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At least 127 records · Page 7Linked to original sources
PubMed1975

Alterations in normal esophageal motility in patients with Chagas' disease.

Eight adult patients with visceral Chagas' disease were studied twice within an interval of 64 months. In each case the esophagus was evaluated radiologically and manometrically. None of the patients had esophageal symptoms and no significant change in resting gastroesophageal sphincter pressure was observed during the study. However in 3 patients incomplete sphincteric relaxation was noted. Normal progressive contractions did not change. The importance of these findings are discussed.

Adult↗
PubMed1975

The adverse effect of chocolate on lower esophageal sphincter pressure.

Decreased lower esophageal sphincter (LES) pressure after ingestion of chocolate has been previously noted. We have further evaluated the effect of chocolate on the known ability of gastric alkalinization or bethanechol to increase LES tone. 9 normal subjects were studied using an infused open-tip recording system. Pressure was monitored for a 15-min basal period, and for 60 min after ingestion of 120 ml of chocolate syrup either alone or with the concurrent administration of commercial antacid, oral bethanechol, or subcutaneous bethanechol. After chocolate ingestion, mean basal LES pressure of 14.6 +/- 1.1 (+/-SEM) mm Hg decreased significantly (P less than 0.01) to 7.9 +/- 1.3 mm Hg. An identical LES response occurred when antacid was given with the chocolate dose. Oral bethanechol (25 mg) and chocolate together resulted in lesser decreases in LES pressure. Subcutaneous bethanechol (5 mg) and chocolate produced significant increases (P less than 0.05) in sphincter pressure, although of lesser magnitude than reported with bethanechol alone. These results indicate that the adverse effect of chocolate on the LES is not reversed by gastric alkalinization and suggest that bethanechol in sufficient dose may overcome chocolate-induced decreases in LES pressure.

Adult↗
PubMed1975

The mucosal lining of the intramural common bile duct as a determinant of ductal opening pressure.

Microanatomical evidence is presented which shows that the lumen of the intraduodenal portion of the common bile duct is almost completely filled by folds of a highly vascularized mucosa in the dog, cat, rabbit, and human. These folds are most apparent near the intraduodenal ductal orifice, where they almost completely occlude the lumen. Physiological data are presented which indicate that changes in systemic arterial blood pressure are associated with changes in the opening pressures of the choledochoduodenal junction of the cat and dog, which vary in the same direction. Experimental results indicate that bile duct opening pressures of these two species are increased by the intraductal administration of histamine and reduced by the intraductal administration of norepinephrine. A histological examination of the intraductal mucosal folds in this area, subsequent to the administration of the elevating agent, revealed a marked presence of vascular engorgement. It is concluded that the most significant determinant of changes in ductal opening pressures in the cat and dog is probably the state of the mucosal vasculature of the terminal portion of the common bile duct.

Animals↗
PubMed1977

Effect of bethanechol on gastroesophageal reflux.

In this study we determined the acute effect of bethanechol (5 mg SC) on gastroesophageal reflux (GER) and lower esophageal sphincter pressure (LESP) in 27 patients with symptomatic esophagitis. The effect of bethanechol on esophageal acid clearance was also determined in 7 of the patients. Intraluminal pH monitoring prior to bethanechol administration demonstrated free or stress-induced reflux episodes in 18 of the 27 patients. Following bethanechol (1) LESP increased significantly, (2) GER diminished or ceased in many of the patients, and (3) acid clearance times decreased significantly. Some individuals, however, continued to reflux despite LESP elevation to 30 mm Hg or more. This latter finding suggests that LESP alone is not the sole factor governing LES competency. Other factors such as improved esophageal emptying may also contribute to the beneficial therapeutic effect of bethanechol in patients with heartburn.

Bethanechol Compounds↗
PubMed1977

Myoelectrical and mechanical activity of stomach and intestine in hypothyroid dogs.

Myoelectrical activity was studied in normothyroid and hypothyroid Labrador dogs in the resting state, following injection of pentagastrin, bethanechol chloride, and after feeding. Hypothyroidism was produced by total thyroidectomy and chronic treatment with thiouracil. Electrodes were surgically implanted over the serosa of the stomach, duodenum, jejunum, and ileum and used for repeated recording of myoelectrical activity of gastrointestinal muscles. A strain gauge was implanted over the gastric antrum and served to record mechanical activity of the stomach. As compared with control dogs, hypothyroid animals showed (a) decreased frequency of electrical control activity of the stomach and jejunum, (b) decreased occurrence of electrical response activity (spike potentials) following stimulation, and (c) decreased mechanical response to the same stimulants, ie, pentagastrin, bethanechol chloride, and food.

Animals↗
PubMed1978

The role of aspirin in gastric ulceration . Some factors involved in the development of gastric mucosal damage induced by aspirin in rats exposed to various stress conditions.

The gastric irritant effects of aspirin were studied in rats treated with a variety of physical and "disease" (inflammatory) stress conditions (which may mimic responses to some stress states encountered clinically) with the object of establishing whether these stress states increase the susceptibility of the gastric mucosa to the potentially ulcerogenic actions of aspirin. While exposure to physical (eg, cold) stress conditions markedly increased the sensitivity of the gastric mucosa to aspirin, exposure to various disease stressors (eg, adjuvant arthritis, acute pain, or paw inflammation) did not appreciably affect the mucosal sensitivity to this drug. Attempts were made to determine the mechanisms of the physical stress plus aspirin interaction by use of pharmacological agents. The results suggest a major involvement of the parasympathetic-vagal, sympathetic, and histamine-producing systems, but not the adrenocortical axis, in this model of gastric ulcerogenesis. No differences were observed in the mucosal uptake of [14C]aspirin, showing that accelerated uptake of the drug is not a factor in the development of gastric ulceration.

Animals↗
PubMed1977

Long-term effects of highly selective vagotomy (HSV) in dogs on acid and pepsin secretion.

Gastric H+ and pepsin studies before and at intervals for 4o months after fundic vagotomy (HSV) in 3 fistula dogs were done with the vagal stimulant 2-deoxyglucose (2-DG), and blocked the secretory response to 2-DG, but secretion began to recover by 5-6 months, and from 16 months on stabilized at 60% H+ and 13-17% pepsin (preoperative = 100%). After HSV the stomach showed hypersensitivity to urecholine with a lower threshold and lower Km, but unchanged Vm, while with histamine the curves were shifted to the right, with Vm unchanged and Km increased. With pentagastrin there was also a small decrease in Vm. Pepsin responses to urecholine recovered and exceeded control by 16 months, but remained relatively unresponsive to histamine or pentagastrin. A cholinergic background provided by urecholine at subthreshold doses (less than 10 mug/kg-hr) restored both pentagastrin and histamine responses to prevagotomy levels. Gastrin release from the innervated antrum by 2-DG was several times greater than in controls and was atropine sensitive. The results indicate that denervation of the secretory mucosa, especially of the peptic cells, is never more than partially reversed even after 3 years. Even though the response to vagal stimulation is partial, the mucosa remains capable of normal response, ie, there is no atrophy, and therefore, the vagus is not directly trophic to the gastric fundus. Moreover, vagotomy was followed by some hypersensitivity to urecholine, indicating changes in cholinergic receptors like those seen in denervated muscle cells.

Acetylcholine↗
PubMed1983

Biphasic action of intravenous ethanol on dog exocrine pancreatic secretion.

The effect of a 20-min intravenous infusion of 1 g/kg of ethanol on a 15% (w/w) solution in isotonic saline on pancreatic secretion was determined in six conscious Beagle dogs provided with Thomas cannulae. Ethanol was given on a background of a prolonged infusion of 0.5 CU/kg/hr of secretin alone or secretin plus either different doses of cerulein (12.5-200 ng/kg/hr), 3 micrograms/kg/hr of pentagastrin, or 200 micrograms/kg/hr bethanechol. Intravenous ethanol had a biphasic action on pancreatic secretion: inhibition during the first 40 min followed by stimulation. When compared to control experiments with intravenous infusion of saline, the inhibition was statistically significant only for volume and bicarbonate output against a background of pentagastrin and for protein output against a background of bethanechol. We propose that alcohol inhibits acetylcholine-mediated protein secretion. The delayed stimulatory effect of ethanol was statistically significant for both ecobolic (protein output) and hydralatic (water and bicarbonate) secretion during infusion of secretin plus 12.5-25 ng/kg/hr cerulein, but not with doses of 50 ng/kg/hr. Although the plateau of secretion before alcohol was roughly similar in the experiments using cerulein and bethanechol, ethanol inhibited protein output and had no effect on bicarbonate output during stimulation with bethanechol. Therefore, the effects of alcohol on pancreatic secretion are influenced by both the type of stimulation and its intensity (dosage).

Animals↗
PubMed1987

Effects of antireflux therapies on salivary function in normal humans.

Saliva has received recent attention because of its potential role in esophageal clearance and neutralization of refluxed gastric contents. Gastric antisecretory drugs or promotility drugs used to treat reflux have not been studied for their ability to affect salivary function. We conducted a double-blind randomized study of four antisecretory drugs, two promotility drugs, and placebo (PL) on 12 healthy volunteers on seven different days. Following a 6-hr fast, accumulated saliva was expectorated at least once per minute. The initial 10-min sample was discarded and a baseline 20-min sample collected. One of the following was given per os: PL, pirenzepine (PIR), 50 mg; propantheline (PRO), 30 mg; cimetidine (CIM), 300 mg; ranitidine (RAN), 150 mg; bethanechol (BET), 25 mg; or metoclopramide (MET), 10 mg. Saliva was collected for 60 min. Saliva was then stimulated (STIM) by sucking a peppermint lozenge for 30 min. Specimens were collected under oil, kept on ice, and analyzed within 30 min. Saliva flow in milliliters per minute and capacity for acid neutralization (CAN) in microequivalents acid per milliliter saliva were analyzed on all samples. The known effect of PRO to inhibit both basal saliva flow and STIM flow and CAN was seen. In contrast, the selective antimuscarinic PIR did not significantly decrease saliva flow or CAN. CIM, RAN, and MET did not significantly effect salivary function, but both CIM and RAN showed a tendency to increase CAN. Oral BET had no detectable effect on salivary function.

Adult↗
PubMed1984

Relationship between swallow rate and salivary flow.

Recent studies indicate that swallow-induced, primary peristalsis is a major determinant of normal esophageal acid clearance. However, factors that regulate the rate of spontaneous swallowing in normal subjects are incompletely understood. We postulated that the rate of salivary flow influences the rate of spontaneous swallows. To test this hypothesis, we did a total of 60 studies measuring salivary flow or the rate of spontaneous swallowing in 10 healthy volunteers, age 10-30 years. Saliva was collected by expectoration. Swallow rate was recorded by a small, transnasal catheter stationed in the pharynx and also, in some circumstances, by cervical electrodes. On separate sessions, we evaluated the effect of five test manipulations on salivary flow and swallowing rate, respectively. The test manipulations consisted of: (1) pharyngeal intubation, (2) sucking of a dummy lozenge, (3) sucking of a peppermint lozenge, (4) bethanechol injection (5 mg subcutaneously), and atropine administration (12 micrograms/kg intravenously). Pharyngeal intubation caused a small, but significant increase in the rate of salivation and spontaneous swallows. Sucking of a peppermint lozenge caused a sixfold increase in salivary flow while nearly doubling the swallowing rate whereas the dummy lozenge caused only a modest increase in salivary flow and swallowing. Cholinergic stimulation by bethanechol elicited a substantial increase in salivary flow and swallowing rate. In contrast, atropine caused a significant decrease in both salivary flow and swallowing. We conclude that in awake, normal subjects the rate of spontaneous swallows is influenced directly by salivary flow. Because oral lozenges substantially increase both swallowing rate and salivary flow, such agents merit investigation as a potentially useful ancillary treatment for the relief of heartburn.

Adolescent↗
PubMed1991

Intestinal mucin secretion in streptozotocin-diabetic rats: lack of response to cholinergic stimulation and cholera toxin.

In diabetic rats, intestinal mucin secretion is unusually high compared with that in normal rats. These studies demonstrate that mucin synthesis is also increased in the diabetic intestine. alpha- and beta-adrenergic agonists or antagonists did not affect mucin output in either normal or diabetic animals, suggesting that altered release in diabetes was not due to goblet cells responding abnormally to adrenergic agents. The cholinergic agonist bethanechol caused a dose-dependent and atropine-sensitive increase in mucin secretion from the normal intestine but had no effect on mucin release from diabetic tissue. Atropine alone did not reduce mucin secretion from the diabetic intestine to levels found in normal tissue. Cholera toxin caused an approximately fivefold increase in mucin output from normal rats but had no effect on mucin secretion from diabetic animals. Thus, goblet cell responses to cholinergic stimulation and cholera toxin in the diabetic intestine are markedly impaired. However, loss of cholinergic control does not appear to be responsible for altered baseline mucin secretion in diabetes.

Animals↗
PubMed1979

L-Dopa inhibits metoclopramide stimulation of the lower esophageal sphincter in man.

Opossum lower esophageal sphincter smooth muscle contains inhibitory dopaminergic receptors. Since metoclopramide is a dopaminergic antagonist in many experimental situations, the present study was designed to investigate whether this mechanism could explain the lower esophageal sphincter (LES) stimulating action of metoclopramide in man. The interactions of (1) oral L-dopa, a dopamine precursor, and metoclopramide; and (2) L-dopa and the cholinergic agent, bethanechol, on lower esophageal sphincter pressure (LESP) in normal subjects were examined. Oral L-dopa significantly inhibited LESP response to either oral metoclopramide 20 mg (P less than 0.05), or intravenous metoclopramide 20 mg (P less than 0.05). In contrast, L-dopa did not inhibit the LESP response to subcutaneous bethanechol (0.07 mg/kg). Mean basal LESP measured 50 min after ingestion of 1000 mg L-dopa, 19.3 +/- 3.1 mm Hg, was significantly less than basal LESP after L-dopa placebo, 29.3 +/- 4 mm Hg (P less than 0.01). It is concluded that (1) L-dopa inhibited the metoclopramide-induced rise in LESP but not peak stimulation of LESP by bethanechol; (2) there is evidence for the possibility of LES dopaminergic inhibitory receptors in man; and (3) these data are consistent with the hypothesis that metoclopramide acts on the LES by blocking a dopaminergic pressure-lowering mechanism.

Adult↗