Oxygen free radicals, lipid metabolism, and whole blood and plasma viscosity in the prevention and treatment of human cardiovascular diseases.
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Animals↗
Biomedical subjects
G Mózsik
Publications and source records attributed to G Mózsik.
Is acute surgical vagotomy an aggressor to gastric mucosa in pylorus ligated rats with and without indomethacin treatment?
Previously it was proved that intact vagal nerve is basically necessary for the development of gastric cytoprotection. The aims of this study were to receive further data about the role of vagal nerve in the development of gastric mucosal damage. The observations were carried out on Sprague-Dawley rats. Acute bilateral surgical vagotomy was done with pylorus ligation and/or indomethacin (IND) treatment (20 mg/kg, sc.) at the time of operation. The animals were sacrificed 4 h after the operation. The number, the severity (semiquantitative method), the mean size and summed surface (computer assisted quantitative method) of gastric mucosal damage, the H+ output and the mucosal PGE2 level were determined. It has been found that 1) the ASV itself (without IND or pylorus ligation) provoked gastric mucosal damage, which was more severe than in the pylorus ligated animals at 4 h; 2) IND was able to reduce the summed surface of mucosal damage after ASV; 3) ASV aggravated the gastric mucosal damage in pylorus ligated animals in spite of the decreased H+ output; 4) the PGE2 level was lower in vagotomized and vagotomized+pylorus ligated animals then in the control group, and the IND did not cause further decrease in its level after ASV. It has been concluded that the balance between aggressive and defensive factors of gastric mucosa was shifted to the aggressive side in surgically vagotomized animals.
Animals↗
Effect of acute surgical vagotomy on the mucosal content of 6-keto-PGF1 alpha, PGE2 and glutathione after intragastric 96% ethanol treatment in rats.
It has been observed earlier that gastric cytoprotection produced by PGI2, beta-carotene, small doses of atropine or cimetidine has failed in surgically vagotomized rats. This phenomenon may be in connection with endogenous prostaglandins (PGs) and glutathione (GSH) level of the gastric mucosa. The aims of the study were to evaluate the effect of vagus nerve on the gastric mucosal 6-keto-PGF1 alpha, PGE2 and glutathione after intragastric 96% ethanol (ETOH) treatment. The observations were carried out on CFY rats. The gastric mucosal damage was produced by intragastric administration of 1 ml 96% ETOH. Acute bilateral surgical vagotomy (ASV) was carried out 30 min prior to ETOH application. The animals were sacrificed 1, 5, 15 or 60 min after ETOH installation. The number and the severity of gastric mucosal lesions were noted and 6-keto-PGF1 alpha, PGE2 an GSH contents of gastric mucosa were measured. It has been found that: 1. the number and the severity of gastric mucosal lesions were increased after ASV compared to those with intact vagal nerve, 2. 96% ETOH treatment increased both the gastric mucosal PGs and GSH levels, 3. 6-keto-PGF1 alpha peaked at 5 min PGE2 and GSH peaked at 15 min after ETOH treatment, 4. ASV decreased the gastric mucosal PGs content and delayed the peaks of PGE2 and GSH. It has been concluded that the decreased content of PGs and the delayed GSH increase may play a pathological role in the failure of gastric cytoprotection of rats after ASV.
6-Ketoprostaglandin F1 alpha↗
Correlation between the cytoprotective effect of beta-carotene and its gastric mucosal level in indomethacin (IND) treated rats with or without acute surgical vagotomy.
As to earlier observations that beta-carotene prevents the development of gastric mucosal injury produced by different noxious agent, however, its cytoprotective effect can be abolished by acute surgical vagotomy. The aim of this study was to evaluate the possible correlation between the gastric mucosal cytoprotective effect of beta-carotene and its gastric mucosal level in rats treated with IND. The gastric mucosal damage was produced by the administration of IND (20 mg/kg s.c.). The instillation of beta-carotene and acute surgical vagotomy (ASV) or SHAM operation were carried out 30 min before IND treatment. The rats were sacrificed 4 h after IND application, and the number and severity of gastric mucosal erosions were noted. The blood rats was collected quantitatively, the liver and the gastric mucosa were removed, and the beta-carotene and vitamin A level of the gastric mucosa, serum and liver were measured with HPLC. It was found that: 1. Beta-carotene induced gastric cytoprotection in SHAM-operated rats treated with IND but its effect disappeared after ASV. 2. Although the beta-carotene level of the gastric mucosa increased its concentration was not elevated in the serum of intact and vagotomized animals either. 3. Vitamin A Formation was not detected in the liver of animals with or without ASV. It was concluded that the lack of intake of beta-carotene into the gastric mucosa can not play etiologic role in the failure of gastric cytoprotection of rats with acute bilateral surgical vagotomy.
Animals↗
Acute and chronic surgical vagotomy (SV) and gastric mucosal vascular permeability in ethanol treated rats.
The role of vagus nerve was studied in the development of gastric mucosal damage induced by ethanol (ETOH). The investigations were carried out on Sprague-Dawley rats. The gastric mucosal damage was produced by i.g. administration of 1 ml 96% ETOH. Acute surgical vagotomy (ASV) was carried out 30 min, chronic surgical vagotomy (CSV) 14 days before the ETOH application. The animals were sacrificed at 0, 1, 5, 15, 60 min after ETOH. Evans blue (EB) (1 mg/100 g) was given i.v. 15 min before autopsy. The number and severity of lesions the EB accumulation of the gastric juice and gastric mucosa were noted. It was found, that: 1. The vascular permeability increased after ETOH treatment at an early state (within 1-5 min) in association to the macroscopic appearance of erosions. 2. The number and extension of lesions, the EB concentrations in gastric juice and gastric mucosa were significantly higher both after ASV and CSV. 3. Surgical vagotomy alone did not increase the vascular permeability. 4. No significant ulcer formation was observed in vagotomized rats without ETOH treatment. It was concluded, that 1. Both ASV and CSV enhanced the development of gastric mucosal injury induced by ethanol. 2. Neither acute nor chronic surgical vagotomy exerted an effect of the development of mucosal injury and vascular permeability without the application of the noxious agent. 3. The further increase of enhanced vascular permeability by vagotomy probably has an etiologic role in the aggravating effect of ASV and CSV on the development of chemical-induced lesions.
Animals↗
ATP breakdown and resynthesis in the development of gastrointestinal mucosal damage and its prevention in animals and human (an overview of 25 years ulcer research studies).
The changes in membrane-bound ATP systems (breakdown and resynthesis) were analyzed in different experimental ulcer models (such as ETOH, HCl, NaOH, 25% NaCl-induced, pyloric ligated + epinephrine treated, stress, reserpine treated, indomethacin treated rat models) and chronic antral, duodenal and jejunal ulcers in patients. The energy system parameters (adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), cyclic AMP (cAMP), lactate) were measured from different sites of gastrointestinal mucosa, and values of ATP/ADP, adenylate pool (ATP + ADP + AMP) and energy charge ((ATP + 0.5 ADP)/(ATP + ADP + AMP)) were calculated. The biochemical measurements were done at different times during the development of gastrointestinal mucosal lesions, without and with application of different drugs (PGI2, atropine, cimetidine) and bilateral surgical vagotomy. The aims of our present paper were: 1.) To summarize the main directions of ATP breakdown during the development of gastrointestinal lesions or ulcers in different experimental models and human beings: 2.) To summarize the biochemical steps of defense of gastrointestinal mucosa against chemicals, drugs or unknown pathogenic factors; 3.) To analyze the importance of membrane-bound ATP-dependent energy systems in order to understand the mucosal lesions and their prevention; 4.) To evaluate the real values of changes in these parameters from the point of view of ulcerogenesis and its prevention; 5.) To find some correlation between the energy parameters during mucosal damage and its prevention: 6.) To understand better the types of tissue reactions (metabolic) due to development of mucosal lesions and prevention.(ABSTRACT TRUNCATED AT 400 WORDS)
Adenosine Triphosphate↗
The energy systems of gastric tissues, their neural, hormonal and pharmacological regulations in order to gastric H+ secretion and ulcerogenesis. (A review of animal experiments and clinical biochemical studies).
In studies conducted over the last 10 years, the ATP, ADP, AMP concentrations, the adenylate pool (ATP + ADP + AMP), the "energy charge" and the cAMP levels were determined:(1) in gastric tissues of pylorus-ligated rats, (2) in gastric and duodenal mucosa and muscular layer (musculature) of human subjects qualified as "hypacid", "normacid" and "hyperacid" on the basis of basal (BAO) and maximal acid output (MAO), (3) in ulcer-bearing and non-ulcerous antral, duodenal and jejunal mucosa and muscular layer of patients with peptic ulcer, including chronic (essential) antral, duodenal ulcer and jejunal ulcer following gastric resection of Billroth II-type. Close analysis of the results centres on: (1) the biochemical background of gastric hypersecretion and of ulcerogenesis in pylorus-ligated rats;(2) the extra- and intracellular feedback system operating between the gastric membrane ATPase and adenylate cyclase systems, under normal and abnormal conditions of the effector organ; (3) questions related to the regulatory mechanisms of functional activity of the effector organ under drug effect; (4) the energy structure of the mucosa and muscular layer of corpus ventriculi, antrum and duodenum in patients considered "hypacid", "normacid" and "hyperacid" on the grounds of the BAO and MAO values; (5) the interrelationships between human gastric H+--K+-dependent ATPase system of gastric corpus mucosa; (6) pharmacological regulation of the ATP--ADcer-free mucosa and musculature of patients with antral, duodenal and jejunal ulcers.
Adenosine Diphosphate↗
The role of the ATP--adenylate cyclase--cAMP system and its pharmacological regulation in the development of gastric hypersecretion and ulceration.
The role and pharmacological regulation of the ATP-adenylate-cyclase--cAMP system were studied in the mucosa of the gastric fundus, and in the forestomach, of pylorus-ligated rats to elucidate the development of gastric hypersecretion and ulceration. (1) cAMP content of the tissue of the fundus mucosa and of the forestomach decreased before the significant increase of gastric H+ output and ulcer development; (2) the gastric H+ outputs depended on the breakdown of ATP in the fundus mucosa; (3) the gastric H+ secretion was inhibited in a dose-dependent way by theophylline, epinephrine and cimetidine; (4) the inhibition of gastric H+ secretion by epinephrine , theophylline or epinephrine plus theophylline associated with a significant increase in the mucosal cAMP of the gastric fundus (5) the significant increase in gastric H+ secretion due to histamine associated with a significant decrease in fundic mucosal cAMP; (6) the gastric H+ secretion could be inhibited dose-dependently by ADP, AMP, cyclic 2', 3'-AMP and cAMP; (7) the inhibition of gastric H+ secretion by cimetidine developed without and with histamine application in pylorus-ligated rats; (8) the histamine on gastric H+ secretion could not be stimulated further with theophylline (9) no significant correlation was found between the mucosal cAMP level and the gastric H+ secretion and/or between the decrease of mucosal cAMP content and gastric H+ secretion. It has been concluded that in pylorus-ligated rats (1) the gastric H+ secretion is an ATP-dependent process; (2) the cAMP system has an inhibitory effect as regards the development of gastric hypersecretion and of ulceration; (3) histamine and cimetidine show no close correlation with the cAMP system; (4) an extracellular and intracellular feed-back mechanism system exists between th ATP-membrane-bound ATPase-ADP and the ATP--adenylate cyclase--cAMP systems in the background of the development of gastric hypersecretion and ulceration.
Adenosine Diphosphate↗
A comparative molecular--pharmacological study of drugs inhibiting Na+--K+-dependent ATPase separated from human gastric fundic mucosa. (One receptor system and more drugs).
The inhibitory effects of atropine, epinephrine, cyclic 3', 5'-AMP (cAMP), the prostaglandins E1 (PGE1) and E2 (PGE2) pentagastrin, histamine and ouabain have been studied on the activity of Na+--K+-dependent ATPase obtained from human gastric fundic mucosa. This study compares the sensitivity of the enzyme to a variety of drugs, applying the law of one receptor and more drugs. It was found that (1) the doses of drugs necessary to produce 50% inhibition to Na+--K+-dependent ATPase activity (affinity, pD2 value) significantly differ from each other C (atropine, 9.50; epinephrine, 8.60; cAMP: 11.30; PGE1, 9.30; PGE2, 9.45; pentagastrin, 9.45; histamine, 9.70 and ouabain, 9.50); (2) the intrinsic activities of drugs to Na+--K+-dependent, ATPase in comparison with ouabain (alpha=1.00) differ: atropine, PGE1, PGE2 and histamine, 1.00; pentagastrin, 0.87; cAMP, 0.48 and epinephrine, 0.41; (3) the inhibitory effects of different drugs, on Na+--K+-dependent ATPase system, depend on the magnitude of enzyme activity from human gastric fundic mucosa. It has been concluded that (1) the sensitivity of these drugs to the Na+--K+-dependent ATPase system and to the adenylate cyclase system, both obtained from human gastric mucosa, significantly differs from each other; (2) the main effect of pentagastrin and histamine on human gastric secretory function differs from the function of Na+--K+-dependent ATPase system; (3) the role of Na+--K+-dependent ATPase system and of adenylate cyclase can be separated pharmacologically from the point of view of human gastric H+ secretion.
Atropine↗
Biochemical and energetic gradients in the mucosa of stomach and duodenum of patients with antral ulcer.
Separation and measurement of adenine-adenosine, adenosine monophosphate (AMP), adenosine diphosphate (ADP), adenosine triphosphate (ATP), lipid phosphates, RNA and DNA, further, separation and measurement of Mg2+-dependent, total (Mg2+-dependent plus Na+--K+-dependent, Mg2+-Na+-K-dependent) and Na+-K+-dependent ATPases were carried out in the mucosa and muscles of the corpus, antrum and duodenum of 68 patients with antral ulcer. It was found that (1) the substrate levels of adenosine nucleotides, lipid phosphates and RNA were significantly higher in the corpus mucosa than those in the mucosa of the antrum and duodenum (calculated for 1.0 mg DNA content); (2) the amounts of adenosine nucleotides and the sum of ATP + ADP + AMP did not alter significantly in the muscles of the corpus, antrum and duodenum; (3) the levels of adenosine nucleotides, sum of ATP + ADP + AMP, lipid phosphates and RNA, further the activities of Mg2+-dependent , total (Mg2/-dependent plus Na+-K+-dependent) and Na+-K+-dependent ATPases were significantly higher in the corpus mucosa than those in the corpus muscles. It was concluded that (1) energetic and biochemical gradients are present between the substrate levels in the mucosa of the corpus, antrum and duodenum; (2) the neural and/or humoral regulatory mechanisms differ in the mucosa and muscles of the corpus, in order to their biochemistry.
Adenine Nucleotides↗
Interrelationships between the gastric secretory responses, prostaglandin E2 inhibition and serum level of immunoreactive gastrin in pylorus-ligated and antrectomized rats.
The effects of prostaglandin E2 (PGE2) have been studied on the gastric secretion and the serum level of immunoreactive gastrin in pylorus-ligated and antrectomized rats. It has been observed that: (1) a significant inhibition of gastric secretion (volume and acid output) was caused by PGE2, applied in doses of 75, 150 and 300 microgram/kg body weight, subcutaneously, in both pylorus-occluded and antrectomized rats: PGE2 inhibition of gastric secretion was more pronounced in rats with antrectomy; (2) no significant changes were found in the serum gastrin levels of both pylorus-ligated and antrectomized rats, and (3) no significant changes in serum levels of immunoreactive gastrin were produced by different doses of PGE2, in comparison with their marked inhibitory effects on gastric H+ secretion. It was concluded that there is no essential role of the immunoreactive gastrin, originated from the antral part of the stomach, neither in development of gastric hypersecretion nor in PGE2-produced inhibition on gastric secretion of the pylorus-occluded rats.
Animals↗
Interrelationships between the gastric mucosal cAMP and gastric H+ secretion in pylorus-ligated rats.
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Animals↗
Surgical vagotomy and stomach wall ATP and ADP in pylorus--ligated rats.
The stomach wall ATP and ADP have been studied in rats, with and without bilateral surgical vagotomy, 24 hr after pylorus ligation. It was observed that the amounts and concentrations of ATP significantly decreased in both parts (corpus + antrum and forestomach) in pylorus-ligated rats, while the amounts and concentrations remained at a significantly higher level in pylorus-ligated + vagotomized rats. Changes in amounts and concentrations of ADP paralleled those of ATP. It has been concluded that a significant decrease of cellular ATP is necessary to produce gastric hypersecretion in ulceration in pylorus-ligated rats. This significant decrease of cellular ATP, in corpus + antrum and forestomach, can be prevented by bilateral surgical vagotomy.
Adenosine Diphosphate↗
[Protein-losing (lymphogenic) enteropathy caused by the occlusion of the thoracic duct].
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Biopsy↗
[D-xylose absorption in patients treated with combined cytostatic drugs].
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Antineoplastic Agents↗
Examination of stomach wall Mg2+-Na+-K+-dependent ATPase, ATP, and ADP in pylorus-ligated rats.
Stomach wall Mg2+-Na+-K+-dependent ATPase, ATP, and ADP were studied in rats, at 4, 7, 17, and 24 hr after pylorus ligation, in order to relate H+ secretion and ulcer development. It was observed, in both parts of forestomach and corpus + antrum, that the stomach wall Mg2+-Na+-K+-dependent ATPase significantly increased at 4 and 7 hr, while it significantly decreased at 24 hr, after pylorus ligation. Contrary to this, stomach-wall ATP decreased at 4 hr, relatively increased at 7 hr, thereafter significantly decreased in forestomach and corpus + antrum. Ouabain inhibited the H+ secretion, ulcer development, and stomach wall Mg2+-Na+-K+-dependent ATPase activity. The possible causal interrelationships between the examined parameters are studied.
Adenosine Diphosphate↗