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V Varró

Publications and source records attributed to V Varró.

At least 91 records · Page 5Linked to original sources

Gastrointestinal mucosal gamma-glutamyl transpeptidase activity changes in different ulcer models of rat.

The experiments presented gave evidence that changes in gamma-glutamyl transpeptidase activity-under experimental circumstances-seem to be in close connection with gastro-intestinal ulceration. In the pre-ulcerative period in both gastric and duodenal ulcer models, the mucosal gamma-glutamyl transpeptidase activity is higher than normal, while in the definitive ulcerative stage the gastric gamma-glutamyl transpeptidase activity is significantly decreased but in the duodenum it remained on normal level. This phenomenon may reflect to a difference in the pathomechanism of the gastric and duodenal ulceration.

Animals↗

Effect of long-term prostacyclin treatment on the gastric mucosa of rat.

According to Bálint and Varró, oral administration of prostacyclin (PGI2) resulted in a significant increase of the DNA-content of the gastric mucosa within a short period of time. In the present study, there was no change in the protein content of the gastric mucosa after oral administration of 100 micrograms/kg/day of PGI2 for 80 days, while the DNA-content increased significantly. The RNA/DNA ratio decreased. Histologically a significant increase in the thickness of the gastric mucosa, as well as in the number of parietal and epithelial cells were found. The cell hyperplasia in the corpus mucosa was accompanied by a decreased number of G-cells of the antral mucosa. The increase of parietal cell number and the decrease of G-cell number after long term PGI2 administration might be explained by the divergent effect of treatment on the kinetics of the different cell types in the gastric mucosa.

Animals↗

The effect of prostacyclin on gastric mucosal protein, DNA and RNA content, with special reference to different ulcer models.

The effect of prostacyclin on gastric mucosal protein, DNA and RNA content has been investigated, either administered alone or in the course of indomethacin and stress-induced experimental ulcer models. It seems that: The oral administration of 100 micrograms/kg prostacyclin caused a prevailing DNA increase (decrease of the RNA/DNA ratio) in the rat gastric mucosa. Indomethacin and stress (restraint) ulcer formation were also followed by a predominant mucosal DNA increase which was maintained even during PGI2 treatment. The observed changes in RNA/DNA ratios were interpreted as a sign of accelerated cell renewal.

Animals↗

Proteolytic inactivation of lipase as a possible cause of the uneven results obtained with enzyme substitution in pancreatic insufficiency.

Inactivation of lipase in four commercially available pancreatin preparations in buffer solution, in duodenal juice stimulated by secretin-cholecystokinin or by Lundh test-meal, and in duodenal juice supplemented with a meat-meal homogenate, was examined during a four-hour incubation period. In the buffer solution and in the secretin-cholecystokinin-stimulated duodenal juice 64-89% of lipase activity was already lost within two hours. Trypsin activity was in inverse relation to that of lipase and soybean trypsin inhibitor. The Lundh test meal and the meat-meal homogenate significantly diminished inactivation of lipase. Substitution therapy of pancreatic insufficiency with crushed and soybean-trypsin-inhibitor supplemented preparations diminished steatorrhoea more effectively than the simple tablets. The demonstrated proteolytic inactivation of lipase indicates that pancreatic supplements have to be given in crushed or granulated form, well mixed with protein-containing meals, and that a physiological ratio of trypsin-lipase activity ought to be preserved in the preparations.

Amylases↗

Effect of different prostaglandin analogues on gastric acid secretion and mucosal blood flow in the dog: action on stimulated and resting mucosa.

The effect of PG-E2, 16-16-DMPGE2, PG-F2 alpha and PG-I2 was investigated on histamine stimulated and resting canine gastric mucosa. PG-F2 alpha had no effect on mucosal circulation or acid secretion. PG-E2 and 16-16-DMPGE2 showed an increasing effect on blood flow of the resting mucosa. PG-E2, 16-16-DMPGE2 and PG-I2 decreased of acid secretion; the effect seemed to be due to a direct action on the parietal cells.

16,16-Dimethylprostaglandin E2↗

Effect of prostacyclin on the mixed function microsomal oxigenase system in the rat liver.

The microsomal fraction of the liver was studied for protein and cytochrome P450 contents as well as for aminopyrine-N-demethylase and aniline-hydroxylase activity and for its BIC spectrum under the effect of PG-I2 treatment. A significant increase was found in the cytochrome P450 content after short term treatment, while continuation of PG-I2 administration caused a significant and long lasting decrease of cytochrome P450. After prolonged application of PG-I2 the aniline-hydroxylase content decreased significantly, while the aminopyrine-N-demethylase enzyme showed no change. The BIC spectrum after 80 days PG-I2 treatment significantly decreased in the 431-432 nm region, corresponding to the decrease of cytochrome P450. Long term PG-I2 application caused no detectable ultrastructural changes in the liver.

Aminopyrine N-Demethylase↗

The effect of different prostaglandins on cysteamine-induced duodenal ulcer in the rat.

Most of the experiments have verified the cytoprotective effect of prostaglandins on the gastric mucosa and only few observations are known to deal with "cytoprotection" exerted on the duodenal or intestinal mucosa. Duodenal ulcers were produced by cysteamine (CEA). The treatment with different prostaglandins (PGI2, PGF2 alpha, PGE2) was carried out every six hours during the 48-hour experimental period. The obtained results indicate that neither prostacyclin nor prostaglandin-F2 alpha has any significant effect on CEA-induced duodenal ulceration, while prostaglandin-E2 exerts a slight anti-ulcerogenic effect. It is possible that cytoprotection is not the result of the same process in the duodenal and gastric mucosa: alternatively, three prostaglandins are not involved in the pathomechanism of CEA-induced duodenal ulceration.

Animals↗

The diagnosis of hypertonic Oddi's sphincter dyskinesia.

The diagnostic possibility of hypertonic Oddi's sphincter dysfunction was evaluated in 100 cholecystectomized and 28 noncholecystectomized patients. An organic lesion interfering with free bile flow was ruled out in every case. The existence of the syndrome, i.e., the dysfunction of the Oddi's musculature, was verified using the morphine-choleretic test combined with either dynamic hepatobiliary scintigraphy or (in selected cases) percutaneous transhepatic cholangiography. Hypertonic Oddi's sphincter dyskinesia can be regarded as an independent clinical syndrome.

Ampulla of Vater↗

Cytoprotective effect of prostacyclin and protein synthesis.

It is shown that de novo synthesis of protein is essential for the healing process of experimental gastric ulcer and that the cytoprotective effect of prostacyclin is connected with protein synthesis. In preliminary experiments the influence of prostacyclin on hepatic protein synthesis has also been shown.

Animals↗

Secretin-pancreozymin test with synthetic secretin and cholecystokinin octapeptide.

Pancreatic responses to submaximal doses of synthetic secretin (125 ng/kg) and cholecystokinin octapeptide (50 ng/kg) were investigated in controls and patients with pancreatic disease. Doses of stimulants were chosen from dose-response experiments to avoid supramaximal amounts which inhibited the pancreatic response. Injection of secretin resulted in duodenal juice in less trypsin but more lipase activity than that elicited by cholecystokinin octapeptide. The increase of amylase was about the same. Diagnostic efficacy of pancreatic responses to the individual hormones was similar. An overall evaluation of the results seems to be the most reliable method for diagnostic purposes.

Amylases↗

Prostaglandins and gastrointestinal cytoprotection.

One of the important and interesting effects of prostaglandins in the gastrointestinal tract is cytoprotection: protection of the gastrointestinal mucosa against nonspecific injuries (physical, chemical, drugs, etc.). The characteristic features of cytoprotection, the possible mechanism of protection and the theoretical and clinical perspectives of prostaglandins and their analogues are discussed.

Animals↗

The effect of naloxone in different gastroduodenal ulcer models.

On the basis of our investigations it seems that: The opiate antagonist naloxone in a dose of 5.0 mg/kg has a significant protective effect in stress-ulcer model in the rat; No such effect was seen in drug (indomethacin) or cysteamine induced (duodenal) ulcer models; The interaction of naloxone with indomethacin seems to show a sex-difference.

Animals↗

Cytoprotection and 6-keto-prostaglandin-F1 alpha.

Several prostaglandins were found to protect the gastric mucosa against the ulcerogenic effect of immobilization (stress) and of indomethacin in the rat. The analogue 6-keto-prostaglandin-F1 alpha had no cytoprotective effect in the same region and even seemed to facilitate ulceration in the stomach in a dose-dependent manner. Unusually high doses of this prostaglandin analogue also exerted a slight cytoprotective effect.

6-Ketoprostaglandin F1 alpha↗