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PubMed1975

Recent advances in management of gastroesophageal reflux.

Gastroesophageal reflux is not synonymous with sliding hiatus hernia. It should be approached as a condition dependent on the intrinsic strength of the lower esophageal sphincter rather than on the presence of a hiatus hernia. The patient's account of symptoms is probably the most important means of diagnosis, but in addition the patient's history should be supplemented by radiographic evaluation. Initially the treatment of gastroesophageal reflux is one of prevention. If this conservative approach proves ineffective, drugs that restore sphincter strength can be tried. Surgery should be resorted to only if medical treatment fails, and then one of the newer specific antireflux procedures should be the operation of choice.

Antacids↗
PubMed1989

Muscarinic poisoning from medications and mushrooms. A puzzling symptom complex.

A mixture of signs and symptoms can occur with muscarinic poisoning from medications or mushrooms. Manifestations may vary even among persons who ingested mushrooms grown in the same patch and gathered at the same time. Confusion can occur if mushroom poisoning is attributed to a suspected species rather than to the toxin suggested by signs and symptoms. Accurate diagnosis depends on clinical suspicion and recognition of muscarinic manifestations, notably diaphoresis, salivation, bladder cramping, diarrhea, and difficulty with visual accommodation. Muscarinic toxicity due to medications necessitates an adjustment in drug dosage. In mushroom poisoning that produces primarily muscarinic effects, atropine is the treatment of choice.

Adult↗
PubMed1992

Gastroesophageal reflux: diagnosis and management.

The pathologic potential of chronic esophagitis cannot be overemphasized. Persistent reflux causing cycles of mucosal damage followed by healing may eventually lead to end-stage disease, with development of peptic stricture. The most effective drugs available are those that inhibit acid production. Drugs that will enhance lower esophageal function are still in the future.

Alginates↗
PubMed1985

The muscarinic receptor of chick embryo cells: correlation between ligand binding and calcium mobilization.

In this report we characterize muscarinic cholinergic receptor on embryonic cells. We established dose-response curves by fluorometric measurement of Ca2+ mobilization in cell suspensions of whole chick embryos stage 23/24. Ca2+ mobilization was quantitated by standardization of chlorotetracycline (CTC) fluorescence changes after stimulation with muscarinic agonists. We determined ED50 values for the agonists acetylcholine and carbachol as 3.4 X 10(-6) and 2.7 X 10(-5) M, respectively. Pilocarpine and oxotremorine were found to act as reversible competitive antagonists with inhibition constants (Kl) of 5.0 X 10(-6) and 1.4 X 10(-6) M, respectively. Bethanechol, which induced only 23% of the maximal effect obtained by acetylcholine, was a partial agonist with an ED50 of 4.8 X 10(-4) M. Its antagonistic component is expressed by an inhibition constant of 1.9 X 10(-4) M. In parallel, binding studies were performed in a competition assay with [3H]-quinuclidinylbenzilate. For the agonists acetylcholine and carbachol, binding parameters were best fitted by a "two binding-sites model." Comparison with dose-response curves indicated that Ca2+ mobilization was triggered via the high-affinity binding site. The inhibition constants of antagonists derived from the shift of dose-response curves corresponded to the fitted KD values of the binding studies when a "one binding-site model" was applied. Combination of dose-response and binding data showed close proportionality between receptor occupancy and calcium mobilization. No spare receptors were present.

Acetylcholine↗
PubMed1976

Microtubules and pancreatic amylase release by mouse pancreas in vitro.

The effects of vinblastine and colchicine on pancreatic acinar cells were studied by use of in vitro mouse pancreatic fragments. Vinblastine inhibited the release of amylase stimulated by bethanechol, caerulein, or ionophore A23187. Inhibition required preincubation with vinblastine,and maximum inhibition was observed after 90 min. Inhibition was relatively irreversible and could not be overcome by a high concentration of stimulant. Inhibition could also be produced by colchicine although longer preincubation was required and inhibition was only partial. Uptake of [3H]vinblastine and [3H]colchicine by pancreatic fragments was measured and found not to be responsible for the slow onset of inhibition by these drugs. In incubated pancreas, microtubules were present primarily in the apical pole of the cell and in association with the Golgi region. Vinblastine, under time and dose conditions that inhibited the release of stimulated amylase, also reduced the number of microtubules. The only other consistent structural effects of vinblastine were the presence of vinblastine-induced crystals and an increased incidence of autophagy. The remainder of cell structure was not affected nor were overall tissue ATP and electrolyte contents or the stimulant-induced increase in 45Ca++ efflux. It is concluded that the antisecretory effects of vinblastine and colchicine are consistent with a microtubular action, but that acinar cell microtubules are more resistant to the drugs than many other cell types.

Adenosine Triphosphate↗
PubMed1982

Secretion of endogenous lectin by chicken intestinal goblet cells.

The two lactose-binding lectins found in adult chicken intestine, chicken-lactose-lectin-1 (CLL-1) and chicken-lactose-lectin-11 (CLL-11), were localized within the vesicles of the mucin-secreting goblet cells by indirect immunofluorescence and immunoperoxidase staining methods. Attention was concentrated on CLL-11 which is 200 time more abundant than CLL-1 in adult intestine. The localization of CLL-11 in secretory vesicles, combined with its demonstration on the intestinal epithelial surface by immune staining methods and by specific elution with lactose, suggested that at least a portion of the CLL-11 in the vesicles was secreted by the goblet cells and then became associated with the mucosal surface. In support of this, treatment of isolated intestinal strips with a cholinergic agent, bethanechol (10(-7 M) produced a small but significant increase in the amount of CLL-11 that could be eluted from their surface with lactose. Secretion of lectin may occur in conjunction with mucin because both are localized in the secretory vesicles and CLL-1 and CLL-11 apparently bind to purified chicken intestinal mucin, which is a potent inhibitor of their hemagglutination activities. The mucin is six orders of magnitude more potent than lactose as a hemagglutination inhibitor of CLL-1 or CLL-11 on a molar basis, and three orders of magnitude more potent when expressed per mole of hexose. These results suggest that CLL-11, and perhaps CLL-1, are secreted from the goblet cells along with mucin. They may function in the organization of mucin for secretion and/or in its association with the intestinal mucosal surface.

Animals↗
PubMed1988

In vitro assay of pancreatic acinar-cell function of rats made chronically riboflavin deficient.

To determine the effect of riboflavin deficiency on the rat pancreas, one-third of a group of rats was fed a purified riboflavin-sufficient diet ad libitum and two-thirds were fed isocaloric amounts of riboflavin-deficient diet for 13 wk; one-half of the latter group was replenished with daily intraperitoneal injections of riboflavin for the last 3 wk. Body weight, pancreas weight, DNA, protein, amylase, chymotrypsinogen, and trypsinogen decreased in riboflavin-deficient animals. In vitro basal secretion of chymotrypsinogen decreased and basal and bethanechol-stimulated secretions of trypsinogen increased in riboflavin-deficient rats. These changes were considered to be caused by relative inanition resulting from decreased food consumption. On replenishment of riboflavin, amylase content reverted to that of animals fed ad libitum whereas increases in body weight, pancreas weight, DNA, protein, chymotrypsinogen, and trypsinogen were not statistically significant. Both basal- and bethanechol-stimulated secretions of chymotrypsinogen increased. These data indicate that riboflavin deficiency, which commonly accompanies chronic alcoholism, may contribute to the pancreatic injury in chronic alcoholism.

Amylases↗
PubMed1984

Intracellular Escherichia coli in urinary malakoplakia: a reservoir of infection and its therapeutic implications.

Urinary malakoplakia may pursue an aggressive clinical course with persistent infection, despite seemingly appropriate antibiotic therapy. The authors studied seven adult females with urinary malakoplakia. Specific immunocytochemical staining demonstrated intracellular Escherichia coli in malakoplakia tissue in four patients. In two of the four patients, the bacteria were present despite antibiotic-induced sterile urines at time of biopsy. Cessation of therapy consistently lead to recurrent bacteriuria in these patients. In one such patient, the intracellular bacilli were confirmed as E. coli by culture of crushed malakoplakia tissue and electron microscopic study; the organisms were a routine E. coli strain susceptible to multiple previously administered antibiotics. Only sequential treatment with bethanechol chloride and trimethoprim-sulfamethoxazole, however, eliminated the infection; all three drugs are thought to be capable of enhancing intracellular killing of bacteria. Conventional antibiotic therapy failed to halt progression of disease in other malakoplakia patients. The data indicate that intracellular bacteria may serve as a reservoir of persistent/recurrent infection in urinary malakoplakia. Optimal therapy should include therapeutic agents that may control intracellular organisms.

Adult↗
PubMed1994

Bilateral renal parenchymal malacoplakia presenting as fever of unknown origin: case report and review.

Malacoplakia is a rare inflammatory disorder seen most often in the urinary tract, where it is highly associated with coliform infection. Although first recognized by pathologists in 1902, it has received little attention from the infectious disease community. While there remains much uncertainty regarding the specific cause of malacoplakia, it appears to be associated with a defect in intracellular killing of ingested microorganisms by macrophages. We report a case of bilateral renal parenchymal malacoplakia that presented as fever of unknown origin, and we review 33 previously identified cases. Renal malacoplakia has traditionally been associated with high morbidity and mortality. More recently, treatment with antimicrobial agents such as trimethoprim or ciprofloxacin has yielded a better outcome than had been documented with other therapy. Malacoplakia should be considered in the evaluation of fever of unknown origin or of relapsing or refractory urinary tract infection. Therapy with antimicrobial agents capable of intracellular penetration is recommended.

Anti-Infective Agents↗
PubMed1974

The effect of parietal cell and truncal vagotomy on gastric and duodenal contractile activity of the unanesthetized dog.

The antral-duodenal contractile relationship was studied in control, after parietal cell vagotomy and truncal vagotomy conditions using extraluminal strain gage transducers. All conditions were investigated under interdigestive and digestive states and after insulin, bethanechol and histamine. After parietal cell vagotomy, there was minimal alteration of the antral-duodenal relationship in both the interdigestive and digestive states. The number and amplitude of contractions on both the antrum and duodenum (as reflected by a motility index) were not changed from control by the various stimulants. The one exception was that histamine markedly stimulated the duodenal contractile activity. In the truncal vagotomy condition, there was a total disruption of the antral-duodenal relationship in the interdigestive and digestive states. There was a significant decrease in the number and amplitude of contractions occurring on the antrum during the interdigestive and after insulin stimulation. Food was ineffective in stimulating the antrum in 2 of 3 dogs. In contrast, motor activity of the duodenum was minimally influenced by truncal vagotomy. In conclusion, parietal cell vagotomy has minimal disruptive effects on the antralduodenal relationship while truncal vagotomy reduces antral contractile activity.

Animals↗
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↗
PubMed1982

Effect of bethanechol on gastric acid secretion and serum gastrin concentration after proximal gastric vagotomy.

It has been suggested that maximal acid output decreases after vagotomy as a result of reduced cholinergic activity and that maximal acid secretion can be restored to prevagotomy levels with cholinergic agonists. To test this, a maximally tolerated dose of bethanechol (50 micrograms/kg/hr) or saline was infused intravenously in nine duodenal ulcer patients who had been treated by proximal gastric vagotomy. Bethanechol infusion significantly (p less than 0.05) increased basal acid secretion without affecting basal serum gastrin concentrations. Despite stimulation of basal acid secretion, bethanechol had no significant effect on maximal acid output in response to subcutaneous pentagastrin. Although bethanechol significantly increased maximal acid output in response to subcutaneous histamine, maximal acid secretion in response to histamine (or to pentagastrin) was not restored to the prevagotomy level in any patient. Thus, factors other than loss of cholinergic activity appear to be responsible for the large reduction in maximal secretory capacity after vagotomy.

Adult↗