Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Basal serum gastrin in 40 patients with benign gastric ulcer was 103 +/- 10.7 pg/ml, a level significantly higher than corresponding estimations in normal subjects and patients with duodenal ulcer. Following stimulation by a protein meal, a mean rise of 124 pg/ml was achieved at 75 minutes and prior atropinization induced a rise of 208 pg/ml at 90 minutes. Insulin hypoglycaemia produced a rise of 63 pg/ml which was not significantly changed with concomitant neutralization of gastric contents. These results suggest that patients with gastric ulcer have higher basal gastrin levels than normal and this is probably related to the lowered antral acidity. In addition, the protein meal and insulin hypoglycaemia responses suggest an increased antral G cell mass and the possibility of additional gastrin release from sites outside the antrum. It is doubtful whether the relative hypergastrinaemia has an aetiological role in gastric ulcer but it may have a role in the maintenance of gastric ulcer.
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PMID:Gastrin studies in gastric ulcer. 502 20

Serum gastrin has been measured by radioimmunoassay in normal subjects and patients with proven duodenal ulcer in response to insulin hypoglycaemia in conjunction with manoeuvres to decrease the intragastric acidity. Insulin hypoglycaemia alone caused a rise in the serum gastrin level from 5 +/- 1.0 to 49 +/- 2.9 pg/ml in duodenal ulcer and from 17 +/- 5.6 to 42 +/- 7.7 pg/ml in normals. With complete intragastric neutralization of acid and the same stimulus, the rise in duodenal ulcer was from 5 +/- 1.3 to 128 +/- 13.6 pg/ml and in normals from 13 +/- 2.6 to 84 +/- 2.6 pg/ml. These studies suggest an increased production rate of gastrin in response to vagal stimulation in duodenal ulcer, and indicate the precise role of acid inhibition in the control of gastrin release and support the concept of both an increased ;G cell' mass and parietal cell mass in duodenal ulcer. They have also offered an explanation of the variable vagal stimulation of gastrin release in normal subjects.
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PMID:Serum gastrin in duodenal ulcer. II. Effect of insulin hypoglycaemia. 515 33

Esophageal ligation in the pylorus-ligated rat significantly inhibited volume, titratable acidity, and titratable acid output and reduced the incidence of ulcers, perforations, and death of 18-hr pylorus-ligated rats. Draining the saliva outside the body of the rat by esophageal cannulation produced a significant increase in volume and gastric acidity over the esophagus-ligated preparation. A method for collection of saliva in the unanesthetized unstimulated rat was developed, and basal salivary flow was found to be 0.84 ml/4 hr. Administration of 1.0 ml of freshly collected saliva to esophagus + pylorus-ligated rats increased titratable acidity, but not volume of secretion, to the level found in the pylorus-ligated rat. A similar effect was obtained with administration of 1.0 ml of a phosphate buffer. Removal of the salivary glands had no significant effect on gastric acidity in the pylorus-ligated rat and the reduction in volume could be accounted for by the lack of saliva. Gastric secretion in the esophagus + pylorus-ligated rat was stimulated by histamine, carbachol, insulin, and 2-deoxyglucose. When the vagus nerves were cut, stimulation was still obtained with carbachol but not with insulin or 2-deoxyglucose. The data indicated that rat saliva did not contain a specific gastric stimulant material, and esophageal ligation depressed gastric secretion in the pylorus-ligated rat by inhibition of the central vagal activity.
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PMID:The mechanism of the inhibition of gastric secretion produced by esophageal ligation in the pylorus-ligated rat. 521 80

Anticholinergic agents are most often divided into tertiary and quaternary ammonium compounds. Tertiary ammonium agents are fully and rapidly absorbed. Quaternary ammonium agents are slowly and incompletely absorbed, but do not cross the blood-brain barrier, or do so to a very limited degree, and have a very low rate of central nervous system side-effects. There are probably subclasses of cholinergic receptors, and anticholinergic agents have different affinities for these. Anticholinergics can decrease the basal acid secretion as well as secretion stimulated by histamine, pentagastrin, insulin or food. Combined therapy with antacids and anticholinergics will give a more long-lasting decrease in acidity than with either drug alone. The reported controlled studies with anticholinergic agents suggest that they can induce healing of duodenal ulcer to the same degree as cimetidine but at the cost of more frequent side-effects. Except for the studies on pirenzepine there are, however, too few studies in which anticholinergics have been compared with histamine H2-receptor antagonists; thus the place of anticholinergics in the treatment of an active duodenal ulcer is not clear. In doses of not less than 100 mg daily, pirenzepine is a candidate-drug for the short-term treatment of duodenal ulcer. At these doses, side-effects of dry mouth and visual disturbance are, however, rather frequent, and more serious side-effects such as urinary retention do also occur. More studies with both the conventional anticholinergics and pirenzepine, with emphasis not only on the desired effects but also on side-effects, are needed before anticholinergics can be taken into consideration as alternatives to histamine H2-receptor antagonists for healing and maintenance treatment. There is some evidence that long-term treatment with anticholinergic agents can decrease recurrences and complications of peptic ulcer disease. Even if there are some encouraging reports on the combination of anticholinergics and antacids, we need more such studies with lower doses of antacids and lower doses of anticholinergics before this combination therapy can be regarded as an equally good alternative to histamine H2-receptor antagonists for ulcer healing and symptom relief.
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PMID:Antacids and anticholinergics in the treatment of duodenal ulcer. 608 86

After various types of sympathectomy (surgical, chemical, isolated adrenodemedullation; AMX, combined procedures) in the rat, basal gastric secretion, gastric mucosal blood flow (MBF), associated glucose and a variety of hormones in the blood were measured. With the exception of the ineffective surgical sympathectomy, all the other forms variously influence gastric secretion qualitatively (volume, acidity, pepsin) and quantitatively (output per unit time). Chemical sympathectomy has an augmenting effect both on acid (volume, acidity, output) and on pepsin. In general the MBF parallels acid, but the MBF is decreased after AMX despite stable or increased gastric secretion. Sympathectomy, except procedures involving AMX or AMX + surgical sympathectomy, increases spontaneous gastric mucosal lesions. With AMX glucose is diminished, but is elevated following surgical and chemical sympathectomy. Gastrin, insulin and somatostatin are always higher than in sham-operated controls, glucagon after surgical sympathectomy only. It is concluded that (1) the sympathoadrenal system in the rat modulates both basal gastric secretion and blood hormones; (2) the adrenal medulla may participate in the control of gastric MBF, and (3) gastric mucosal lesions are not correctly reflected by the ration MBF/acidity.
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PMID:Basal gastric secretion, mucosal blood flow and associated fasting blood hormones in the rat. Effects of various forms of sympathectomy. 612 14

After vagotomy (truncal, highly selective, superselective) in rats, basal gastric secretion, gastric mucosal blood flow, associated fasting blood glucose and a variety of hormones were measured. All forms of vagotomy reduce acid (volume, acidity, output), but highly selective and superselective--though not truncal--procedures stimulate basal pepsin secretion, whereas mucosal blood flow roughly parallels acid production. Spontaneous gastric mucosal lesions increase after highly selective vagotomy. Both highly selective and superselective--but not truncal--vagotomy tend to increase plasma glucose and somatostatin, while only the former reduces insulin and glucagon. Common to all vagotomies is the development of virtually undetectable calcitonin (less than 25 pg/ml) and of hypergastrinemia. It is concluded that in the rat with draining gastric fistula in response to vagotomy there are moderate differences in regard to gastric mucosal ulcer index, gastric secretion, glucose, glucose-regulating hormones, while lowered calcitonin may be a general feature of low vagal tone.
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PMID:Basal gastric secretion, mucosal blood flow and associated fasting blood hormones in the rat. Effects of various forms of vagotomy. 612 15

The modified sham feeding procedure has been advocated to replace the insulin test as the method of choice for the assessment of denervation after vagotomy. One of the reasons for this changing attitude is the assumption that insulin hypoglycaemia causes non-cholinergic stimulation of acid secretion, possibly mediated via the sympatho-adrenal system. This study has therefore compared the effects of these two different tests on acidity and release of catecholamines into the circulation in 7 duodenal ulcer patients 6 weeks after highly selective vagotomy. It was found that insulin, but not modified sham feeding, caused a marked increase in plasma adrenaline and noradrenaline concentrations whereas gastric acid secretion was of a similar magnitude in the two tests. The results suggest that the increased plasma catecholamine levels during insulin hypoglycaemia do not influence gastric acid secretion in duodenal ulcer patients.
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PMID:The role of catecholamines in the control of gastric acid secretion during insulin hypoglycaemia and modified sham feeding. 635 21

In non-stressed rats and rats stressed by immobilization, gastric secretion (acid, pepsin), mucosal blood flow (MBF), stress ulcers as well as glucose, insulin, and glucagon in blood were studied during 8 h, with and without additional infusion of exogenous glucagon (0.2, 1.4, 9.8 micrograms/kg/h). Metabolic clearance of glucagon and the disappearance half-time of exogenous glucagon from blood do not differ during zero stress and stress, a fact that favors the assumption of hypersecretion of glucagon as the cause of stress hyperglucagonemia. During stress alone acid secretion (volume, acidity) and MBF are lower than during zero stress; pepsin remains unchanged. Under zero stress condition additionally administered glucagon inhibits pepsin and MBF, but not acid secretion, in a dose-dependent manner. The ulcer index increased without changing the severity of ulcers. During stress the intermediate and highest glucagon doses stimulate MBF and pepsin secretion, other variables remaining unchanged. It is concluded that glucagon effects on functions of the gastric mucosa in the rat vary fundamentally, depending upon the environmental conditions.
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PMID:Influence of exogenous glucagon on gastric acid secretion, mucosal blood flow, and stress ulcers in the rat: dose-response results under non-stress conditions and immobilization stress. 661 2

The demand of the untrained skeletal muscle to produce additional mechanical work by utilizing more nutrients is the origin of the structural and metabolic adaptation of the muscle. The expanding capillary surface, in response to a lower vascular resistance during repeated contraction, enables the different fibre types to increase their oxygen extraction, and to adapt their uptake of substrates (glucose, FFA). The muscle fibre types in humans are selectively recruited for differing work intensity but the oxidative potential (SDH) increases in all types with long-term physical training. Details of the mechanism by which insulin promotes glucose uptake are unclear but there is some evidence that the hormonal stimulation involves cellular uptake of the insulin-receptor complex of the membrane. Hypoxia and raised cytoplasmic levels of calcium in muscle cells after work exert an insulin-like action on glucose uptake, which may be ascribed to the intracellular acidity.--The interrelationship between glucose and FFA oxidation is in part regulated by known key enzymes of the contracting muscle, but the exact extramuscular substrate mobilization appears to require both hormonal and supplementary feed-back control in storage organs.--During prolonged muscular exercise, the successive utilization of carbohydrate and fat from endogenous and exogenous stores can, however, in principle be attributed to known hormonal regulation.--Oral intake of glucose solution before and during work evokes a prolonged glucose utilization with relative hyperinsulinemia and hypoglucagonemia, preventing hepatic glycogenolysis. A prerequisite for successful endurance training is the improved capacity to use FFA as substrate. The necessary lipolysis in adipocytes is mainly mediated by an increased cellular exposure and sensitivity to catecholamines, but the delayed adaptation of the fat cells to their hormonal environment, especially insulin, in relation to the progress of the training is likely to modify the lipolytic response.
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PMID:Obesity, diabetes mellitus and physical activity--metabolic responses to physical training in adipose and muscle tissues. 675 74

Patients with dyspepsia were asked to volunteer for two gastric secretion tests preceded by a single intravenous injection of pirenzepine 10 mg in the one and 0.9% saline in the other (in random order). In each test gastric secretion was aspirated continuously. 0.9% saline was infused intravenously for 30 minutes followed by insulin 0.15 micrograms/kg-h for 90 minutes, saline for 30 minutes and finally pentagastrin for 90 minutes in doses of either 6, 1, 0.5 or 0.25 micrograms/kg-h. Gastric samples were analysed for volume, pH, titratable acidity and pepsin. Basal outputs of acid and pepsin were not altered by pirenzepine. Insulin-stimulated acid output was significantly reduced (p less than 0.05) from a mean of 32.7 to 22.6 mmol/h (-31%). The mean percentage reduction was 16%. Acid and pepsin outputs after pentagastrin 0.25-6 micrograms/kg-h were not significantly altered by this dose of pirenzepine.
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PMID:Influence of intravenous pirenzepine on gastric acid and pepsin in man. 678 94


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