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At least 919 records · Page 51Linked to original sources
PubMed1984

The developmental physiology of the stomach: possible contributions to the regulatory disturbances of duodenal ulcer disease.

Several different disturbances in the regulation of acid secretion have been found in persons with duodenal ulcer disease (DU). This paper examines the possibility that some of these regulatory disturbances might arise during postnatal development. The regulation of acid secretion is not fixed in adult form at birth, in either animals or humans. Instead, these regulatory processes continue to change during postnatal development. Examples are developmental changes in the responsiveness of the stomach to parietal cell stimulants and developmental increases and decreases in basal and maximal acid output. The unfolding of these developmental changes requires complex regulatory adjustments. It is possible that untoward environmental circumstances could induce "errors" in these regulated changes or adjustments. Some errors might persist as disturbances in the regulation of acid secretion seen in patients with DU.

Adult↗
PubMed1988

Comparison of somatostatin and its highly potent hexa- and octapeptide analogs on exocrine and endocrine pancreatic secretion.

The effects on pancreatic responses of highly potent cyclic hexapeptide (cyclo (N-Me-Ala-Phe-D-Trp-Lys-Thr-Phe)) (Veber analog) and octapeptide analogs of somatostatin such as D-Phe-Cys-Phe-D-Trp-Lys-Thr-Cys-Thr-ol (SMS 201-995), D-Phe-Cys-Tyr-D-Trp-Lys-Val-Cys-Thr-NH2 (RC-121), and D-Phe-Cys-Tyr-D-Trp-Lys-Val-Cys-Trp-NH2 (RC-160) have been compared with somatostatin tetradecapeptide (SS-14) and atropine. The parameters evaluated were pancreatic responses to secretin and meat feeding in conscious dogs with chronic pancreatic fistula and amylase release from the dispersed pancreatic acini. The analogs were administered intravenously or intraduodenally. The cyclic hexapeptide and octapeptide analogs, given iv in graded doses against a constant background stimulation with secretin, produced similar and dose-dependent inhibition of pancreatic HCO3- and protein secretion. Analogs RC-121, RC-160, and the Veber analog were about two to four times more active than SS-14 in suppressing HCO3- secretion and equipotent in reducing protein secretion, but SMS 201-995 was only about half as potent as somatostatin in inhibiting HCO3-. RC-160 was effective in inhibiting secretin-induced protein secretion at lower doses than other analogs. In tests with feeding, SMS 201-995, the Veber analog, RC-121, and RC-160 were more potent inhibitors of exocrine pancreatic secretion of HCO3- and protein and exhibited more prolonged inhibitory effects than SS-14. The Veber analog, RC-121, and RC-160 were also more effective after intraduodenal administration. Atropine also caused significant inhibition of both HCO3- and protein responses to secretin and meal feeding. All four analogs decreased the postprandial insulin and pancreatic polypeptide release to a similar degree as SS-14. Neither SS-14 nor the analogs tested significantly affected basal or caerulein-, gastrin-, secretin-, or bethanechol-stimulated amylase release from the dispersed canine pancreatic acini. Atropine reduced amylase release induced by bethanechol, but not that stimulated by caerulein, gastrin, or secretin. This indicated that the analogs, as somatostatin, are ineffective as secretory inhibitors in vitro. We conclude that cyclic hexapeptide and octapeptide analogs are more potent and longer acting inhibitors of pancreatic secretion than somatostatin-14 in vivo.

Amylases↗
PubMed1980

Treatment of diabetic cystopathy.

Neurogenic bladder disorders in diabetic patients may result in insufficient bladder emptying because of loss of reflex detrusor contraction. In those who are asymptomatic or have only moderate signs of diabetic cystopathy, treatment choices are scheduled voiding by the triple-voiding technique, cholinergic treatment either daily or twice weekly, and transurethral surgery of the bladder neck. In patients with total urine retention, an indwelling catheter will decrease the overstretched detrusor muscle. Cholinergic treatment with initially high parenteral doses of bethanecol may help to diminish residual urine. Transurethral surgery is often mandatory in such cases. Decensus of the bladder in females often requires surgery. Deficient bladder sensation is irreversible in diabetics, and follow-up of treatment should be lifelong.

Bethanechol Compounds↗
PubMed1980

Reflux esophagitis: effect of oral bethanechol on symptoms and endoscopic findings.

We ascertained the effectiveness of oral bethanechol on symptoms and endoscopic evaluation of reflux esophagitis in a double-blind controlled study. Forty-four patients were treated with either 25-mg bethanechol tablets or placebo, each given four times daily for 4 weeks, in addition to conventional medical therapy. Both therapies significantly decreased symptoms as well as endoscopic lesions; however, endoscopic improvement was significantly better in the bethanechol-treated group. Bethanechol therapy resulted in complete endoscopic healing in 10 of 22 cases, whereas only three of 22 patients in the control group had such healing. No worsening of endoscopic lesions was seen in either group. Our study indicates that bethanechol is an effective drug offering advantages over conventional antacid therapy in the treatment of reflux esophagitis.

Administration, Oral↗
PubMed1982

Gastroesophageal reflux. Pathogenesis, diagnosis, and therapy.

In recent years, considerable new information has become available on the pathogenesis, diagnosis and therapy of gastroesophageal reflux. Gastric contents, mucosal resistance, esophageal acid clearance, and gastric emptying are now recognized, along with incompetency of the lower esophageal sphincter, as contributing factors to gastroesophageal reflux disease. The potential tests for reflux are reviewed and the diagnostic accuracy of each is evaluated. A diagnostic approach to the patient with reflux symptoms is outlined that considers the sensitivity and specificity of these various tests as well as their availability to the generalist and gastrointestinal specialist. Finally, an overview of the current therapy for reflux disease summarizes the controlled studies in the medical literature.

Alginates↗
PubMed1983

Disorders of gastrointestinal motility associated with diabetes mellitus.

Gastrointestinal symptoms such as vomiting, constipation, diarrhea, and fecal incontinence occur frequently in patients with diabetes mellitus. In a survey of 136 diabetic outpatients, 76% had one or more gastrointestinal symptoms, the commonest symptom being constipation (found in 60%). In many cases these symptoms are thought to be due to abnormal gastrointestinal motility that, in turn, may be a manifestation of diabetic autonomic neuropathy involving the gastrointestinal tract. The pathophysiology of these gastrointestinal symptoms, clarified in recent studies, and the clinical features and treatment of these problems in diabetic patients are reviewed.

Autonomic Nervous System Diseases↗
PubMed1979

Histaminergic involvement in thyrotropin-releasing hormone stimulation of antral tissue in the rat.

The mechanism of action of thyrotropin-releasing hormone on antral motility was investigated in vitro. With the recent detection of thyrotropin-releasing hormone in gastrointestinal tissue, the possibility exists that the peptide may play a physiologic role in gastrointestinal motility. Results indicate that the hormone stimulates antral motility through a non-cholinergic excitatory pathway based on the inability of the muscarinic antagonist, atropine, to block the response. A histaminergic pathway is an attractive possibility to explain the excitatory response, because both pyrilamine and cimetidine inhibit the thyrotropin-releasing hormone induced response and the peptide has no further influence on antral motility after the tissue is exposed to a supramaximal concentration of histamine.

Animals↗