Search PubMed⌕ Search

Biomedical subjects

J Behar

Publications and source records attributed to J Behar.

At least 73 records · Page 4Linked to original sources
PubMed1984

Neural control of the sphincter of Oddi. Physiologic role of enkephalins on the regulation of basal sphincter of Oddi motor activity in the cat.

The effect and physiologic role of enkephalins on the sphincter of Oddi was studied in the cat. Leucine- and methionine-enkephalin caused an initial sphincter of Oddi contraction followed by a more prolonged relaxation. The excitatory effect of leucine-enkephalin was antagonized partially by atropine and by methysergide infusion. It was completely blocked by a combination of atropine and methysergide infusion, by tetrodotoxin, by 5-hydroxytryptamine depletion induced by reserpine, and by 5-hydroxytryptamine tachyphylaxis. Naloxone infusion decreased sphincter of Oddi motor activity, which was reversed by tetrodotoxin. Maximal sphincter of Oddi relaxation was induced by doses of naloxone (40 micrograms/kg) that antagonized a maximal dose of morphine. Higher doses of naloxone (640 micrograms/kg) were needed to block maximal doses of enkephalin (8 micrograms/kg). The enkephalin inhibitory action was blocked only by tetrodotoxin. These findings indicate that (a) leucine-enkephalin has two receptor sites on the sphincter of Oddi--one at the serotonergic neurons and the other at noncholinergic, nonadrenergic inhibitory neurons, and (b) opioid peptides participate in the intramural excitatory pathway to the sphincter of Oddi.

Ampulla of Vater↗
PubMed1983

Neural control of the sphincter of Oddi. A physiological role of 5-hydroxytryptamine in the regulation of basal sphincter of Oddi motor activity in the cat.

The effect of 5-hydroxytryptamine (5-HT) on the sphincter of Oddi (SO) was studied in the cat. The SO had two motor responses to 5-HT: the most common was an initial contraction followed by a more prolonged relaxation, and the other was an exclusive relaxation. Tetrodotoxin did not impair the magnitude of the net contraction induced by 5-HT, but it completely blocked the relaxation. Methysergide partially inhibited the SO contraction in response to submaximal doses of 5-HT (5-20 micrograms/kg). Atropine decreased the SO excitatory response to all doses of 5-HT. The combination of atropine and methysergide completely antagonized the 5-HT excitatory effect, which changed the SO biphasic response to an exclusive relaxation. After tetrodotoxin, the effect of 5-HT was almost completely antagonized by methysergide alone. The SO contraction and relaxation caused by 5-HT were almost completely blocked by 5-HT tachyphylaxis. In contrast, a 5-HT depletion with reserpine enhanced the sensitivity of the SO to 5-HT, responding to doses a thousand times smaller than in control animals. Hexamethonium, phentolamine, propranolol, and 5-methoxy-N,N-dimethyltryptamine did not antagonize the 5-HT-induced contraction or relaxation. These findings indicate that 5-HT caused SO contraction by stimulating postganglionic cholinergic neurons and the smooth muscle directly and caused relaxation by stimulating postganglionic, noncholinergic, nonadrenergic inhibitory neurons. 5-HT blockade or depletion resulted in a significant reduction in basal tonic pressures and in the amplitude of phasic contractions, which suggested that serotonergic neurons may play a physiologic role in the regulation of basal SO motor activity.

Ampulla of Vater↗
PubMed1980

Effect of hemorrhagic hypotension and hypoventilation on lower esophageal sphincter pressure.

Dysfunction of the lower esophageal sphincter has been demonstrated in the cat shock model. Analogies have been drawn to reflux and aspiration in the critically ill patient. In a cat shock model, lower esophageal sphincter pressure is reduced and response to bethanechol is impaired. Upon resuscitation to basal state with heparinized shed blood, the lower esophageal basal pressure returns to normal values, and response to bethanechol is restored. This model may explain reflux and aspiration in the critically ill patient.

Acidosis↗
PubMed1980

Effect of cholecystokinin and the octapeptide of cholecystokinin on the feline sphincter of Oddi and gallbladder. Mechanisms of action.

We studied the effect of cholecystokinin (CCK) and the octapeptide of cholecystokinin (OP-CCK) on the feline gallbladder and sphinecter of Oddi. Both CCK caused a dose-dependent gallbladder contraction and sphincter of Oddi relaxation. The half-maximal responses of the sphincter of Oddi were 6 ng/kg for OP-CCK and 0.15 Ivy-dog U/kg for CCK, which were lower than those of the gallbladder with 28 ng/kg and 0.32 Ivy-dog U/kg, respectively. The effect of OP-CCK on the gallbladder was partially blocked by tetrodotoxin (P < 0.02), hexamethonium alone (P < 0.05), or a combination of hexamethonium and atropine (P < 0.01). The gallbladder response to CCK was not blocked by either atropine alone (P < 0.60) or adrenergic antagonists (P > 0.40). The sphincter of Oddi response to OP-CCK was blocked by tetrodotoxin (P < 0.001) but it was not blocked by cholinergic (P < 0.20) or adrenergic antagonists (P < 0.60). After complete denervation with tetrodotoxin, OP-CCK caused sphincter of Oddi contraction. These findings indicate that there are two excitatory receptors for CCK in the gallbladder, one at the cholinergic neurons and the other at the level of the gallbladder muscle. There are also two receptors for CCK in the sphincter of Oddi, one that is inhibitory, and present at the noncholinergic, nonadrenergic neurons, and the other, excitatory, at the circular muscle.

Ampulla of Vater↗
PubMed1980

Mechanical characteristics of the cat pylorus.

In vitro force-length curves of rings from the gastroduodenal junction were obtained in standard tyrode solution, in tyrode with 140 mM KCl, and in calcium-free tyrode with 5 mM sodium EDTA, to determine basal, total, and passive forces, respectively. Active force was obtained as a difference between total and passive forces. Basal, total, passive, and active forces were higher for pyloric rings than for duodenal and antral rings. Furthermore, in the pylorus the force-length curves were shifted to the left along the length axis due to a narrowing at the gastroduodenal junction. Pressure-diameter relationships calculated from the in vitro force-length data and compared with previously determined in vivo pressure-diameter data, demonstrated good correlation between the in vivo and in vitro data. These data indicate that the higher forces and pressures observed in the pylorus are due to a combination of higher active and passive components. At low levels of stretch, the active forces are higher, while at high levels of stretch the passive forces become prevalent. These data suggest that, because of its passive properties the pylorus may act as a stricture and resist opening to large diameters, thus impeding the passage of large boluses. Near closure, however, any pressure gradient at the gastroduodenal junction would be due to active contraction of the pyloric circular muscles, and thus be susceptible to modulation through neural and/or myogenic factors.

Animals↗
PubMed1980

Pathogenesis of diabetic gastroparesis: a pharmacologic study.

The motor function of the antrum was studied in 7 normal subjects, 4 patients with diabetes without GI symptoms, and 7 patients with diabetic gastroparesis. Both the number of antral contractions and the cumulative antral activity (percent of time during which the antrum contracted) in patients with diabetic gastroparesis were significantly lower than in normal subjects and diabetic patients without gastroparesis (P less than 0.01). Interdigestive motor complexes were observed in all normal subjects, but they were not present in any patients with diabetic gastroparesis. Intravenous metoclopramide did not affect the rate of antral contractions (P less than 0.1), but it increased the cumulative antral activity (P less than 0.001) in normal subjects and diabetics without gastroparesis. Metoclopramide, however, did not alter the rate of antral contractions (P less than 0.09) or the total cumulative antral activity (P less than 0.09) in diabetic patients with gastroparesis. Furthermore, in normal subjects, the action of metoclopramide was blocked by atropine sulfate (P less than 0.003). Bethanechol caused a slight increase in the number of antral contractions (P less than 0.05) and cumulative antral activity (P less than 0.01) in normal subjects. This cholinergic drug caused a marked increase in the rate of antral contractions and the cumulative antral activity in diabetic patients with gastroparesis. Antral contractions and cumulative antral activity were restored by bethanechol to normal values. These findings suggest a variable degree of gastric neuropathy in individual patients with diabetic gastroparesis with functionally intact antral muscles as assessed by their pharmacologic response to cholinergic stimulation.

Adult↗
PubMed1978

Cimetidine in the treatment of symptomatic gastroesophageal reflux: a double blind controlled trial.

The effectiveness of cimetidine for symptomatic relief in patients with chronic gastroesophageal reflux was studied in a multicenter, double blind clinical trial. Patients were entered into the study for a total of 8 weeks, receiving either cimetidine, 300 mg four times daily, or identical placebo tablets. Throughout the trial, frequent assessments were made of symptom severity and frequency, combined with careful measurement of antacid use. Esophagoscopy, esophageal acid sensitivity, and lower esophageal pressures were performed before and at the completion of the treatment period. Significant (P less than 0.05) decreases in symptom frequency and severity were noted throughout the study in the cimetidine-treated patients, as compared with the placebo group. This subjective improvement was corroborated by a concomitant decrease in antacid use, which was significantly (P less than 0.05) reduced in the cimetidine-treated group. In addition, significant improvement in esophageal acid sensitivity resulted from cimetidine therapy. No objective improvement in esophageal endoscopic appearance or sphincter pressures was noted. The results of this double blind trial indicate that cimetidine is more effective than the placebo for the relief of symptoms of gastroesophageal reflux.

Adult↗
PubMed1978

Gastric emptying and antral motility in reflux esophagitis. Effect of oral metoclopramide.

The gastric emptying of the liquid phase of a meal and the fasting antral contractility were studied in 13 patients with reflux esophagitis and in 9 age-matched control subjects. Gastric emptying half-time (t 1/2) in reflux esophagitis patients was no different from that of control subjects (P less than 0.30). Antral contractility (number of antral contractions and the cumulative antral activity), however, was lower in reflux esophagitis patients than in control subjects (P less than 0.001). Oral metoclopramide (15 mg) accelerated gastric emptying, increased the number of antral contractions as well as the cumulative antral activity in patients with reflux esophagitis (P less than 0.001). However, it only increased the cumulative antral activity in normal subjects (P less than 0.01). These results suggest that metoclopramide may be potentially beneficial to reflux esophagitis patients by reducing the volume of gastric contents available for gastroesophageal reflux.

Administration, Oral↗
PubMed1977

Calcium stimulation of gastrin and gastric acid secretion: effect of small doses of calcium carbonate.

Oral calcium carbonate (0-5 g, pH 9-4) increased serum gastrin and gastric acid output with slight but insignificant change in serum calcium. A similar rise in serum calcium during an intravenous infusion of calcium gluconate failed to increase serum gastrin and gastric acid output. Both intragastric calcium actions were abolished by acidification of the calcium carbonate solution (pH 1-0). The increase in serum gastrin and gastric acid output after intragastric calcium carbonate was not affected, however, by a simultaneous intraduodenal acid load. Equivalent neutralising doses of magnesium hydroxide (pH 9-4) did not increase serum gastrin and gastric acid output above basal levels, whereas antral acidification with 20 ml 0-1 N HCl resulted in a slight decrease in serum gastrin. Intraduodenal calcium carbonate (pH 3-0) also increased serum gastrin and gastric acid output, whereas an equivalent volume of intraduodenal saline (pH 3-0) had no effect. These findings indicate that calcium increases serum gastrin by local stimulation of antral and duodenal mucosa. They also suggest that the action of calcium on gastric secretion is partly mediated by gastrin.

Calcium↗