The authors evaluated the influence of the vagal pyloric branches on the gastrointestinal function in patients who underwent a pylorus preserving pancreatoduodenectomy (PPPD). METHODOLOGY: Twenty-seven patients with pancreatobiliary and duodenal diseases underwent a PPPD between 1991 and 1994. We analyzed several variables including the daily volume of gastric juice, days of gastric suctioning, start of diet, gastric acid, and gastrin levels. In addition, a gastric emptying scintigram and gastrointestinal manometry were measured. These variables were compared between two groups, namely, those with retained superior pyloric branches of the vagus nerve (preserved group: n = 14), and those without these branches (non-preserved group: n = 13). RESULTS: There were no significant differences in basal acid output, maximum acid output, or plasma gastrin levels between the preserved group and the non-preserved group. In addition, a gastric emptying scintigram demonstrated no difference between the two groups. Finally, on gastrointestinal manometry, there was no significant difference between the two groups during gastric and jejunal phase III activity of migrating motor complex. CONCLUSIONS: Preservation of the vagal pyloric branches did not influence gastric exocrine and endocrine secretion, nor did it effect the gastric emptying of patients who underwent a PPPD.

Adult↗
PubMed1979

[Action of TRH on gastrointestinal motility in vitro (author's transl)].

Thyrotropin-releasing hormone (TRH) was studied for its effects on some strips of the gastrointestinal tract in vitro. TRH showed to possess a certain stimulatory activity on proximal segments of the g.i. tract being approximately as effective as histamine. This motor activity of TRH is discussed taking into account a possible physiological role outside the brain.

Acetylcholine↗
PubMed1992

Effects of intrathecal and intraperitoneal morphine on gastrointestinal motility in the rat.

A method has been developed to compare gastrointestinal (GI) transit time after intrathecal (i.t.) drug injection in the rat. Each animal had a catheter implanted in the i.t. space. Eight rats, on three separate occasions, had either i.t. morphine 16 micrograms kg-1 (in 50 microliters) or intraperitoneal (i.p.) morphine (0.1%) 7.5 mg kg-1 or i.t. saline (50 microliters). The dose of morphine was the ED50 for analgesia by each route. After halothane and oxygen anaesthesia, 10 steel balls and 1 ml of contrast medium were placed into the stomach, the whole procedure being completed within 5 min. Radiographs were taken at 5 min, 3, 6 and 24 h, and the number of balls in the stomach, small and large intestine were counted. The inhibitory effect of i.t. or i.p. morphine on gut motility caused an equally significant delay at 6 h. In a separate series of eight rats the delay by i.t. morphine could be completely antagonized by i.p. naloxone 1 mg kg-1. Thus, i.t. morphine in an analgesic dose even though smaller than the i.p. dose has a similar inhibitory effect on GI tract motility in the rat. This method would enable comparisons on GI transit to be made between a variety of intrathecally administered drugs.

Animals↗
PubMedDate not supplied

Role of histamine H(3) receptors in the control of gastrointestinal motility. An overview.

Over the last few years, the biochemical and functional characterization of H(3) receptors has been a matter for extensive investigation, culminating in the cloning of the human, guinea pig and rat receptor protein from brain tissues. This discovery contributed to determine the distribution of receptors in the body and to define the molecular mechanisms which follow activation. The major breakthrough in the histamine H(3) receptor field came with the synthesis of selective and potent agonists and antagonists, which unravelled the function of this receptor subtype in the different tissues. As expected from the ubiquitous location of histamine in the body, histamine H(3) receptors have also been identified in virtually every tissue, although they are quantitatively less abundant than H(1) and H(2) receptors. Concerning the gastrointestinal tract, this new receptor subtype seems to have multiple cellular locations, which include neurons, enteric ganglia, paracrine and immune cells and, in some tissues, also smooth muscle cells. Therefore it might be regarded as a general regulatory system of different digestive functions, including motility. The effects mediated by histamine H(3)-receptors mainly reflect the presynaptic inhibition of the release of either excitatory or inhibitory neurotransmitters from the myenteric plexus. The molecular mechanism of presynaptic inhibition seems to involve a restriction of calcium entry into the nerve endings, but other mechanisms (reduction of cAMP), possibly associated to different H(3) receptor subtypes, may be involved. Despite the widespread distribution and the well defined inhibitory effects evoked in the majority of in vitro models of intestinal motility, no clear cut evidence of its involvement in the control of peristalsis could be provided. In vivo models of gastrointestinal transit, indeed, did not reveal a defined effect of histamine H(3) receptor ligands, even though the possibility of a central inhibition was pointed out in several studies. Therefore, it is not clear at the present what is the physiological meaning of the histamine H(3) receptor in the control of gastrointestinal motility and whether it could represent a potential target for novel therapeutic interventions in deranged motility, taking into account that human gastrointestinal tissues are apparently devoid of this receptor.

Animals↗
PubMed1985

[Effect of proglumide on gastrointestinal motility and gastric secretion in the conscious state].

Proglumide suppressed neither phase III activity nor propagation of interdigestive migrating contractions (IMC) in the gastrointestinal tract. Furthermore, proglumide did not inhibit the gastric motor activity stimulated by pentagastrin, however, it suppressed the pH in Pavlov pouch stimulated by pentagastrin in the interdigestive state. On the contrary, in the digestive state, proglumide did not suppress the pH. That might be due to not only various gut hormones including gastrin, but also neural stimulation, mechanical stimulation and so on. In conclusion, antigastrin effect of proglumide is rather remarkable on the acid secretion not on the gastrointestinal motor activity. Proglumide may be an antacid without suppression of motor activity.

Animals↗
PubMed2001

Inhibitory effect of palmitoylethanolamide on gastrointestinal motility in mice.

1. We have studied the effect of palmitoylethanolamide (PEA, 2.5 - 30 mg kg(-1), i.p.) on upper gastrointestinal transit in control mice and in mice with chronic intestinal inflammation induced by croton oil. 2. PEA significantly and dose-dependently decreased intestinal transit. The inhibitory effect of PEA (10 mg kg(-1)) was not modified by the cannabinoid CB(1) receptor antagonist SR141716A (0.3 mg kg(-1), i.p.), the cannabinoid CB(2) receptor antagonist SR144528 (1 mg kg(-1), i.p.), N(G)-nitro-L-arginine methyl ester (L-NAME, 25 mg kg(-1), i.p.), yohimbine (1 mg kg(-1), i.p.), naloxone (2 mg kg(-1), i.p.) or hexamethonium (1 mg kg(-1), i.p.). 3. PEA levels were significantly decreased in the small intestine of croton oil-treated mice. In these animals, PEA also inhibited motility and this effect was not counteracted by SR141716A (0.3 mg kg(-1)), or SR144528 (1 mg kg(-1)). 4. Pre-treatment of mice with the amidase inhibitor phenylmethyl sulphonil fluoride (PMSF, 30 mg kg(-1), i.p.) did not modify the inhibitory effect of PEA, either in control or in mice with inflammation. 5. It is concluded that PEA inhibits intestinal motility with a peripheral mechanism independent from cannabinoid receptor activation. The decreased levels of PEA in croton oil-treated might contribute, at least in part, to the exaggerated transit observed during chronic intestinal inflammation.

Adrenergic alpha-Antagonists↗
PubMedDate not supplied

Gastrointestinal motility in constipation.

This study included ten subjects with normal intestinal habits and 25 with constipation. Data were collected from X-rays of gastrointestinal transit times and from intraluminal pressures in the sigmoid and rectum using electromanometry. A comparison of the results led to the following conclusions: a) transit times to the cecum were essentially similar in both the control group and patients with constipation; b) the barium contrast arrived faster in the proximal sigmoid of patients with constipation compared to the control group; c) the mean of the total time of gastrointestinal emptying was slower in constipation; d) under unstimulated conditions, the electromanometry study of the sigmoid and rectum showed a higher motility index in constipation than in the control group; e) the high values of the percent activity was the most important element in the elevation of the motility index in constipation; f) the propulsion and retention activities of the colon were higher in constipation than in normals, as was demonstrated by radiologic and electromanometric studies.

Adult↗
PubMed1987

Effects of ketamine on nociception and gastrointestinal motility in mice are unaffected by naloxone.

The present study investigates the effects of ketamine on nociception towards chemical and thermic stimuli and on gastrointestinal transit in mice. The reversibility of these effects by the opioid antagonist naloxone (10 mg/kg) was also assessed. Ketamine promoted dose-related analgesia in both the acetic acid-induced writhing and hot plate tests. Analgesia was not influenced by pretreatment with naloxone. Contrasting the constipation induced by opioids, ketamine enhanced gastrointestinal transit in a dose-dependent manner and this was not modified by naloxone. These results suggest that although ketamine can elicit analgesia, it does not activate opioid mechanisms in subanesthetic doses.

Analgesia↗