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At least 163 records · Page 9Linked to original sources
PubMed1989

Relaxatory responses of canine proximal stomach to esophageal and duodenal distension. Importance of vagal pathways.

The viscerovisceral reflex control of gastric tone remains poorly characterized. We have previously demonstrated physiological variations in gastric tone that occur during fasting and after feeding. These variations are neurally regulated. We have now compared the reflex mechanisms modulating gastric tone that are elicited by esophageal or duodenal distension in fasted, conscious dogs. To determine the pathways involved in these reflexes, we combined the technique of vagal blockade (by cooling the supradiaphragmatic vagi isolated within a surgically implanted cooling jacket) with the administration of autonomic drugs. Gastric tone was measured as the air volume within an intragastric bag maintained at a constant, low pressure by an electronic barostat. Standardized distensions were performed by means of an inflatable balloon-catheter positioned either in the mid-esophagus (in three dogs) or in the distal duodenum (in three dogs). A profound and consistent gastric relaxation was induced by distension of either the esophagus (247 +/- 21 ml delta volume, P less than 0.05) or the duodenum (238 +/- 29 ml, P less than 0.05). Supradiaphragmatic vagal cooling abolished the gastric relaxatory response to duodenal distension and significantly reduced, but did not completely suppress, the response to esophageal distension. Neither cholinergic stimulation (intravenous bethanechol) nor adrenergic blockade (combined intravenous phentolamine and propranolol) had any significant effect on either gastric relaxatory response. Combined adrenergic and cholinergic (intravenous atropine) blockade induced gastric relaxation, but failed to suppress the gastric responses. We conclude that both esophageal and duodenal distension elicit gastric relaxation by a noncholinergic vagal mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Characterization of in vivo acid secretory responses of rabbit with comparison to dog and rat.

Even though rabbit gastric glands are a commonly used model for the study of gastric physiology, little is known about the secretion of gastric acid in the rabbit in vivo. Gastric acid secretion in response to pentagastrin, histamine, and bethanechol stimulation, and the effect of specific cholinergic and histamine H2-receptor blockers was studied in 62 urethane-anesthetized rabbits. Additionally, the responses of eight conscious rabbits prepared with chronic gastric fistula were compared with similarly prepared conscious dogs (n = 10) and conscious rats (n = 18). In anesthetized rabbits, maximal pentagastrin stimulation resulted in acid outputs only 22% that of maximal histamine stimulation, but this was enhanced by restoring cholinergic tone with a subthreshold infusion of bethanechol. In conscious rabbits, pentagastrin was an effective stimulant, resulting in maximal acid output 70% that of maximal histamine stimulation. This is in contrast to the in vitro findings reported reported by others utilizing isolated gastric glands and cells. Histamine was a potent stimulant of acid secretion in both the anesthetized and conscious rabbit, an observation that parallels the in vitro findings. Unlike the dog and rat, atropine was ineffective as an inhibitor of histamine-stimulated acid secretion in the conscious rabbit, although it was marginally effective against histamine in anesthetized rabbits and against pentagastrin in conscious rabbits. It is concluded that cholinergic tone plays a crucial role in pentagastrin-stimulated acid secretion in the rabbit. This may be an explanation for the poor response to pentagastrin described in isolated rabbit gastric gland preparations.

Animals↗
PubMed1988

Impaired exocrine pancreatic function in diabetics with diarrhea and peripheral neuropathy.

Exocrine pancreatic insufficiency has been observed in some diabetics with peripheral neuropathy and diarrhea. Several mechanisms may be responsible for this insufficiency: (1) pancreatic atrophy, (2) disruption of the cholinergic enteropancreatic reflexes, or (3) elevated serum levels of peptides such as glucagon and pancreatic polypeptide which are known to inhibit pancreatic exocrine secretion. To clarify the mechanism(s) involved in this exocrine pancreatic impairment, we studied 10 diabetics with diarrhea and peripheral neuropathy. Their results were compared to those of eight normal volunteers. Each subject underwent a standardized pancreatic function study which assessed nonstimulated secretion, the response to intrajejunal infusion of a mixture of amino acids, and the output following intravenous administration of secretin and cholecystokinin (CCK). In separate studies, the effect of a background infusion of bethanechol and secretin on the pancreatic response to CCK was assessed in six patients and six normal controls. Compared to normals, all diabetics exhibited a significant reduction in both enzyme and bicarbonate secretion to all stimuli. This reduction was not corrected by administering bethanechol. Plasma glucagon and pancreatic polypeptide levels in diabetics were not significantly higher than those in controls. We conclude that diabetics with diarrhea and peripheral neuropathy exhibit impairment of their exocrine pancreatic secretion and possible mechanisms for this are discussed.

Adult↗
PubMed1993

Prosexual drugs: empirical status of the "new aphrodisiacs".

The search for an effective aphrodisiac has been a perennial pursuit of most societies throughout history. In the past decade, attention has focused increasingly on the prosexual effects of oral pharmacological agents with central neurotransmitter actions. The role of various dopaminergic, adrenergic, and serotonergic agents, in particular, has been intensively investigated in both human and animal studies. Some of these drugs have been considered for their potential role in the treatment of sexual dysfunction, while others have contributed to our understanding of basic neurophysiological processes in sexual arousal. This review provides a critical evaluation of current laboratory and clinical research on the "new aphrodisiacs," including studies in both patient populations and normal volunteers. Several conceptual and methodological problems are addressed, such as the definition and measurement of sexual response, the need to separate specific and nonspecific drug effects on sexual response, and the lack of studies in women. Although no single drug has proven to be clinically safe and reliably effective for human use, several promising candidates have been identified. Overall, research on prosexual drugs has contributed significantly to our understanding of basic mechanisms in sexual response, as well as providing new treatment options for common sexual disorders.

Aphrodisiacs↗
PubMed1994

Cholinergic dysfunction in Shy-Drager syndrome: effect of the parasympathomimetic agent, bethanechol.

To determine the frequency, severity and organ distribution of cholinergic dysfunction in the Shy-Drager syndrome, eleven patients were prospectively studied. In addition to documenting adrenergic insufficiency, a battery of twelve tests was employed to assess cholinergic function. Six tests demonstrated pupillary, lacrimal, salivary, urinary bladder, sexual and sudomotor dysfunction in the majority of patients. Cardiac vagal function as studied by the heart rate response to deep breathing, the Valsalva manoeuvre, cold face test, apnoeic facial immersion and atropine test was affected in all patients. Oesophageal motility was abnormal in six patients. Cholinergic dysfunction in patients with the Shy-Drager syndrome was widespread but of variable severity and distribution. Subcutaneous administration of the parasympathomimetic agent bethanechol demonstrated hyperresponsiveness of lacrimal, salivary, oesophageal, bowel, bladder and sudomotor functions. It is suggested that the Shy-Drager syndrome is primarily a preganglionic cholinergic disorder with transsynaptic degeneration accounting for the development of postganglionic cholinergic as well as adrenergic dysfunction.

Aged↗
PubMed1980

Gastroesophageal scintigraphy.

The technique of gastroesophageal scintigraphy was developed in order to quantitatively detect reflux from the stomach into the esophagus. The scintigraphic technique was compared to previous diagnostic tests including barium esophagography, fluoroscopy, endoscopy, esophageal biopsy, the acid perfusion test, esophageal manometry, and the acid reflux test. None of the other techniques is as sensitive as gastroesophageal scintigraphy for the detection of reflux, in comparison to the acid reflux test. Gastroesophageal scintigraphy is able to detect gastroesophageal reflux accurately, rapidly, noninvasively, and more sensitively than other diagnostic techniques. In addition, it is able to be employed to quantitate reflux and is suitable for studying the effects of various therapeutic modalities.

Adult↗
PubMed1977

Intracellular uptake and alpha-amylase and lactate dehydrogenase releasing actions of the divalent cation ionophore A23187 in dissociated pancreatic acinar cells.

Intracellular uptake of A23187 and the increased release of amylase and lactate dehydrogenase (LDH) accompanying ionophore uptake was studied using dissociated acinar cells prepared from mouse pancreas. Easily detected changes in the fluorescence excitation spectrum of A23187 upon transfer of the ionophore from a Tris-buffered Ringer's to cell membranes were used to monitor A23187 uptake. Uptake was rapid in the absence of extracellular Ca2+ and Mg2+ (t1/2=1 min) and much slower in the presence of Ca2+ or Mg2+ (t1/2=20 min). Cell-associated ionophore was largely intracellular as indicated by fluorescence microscopy, lack of spectral sensitivity to changes in extracellular Ca2+ and Mg2+, and by equivalent interaction of ionophore with membranes of whole and sonicated cells. A23187 (10 micronm) increased amylase release 200% in the presence of extracellular Ca2+ and Mg2+. In the absence of Ca2+ (but in the presence of Mg2+) A23187 did not increase amylase release. A23187 (10 micronm) also produced Ca2+ -dependent cell damage, as judged by increased LDH release, increased permeability to trypan blue, and by disruption of cell morphology. The cell damaging and amylase releasing properties of A23187 were distinguished by their time course and dose-response relationship. A23187 (1 micronm) increased amylase release 140% without increasing LDH release or permeability to trypan blue.

Amylases↗
PubMed1992

The influence of chronic nicotine treatment on stress-induced gastric ulceration and emptying rate in rats.

Ten-day treatment with nicotine (5, 25 or 50 micrograms/ml drinking water) dose-dependently intensified gastric ulceration induced by cold-restraint, and emptying rate. Stomach contractions produced by graded doses of bethanechol i.v. were elevated further by nicotine treatment. It is suggested that chronic nicotine administration produces hypersensitivity of the gastric muscarinic receptors; stomach hypermotility contributes to the ulcer-worsening action of the alkaloid.

Animals↗
PubMed1982

Calcium causes the biphasic dose-response curve for pancreatic amylase secretion.

High concentrations of bethanechol (10(-4) to 10(-3) M) were effective stimulants of amylase secretion from the mouse pancreas if incubations are performed in low [Ca2+] (0.1 mM) solutions but not if normal Krebs solution (2.56 mM Ca2+) was used. This inhibitory effect of Ca2+ at high secretagogue concentrations did not appear to be mediated through the microtubules or microfilaments.

Amylases↗
PubMed1986

Are prostaglandins involved in somatostatin mediated inhibition of gastric secretion in the cat?

The role of prostaglandins in somatostatin mediated gastric inhibitory effects has been investigated in conscious cats. The effect of somatostatin on pentagastrin-, insulin- and histamine plus bethanechol-stimulated gastric acid and pepsin secretion was determined with and without indomethacin pretreatment. Somatostatin significantly inhibited acid and pepsin secretion and this effect was not diminished by cyclo-oxygenase inhibition. It is concluded that there is no evidence that endogenous prostaglandins mediate the inhibitory effects of somatostatin on gastric acid and pepsin secretion in the cat.

Animals↗
PubMed1983

Cholinomimetics produce seizures and brain damage in rats.

Microinjections of the cholinergic agonists, carbachol and bethanechol, either into the amygdala or into the dorsal hippocampus produced sustained limbic seizures and brain damage in rats. Systemic administration of pilocarpine in rats resulted in a sequence of convulsive disorders and widespread brain damage as well. Scopolamine prevented the development of convulsive activity and brain damage produced by cholinomimetics. These results suggest that the excessive stimulation of cholinergic muscarinic receptors can lead to limbic seizures and brain damage. It is postulated that muscarinic cholinergic mechanisms are linked to the etiology of temporal lobe epilepsy and epileptic brain damage.

Amygdala↗
PubMed1981

The effect of ranitidine on gastric acid secretory response curves to histamine, pentagastrin or bethanechol in the dog with a Heidenhain pouch.

The H2-receptor antagonists ranitidine and cimetidine were tested against gastric secretory dose-response curves to histamine, pentagastrin and bethanechol in the Heidenhain-pouch dog. Histamine-induced gastric secretion was antagonized in a competitive manner by both ranitidine and cimetidine, but ranitidine was approximately 8 times more potent than cimetidine. Pentagastrin -induced secretion was markedly reduced by ranitidine and cimetidine but this antagonism was not competitive in nature. Bethanechol-induced gastric secretion was slightly reduced by both drugs. These findings are discussed in relation to the physiological control of gastric secretion.

Animals↗
PubMed1994

Effect of CGRP antagonist, alpha-CGRP 8-37, on acid secretion in the dog.

The recently synthesized calcitonin gene-related peptide (CGRP) antagonist, human alpha-CGRP 8-37, was used to study its effects on gastric acid secretion. Four dogs with gastric fistula were used to measure the antagonist's physiologic effects in the stomach. All dogs received a bactopeptone dextrose meal (intragastric titration to pH 5.5) with either continuous CGRP 8-37 (1000 pmol/kg/hr) or saline (control). Additionally, intravenous bombesin (75-600 ng/kg/hr) and bethanechol (12.5-100 micrograms/kg/hr) was tested in the presence of the antagonist. Plasma gastrin levels also were measured via radioimmunoassay (RIA) in control and CGRP 8-37-stimulated animals. Gastric acid secretion increased by 100% with infusion of 1000 pmol/kg/hr CGRP 8-37 when compared to the control. Acid output increased 98% with both intravenous antagonist and 600 ng/kg/hr bombesin when compared to bombesin alone. However, no augmentation of acid secretion by CGRP 8-37 was shown with 25 micrograms/kg/hr bethanechol. RIA of plasma gastrin demonstrated no effect with the antagonist when given alone and did not increase bombesin-stimulated gastrin release. We conclude that CGRP 8-37 blocks native CGRP inhibitory effects on gastric acid secretion. Our findings of potentiation of acid secretion by bombesin as well as no change in gastrin levels in the presence of the antagonist is likely due to a blockage in a noncholinergic neuron to the somatostatin cell. Furthermore, CGRP 8-37 did not increase bethanechol-stimulated acid secretion, most likely due to bethanechol's (acetylcholine) nearly ubiquitous positive effects on acid secretion.

Animals↗
PubMed1977

The effect of hexamethonium on gastric acid secretion in the conscious rat.

Evidence against a role for histamine in pentagastrin-stimulated acid secretion has been obtained previously using hexamethonium in gastric fistula rats. This possibility has been re-examined in conscious rats provided with gastric fistulae or Heidenhain pouches. Hexamethonium (20 mg/kg s.c.) inhibited basal acid secretion and acid secretion stimulated by histamine and pentagastrin in gastric fistula rats. The same dose of hexamethonium failed to produce a significant inhibition of acid secretion stimulated by bethanechol, pentagastrin or histamine in the presence of a low dose of bethanechol in Heidenhain pouch rats. These results provide no evidence to oppose the view that pentagastrin-stimulated acid secretion in the rat is mediated at least in part through the mobilization of gastric mucosal histamine. The inhibition of secretagogue induced acid secretion in the gastric fistula rat is mainly the result of a reduction in the basal acid output.

Animals↗