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Biomedical subjects

L Nagy

Publications and source records attributed to L Nagy.

At least 199 records · Page 11Linked to original sources
PubMed1984

The gastric fundic mucosal energy systems and the HCl-induced lesions in rats in dependence on starvation.

Gastric mucosal lesions were produced by intragastric administration of 0.6 M HCl (1 ml) to rats starved for 48 or 24 h, and to unstarved rats which received 5 or 20% glucose solution ad libitum. The number and severity of gastric lesions were recorded and the mucosal levels of ATP, ADP, and AMP were enzymatically measured, cAMP was determined by RIA. Adenylate pool, energy charge, and ATP X ADP-1 were rated. It has been found that: the 20% glucose fed rats showed the highest levels of biochemical constituents, but the lowest number and severity of gastric lesions; there were significant negative correlations between the number and severity of lesions and the mucosal levels of ADP, AMP and cAMP; significant positive correlations were found between the number and severity of gastric lesions and the ratios of ATP X ADP-1 and energy charge. It has been concluded that: the energy turnover processes of the fundic mucosa were significantly higher in the animals fed 20% glucose; the increased energy turnover in the gastric mucosa may produce a better metabolic adaptation against the necrotizing effect of HCl.

Adenosine Diphosphate↗
PubMed1984

Interrelationships between the membrane-bound ATP-dependent energy systems of the gastric mucosa and the gastric cytoprotective effect of beta-carotene on the development of gastric mucosal damage produced by 0.6 M HCl in rats.

The effects of different doses (0.01-0.1-1.0-10.0/mg/kg-1) of beta-carotene were studied on gastric secretory responses of 4 hr pylorus-ligated rats: development of gastric mucosal damage (as assessed by number and severity of lesions) produced by intragastric administration of 0.6 M HCl; tissue level of adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), adenylate pool (ATP + ADP + AMP), ratio of ATP X ADP-1, "energy charge" (ATP + 0.5 ADP X X (ATP + ADP + AMP)-1) (during the development of gastric mucosal damage by 0.6 M HCl and of gastric cytoprotection by beta-carotene. It was found that beta-carotene did not decrease the gastric secretory responses of 4 hr pylorus-ligated rats; The development of gastric mucosal damage could be decreased dose-dependently by the administration of beta-carotene; the ATP transformation could be decreased by beta-carotene; the tissue levels of cAMP and AMP could be increased significantly and dose-dependently by beta-carotene; the ratio of ATP X ADP-1 could be increased significantly and dose-dependently by beta-carotene; the values of adenylate pool and "energy charge" remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1984

A comparative dynamic study of the effectiveness of gastric cytoprotection by vitamin A, De-Nol, sucralfate and ulcer healing by pirenzepine in patients with chronic gastric ulcer (a multiclinical and randomized study).

The gastric cytoprotective effects of vitamin A, De-Nol and sucralfate were compared with the effectiveness of pirenzepine in healing ulcer in patients with chronic gastric ulcer. A total of 100 patients was randomized into different groups: the patients were treated with antacids, vitamin A (3 X 50.000 IU), De-Nol liquid (4 X 5 ml), sucralfate (4 X 1 g) or pirenzepine (3 X 50 mg). The treatment was continued for 4 weeks. At the beginning, 2 and 4 weeks after starting treatment the patients were subjected to endoscopy and the size of the ulcer was measured planimetrically. The ulcer-healing effect of De-Nol liquid was significantly better than that of the antacids (p less than 0.01). Ulcer size was reduced significantly in all groups (p less than 0.01), however, at the end of the study the gastric ulcers were smallest in the De-Nol treated group (p less than 0.001). The dynamics of ulcer healing in the second week was most favourable in the patients receiving vitamin A (p less than 0.01). The present data point to the cytoprotective effects of De-Nol liquid, vitamin A and sucralfate and to their ability of healing chronic gastric ulcers.

Adolescent↗
PubMed1984

Evidence for the existence of gastric cytoprotective effect of atropine and cimetidine in humans.

The effects of cimetidine (12.5 mg i.m.) and atropine (0.125 mg i.m.) were studied on the basal (BAO) and pentagastrin (6 micrograms X kg-1 s.c.)-stimulated (MAO) gastric acid secretion; the gastric mucosal microbleeding provoked by one-day treatment with indomethacin (4 X 25 mg orally) in patients with chronic disorders of the joints. The extent of the gastric microbleeding was measured by spectrophotometric determination of haemoglobin in gastric lavage fluid. The aims of this study were to determine the doses of cimetidine and atropine in humans without any significant inhibitory effects either on the basal or on the maximal gastric acid output to evaluate the cytoprotective action of these doses of cimetidine and atropine on the indomethacin-induced gastric microbleeding in the man. It was found that cimetidine (12.5 mg i.m.) and atropine (0.125 mg i.m.) did not cause any significant inhibition either of the BAO or of the MAO; indomethacin (4 X 25 mg orally) significantly increased gastric microbleeding in the patients; cimetidine and atropine, in the above doses, were able to prevent significantly indomethacin-induced gastric microbleeding in the patients. These results provide evidence for the existence of gastric cytoprotective effects of cimetidine and atropine in humans.

Adult↗
PubMed1984

Gastric microbleeding measurements during one day treatment with indomethacin and indomethacin plus sodium salicylate (1 : 10) in patients.

A double-blind, prospective, randomized clinical study was carried out. Gastric microbleeding was provoked in informed patients without gastrointestinal disorders by the administration of indomethacin (4 X 25 mg, orally), sodium salicylate (4 X 250 mg, orally) or indomethacin (25 mg) plus sodium salicylate (250 mg) (Pelsonin, 4 X 1 capsules). The rate of gastric bleeding was estimated on the basis of haemoglobin losses into the gastric juice according to a rapid and sensitive chemical method (Fisher and Hunt, 1976). The observations were done before and after the day of treatment. The basic gastric bleeding was practically the same in the three groups (indomethacin, 0.91 +/- 0.12 ml/day: sodium salicylate, 0.72 +/- 0.20 ml/day: Pelsonin, 0.99 +/- +/- 0.18 ml/day: p less than 0.05). Contrary to this, the increases of gastric bleeding were found to be considerably different after a one-day application of these drugs (indomethacin, 7.3 +/- 1.2 ml/day: sodium salicylate, 1.92 +/- 0.45 ml/day, Pelsonin, 2.1 +/- 0.8 ml/day). It has been concluded that sodium salicylate can reduce the indomethacin-induced gastric microbleeding in patients.

Adult↗
PubMed1983

Effects of indomethacin and prostaglandins I2 and E2 on the tone of human isolated mesenteric arteries.

The actions of indomethacin (IND), PGE2 and PGI2 were studied on the tone of isolated mesenteric arteries obtained from operated patients. The cyclooxygenase inhibitors IND (3 mumol/l) and suprofen (0.58 mumol/l) increased the resting tone and potentiated the contractile responses to electrical stimulation and noradrenaline. Low concentrations of PGE2 (0.7-5.6 X 10(-9) mol/l) decreased the baseline tone and reduced the stimulation-evoked contractions whereas higher concentrations (from 5.7 X 10(-8) mol/l) increased the tone of vessels. PGI2 (0.7-10.8 X 10(-9) mol/l) also relaxed IND-treated arteries but, in contrast to PGE2, it did not produce contraction even at a concentration of 10(-6) mol/l. Prostacyclin reduced the tone evoked and sustained by a high concentration of PGE2 or PGF2 alpha, the IC50 values being 46.2 or 7.9 X 10(-9) mol/l, respectively. The contractile responses to electrical stimulation and to noradrenaline were also inhibited by PGI2 (IC50 5.6 and 6.8 X 10(-9) mol/l, respectively). These results suggest that the smooth muscle cells of human mesenteric arteries are just as sensitive to IND, PGE2 and PGI2 as are those from laboratory animals. Our observations may be of clinical importance.

Adult↗
PubMed1983

Is the knife-cut in the hypothalamus a permanent barrier to regrowth of nerve fibers? -an affirmative answer.

The regenerative capacity of nerve fibers was studied in adult female rats. Horseradish peroxidase was injected into the anterior hypothalamus lateral to the suprachiasmatic nucleus 4 days, 6 weeks and 4 months, respectively, following an archiform retrochiasmatic knife-cut. The trajectory of the stained fibers was examined on horizontal sections of the hypothalamus. No nerve fibers could be seen sprouting across the scar-tissue of the knife-cut regardless of the survival time. In one rat (6-week survival time) a bundle of fine nerve fibers turned in a medial direction at the caudal end of the knife-cut, suggesting that sprouting fibers were destined to reinnervate parts of the deafferented medial-basal hypothalamus.

Animals↗
PubMed1983

Interrelationships between membrane-bound ATP-dependent energy systems, gastric mucosal damage produced by NaOH, hypertonic NaCl, HCl, and alcohol, and prostacyclin-induced gastric cytoprotection in rats.

Rat gastric mucosal lesions (ulcers) were produced by topical application of 0.2 M NaOH, 25% NaCl, 0.6 M HCl and 96% ethanol. The animals were sacrificed 1 hr after administration of the different necrotizing agents. The number of gastric lesions (ulcers) was noted and their severities scored. Different doses (5 and 50 micrograms.kg-1) of prostacyclin (PGI2) were given intraperitoneally at 30 minutes before administration of necrotizing agents, and their effects were studied on the number and severity of gastric lesions (ulcers). At the time of killing of animals, the rat gastric fundic mucosa was removed for biochemical examinations. Tissue levels of adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP) and lactate were determined enzymatically, while the tissue content of cyclic adenosine monophosphate (cAMP) was measured by radioimmunoassay. The values of the adenylate pool (ATP + ADP + AMP), the ratio of ATP X ADP-1 and the energy charge (ATP + 0.5 ADP X ATP + ADP + AMP-1) were calculated. All biochemical results were calculated in relation to one mg mucosal protein. It was found that:1. the tissue levels of ATP, cAMP, AMP decreased significantly, while the tissue level of ADP increased (without statistical significance) in all models, during the development of gastric mucosal damage; 2. the tissue level of lactate increased only in the model produced by 0.6 M HCl, while its level was unchanged in the other models during the development of gastric mucosal damage; 3. PGI2 decreased dose-dependently the number and severity of gastric lesions (ulcers); 4. the tissue level of ATP, ratio of ATP X ADP-1 and energy charge were decreased significantly, while the tissue level of ADP was increased significantly by PGI2 in all models; 5. the tissue level of lactate and the adenylate pool remained unchanged during the PGI2 effects. It was concluded that: 1. the development of gastric mucosal damage, produced by topical application of 0.2 M NaOH, 25% NaCl, 0.6 M HCl and 96% ethanol, is associated with an active metabolic adaptation of the gastric fundic mucosa; 2. the metabolic adaptation of the rat gastric fundic mucosa is further increased by PGI2, without resulting in hypoxaemic damage of the gastric mucosa; 3. the feed-back mechanism system - between the membrane-bound ATP-dependent energy systems - is broken during the development of gastric mucosal damage produced by different necrotizing agents, which is modified further by PGI2 at the time of gastric cytoprotection.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine Diphosphate↗
PubMed1983

Comparison of acetylcholine sensitivity in asthmatics with negative and positive response to exercise.

Airways response to inhaled acetylcholine was studied in asthmatic patients with negative and positive response to exercise. The respiratory threshold of acetylcholine proved to be lower in exercise-responders. Mean value of the bronchoconstrictive dose of acetylcholine was found 72 +/- 78 micrograms in patients with positive, while 510 +/- 360 micrograms in those with negative response to exercise challenge. Our data seem to confirm previous hypotheses, i.e. that exercise-induced asthma is a phenomenon dependent on two factors: mediators generated during exercise (histamine, catecholamines, neutrophil chemotactic factor) and a vagal response from the bronchi.

Acetylcholine↗