Mechanism Of Gastric Secretion Research Articles

Domestic researchers who have made important contributions to the study of digestive system diseases: images in art. Maks Moiseyevich Gubergrits

A few main directions can be distinguished in the scientific and practical activities of M. M. Gubergrits. Even his first studies contributed to the history of the development of domestic cardiology. He continued the work started by V. P. Obraztsov on the III normal heart sound, studied changes in heart tones and the formation of a gallop rhythm, the rhythm of a neurasthenic quail, was one of the first to evaluate the clinical significance of the electrocardiographic technique, and tried to use it for better understanding the effect of certain drugs on the heart. He described disorders of the cardiovascular system in severe infectious diseases (epidemic typhus, relapsing fever, and typhoid fever) and thrombosis of the splenic vein. An important part of the scientific activity of M. M. Gubergrits was the pain problem. An outstanding humanist scientist could not ignore this human suffering from various diseases. He was interested not only in the origin of pain in diseases of the heart, liver, and kidneys but also in pain as a general problem of physiology and pathology. However, he most clearly revealed himself as a talented clinician in gastroenterology by constantly combining thoughtful observation at the patient’s bedside with clinical and physiological experimentation. Back in 1929, in his work on the mechanism of gastric secretion, he established the effect of mechanical irritation of the gastric mucosa on the secretion of gastric juice. He described a unique palpatory symptom of a bigastric stomach (changes in the position of the lower border of the stomach, re‑determined by splashing noise). He had a keen interest in peptic ulcer disease. His studies on pancreatic physiology and pathology have retained their value to the present day: data on excretory function, the adaptability of exocrine function to different diets, the possibility of a partial violation of this function (dyspancreatism), as well as the organ’s functional study technique developed in his clinic. M. M. Gubergrits described the pain zone in the pathology of the head and body of the pancreas. In addition, he described concomitant diseases of the liver and pancreas and the liver’s involvement in the pathological process in gastric, duodenal, and large intestinal diseases. The studies by M. M. Gubergrits on the clinical picture of pancreatic diseases played a significant role in the further research. To a large extent, his statements on the diagnosis of pancreatitis have retained their significance. He emphasized the importance of such symptoms as pathological hunger, thirst, polyuria, weight loss, pain in the epigastric area, sometimes jaundice, diarrhea with creatorrhea and steatorrhea, and changes in the blood and urine.

Omeprazole

OMEPRAZOLE is the first of a new class of drugs that inhibit gastric secretion by altering the activity of H+/K+—ATPase,1 2 3 the final common step of acid secretion, in gastric parietal cells. The discovery of omeprazole has led to new insights into the mechanism of gastric secretion, knowledge of the genesis of certain gastrointestinal tumors, and the development of new treatments for acid-peptic diseases. In the United States, omeprazole has been approved only for short-term use in certain patients with reflux esophagitis and for patients with the Zollinger—Ellison syndrome, because of concerns raised by the results of long-term studies of toxicity . . .

Mechanisms of gastric secretion in dogs induced by infusion of histamine, carbachol, and pentagastrin

Mechanisms of gastric secretion in dogs induced by infusion of histamine, carbachol, and pentagastrin

Inhibition of gastric acid secretion in dogs by a new sympathomimetic drug.

The effect of salmefamol, a new beta 2-agonist, on pentagastrin-induced gastric acid secretion was studied in conscious gastric fistula dogs. Salmefamol inhibited the acid secretion, an effect which was dose dependent. The volume as well as the acidity was inhibited. Salmefamol caused an increase in the pulse rate. Propranolol prevented the inhibition of acid output as well as the increase in pulse rate. Practolol, a beta 1-adrenoceptor blocker, had no effect on the inhibition of acid secretion but prevented the increase in pulse rate. Dose-response experiments with 6 doses of pentagastrin and 1 dose of salmefamol showed a decrease in calculated maximal response (CMR) and an unchanged D50. It is concluded that salmefamol strongly inhibits pentagastrin-induced acid output in the dog, and the inhibition follows a non-competitive kinetic. The mechanism of gastric secretion probably involves a beta 2-receptor.

The antiulcer and autonomic pharmacology of pyridyl-2-thioacetamide (CMN 131).

Pyridyl-2-thioacetamide-CMN 131-possess high ulcer-protective activity which seems closely related to its gastric antisecretory properties previously described. This activity is demonstrated using experimental models whose ulcerogenic stimulus can be related to various origins: 4-hr and 24-hr restraint stress ulcers and aspirin or phenylbutazone gastric erosions in rats, histamine-induced ulcers in guinea pigs, reserpine-induced ulcers in cats. In the same dose range used in the ulcer study, and even at higher doses, CMN 131 fails to show any systemic activity on the cholinergic or adrenergic pathway. At a systemic level no antihistaminic, antiserotonin, or ganglion properties can be observed either. Furthermore, CMN 131 modifies neither the salivary and lacrymal secretions, nor the gastric emptying or the blood pressure. Finally, CMN 131 can be considered an original pharmacological agent whose wide antiulcer and antisecretory properties could enable us to understand more clearly the intrinsic mechanism of gastric secretion.

The endocrine cells of the upper gut mucosa in dogs with transplantation of the pyloric antrum to the colon.

A previous examination, done by others, of the endocrine cells of the canine pyloric antrum following its transplantation to the colon evidenced an increase in their number; the cell types involved, however, were not individualized. The present study further characterizes the changes occurring in the endocrine cells of the pyloric antrum of dogs following transplantation to the colon. The main change observed consists of hyperplasia of the enterochromaffin cells, with minor qualitative modifications in the antral gastrin-producing cells being noted only by electron microscopy. The response of the enterochromaffin cells cannot be readily explained but might be related to similar enterochromaffin cell hyperplasias found in human stomachs with peptic ulcers. Antrum transplantation to the colon in dogs appears to provide a promising experimental model for the study of the relationship between gastrin and other humoral factors (probably biogenic amines) in the mechanism of gastric secretion under normal as well as abnormal circumstances.

An experimental study on the relationship between endogenous histamine metabolism and the liver in the mechanism of gastric secretion

An experimental study on the relationship between endogenous histamine metabolism and the liver in the mechanism of gastric secretion

Recent advances in the physiology of gastrin.

On 18 May 1905 there was presented at a meeting of this Society a paper in the name of John Sydney Edkins entitled ‘On the chemical mechanism of gastric secretion’ (Edkins 1905). It described experiments in which simple aqueous extracts of antral and fundic mucosa were tested for their power to stimulate gastric secretion when injected as single intravenous doses into anaesthetized cats. Antral extracts excited a secretion of acid and pepsin; fundic extracts did not. Edkins concluded that certain cells in the antral mucosa contained a principle which he named ‘gastrin’; this, he considered, entered the circulation during gastric digestion and stimulated the fundic glands to further activity following on the initial vagal reflex excited by the eating of the meal. These experiments, later recounted in detail (Edkins 1906) initiated more than 40 years of controversy as to the existence of a gastric antral hormone. When attempts were made to confirm and extend Edkins’s observations it was soon discovered that a stimulant of gastric acid secretion could be found not only in antral mucosa but also in many other tissues; and when eventually this ubiquitous agent was identified as histamine (Barger & Dale 1910; Dale & Laidlaw 1910; Popielski 1919) it was widely concluded that the activity of Edkins’s antral extract was due to the presence in it of this substance. The situation was further confused by the failure of apparently well-designed attempts to prove by physio­logical experiment that an antral hormonal mechanism existed, whatever the nature of the hormone. For example, Ivy & Whitlow (1922) and Priestley & Mann (1932) provided dogs with fundic and antral pouches and irrigated the latter with solutions regarded at the time as likely to cause a release of the hormone; but no response from the fundic pouch could be detected, and many years elapsed before the probable reason for such failure became appreciated.

Electrophysiology of the elasmobranch stomach.

A consequence of the recent study of the mechanism of gastric secretion has been the presumption, implicit (1) if not explicit (2), that the distinctive gastric transmucosal potential has a fundamental role in the formation of hydrochloric acid. The following report indicates that the isolated surviving elasmobranch gastric mucosa does secrete acid but, unlike that of other vertebrates, does so without developing a significant epithelial potential difference. The gastric transmembrane potential is neither necessary for hydrogen ion secretion nor is its generation a fundamental feature of the mechanism that leads to the formation of hydrochloric acid.

Quantitative studies on the mechanism of gastric secretion in health and disease.

Dragstedt, Lester R. M.D., Ph.D.; Woodward, Edward R. M.D.; Storer, Edward H. M.D.; Oberhelman, Harry A. Jr. M.D.; Smith, Curtis A. M.D. Author Information

The mechanisms of gastric secretion

The mechanisms of gastric secretion

Mechanism of Gastric Secretion. The Nature of Gastric Juice of Constant Maximum Acidity.

In a recent paper,1 it was reported that, by a modification of the usual technic for collecting gastric juice from a dog's auxiliary stomach pouch, a fluid of constant acidity was obtained. Independently of whether the secretory stimulus was food or histamine, the pH of the pouch juice had a constant value of 0.90±D0.01. The difference (a decrease of 0.02 pH) between this and the value originally reported may be due to individual variation as well as to improved technic. With further modifications in the latter, the maximum acidity may be found to be even slightly higher.Subsequent to the above report, the acid values of some representative samples were determined by titration. The micro-method employed involved titration to a definite end point with the aid of comparator tubes of known pH. For total acidity, phenol red at pH 7.8 was used; for free acidity, brom-phenol blue at 3.5. Also, in the case of a few of these samples, total chlorine was determined by the micro-method of Van Slyke.2 From the data s...

The natural channels of absorption evoking the chemical mechanism of gastric secretion

The natural channels of absorption evoking the chemical mechanism of gastric secretion