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Biomedical subjects

B Simon

Publications and source records attributed to B Simon.

At least 325 records · Page 18Linked to original sources

[Onset of effect of an i.v. ranitidine bolus].

Ranitidine 50 mg or 0.9% saline was given i.v. to 12(6) volunteers and pH and volume of the gastric aspirate was measured in short-time intervals over a period of 6 hours. There was an increase in pH above 4 in all subjects starting within 30 min after ranitidine injection. Concomitantly volume secretion was reduced to 35-50%. i.v. administration of ranitidine 30-45 min before induction of anaesthesia should, therefore, reduce the number of patients theoretically at risk of acid-induced pulmonary damage.

Adult↗

[Do prostaglandins protect other cells besides those of the gastrointestinal epithelium?].

Prostaglandins in very low concentrations, which do not inhibit acid secretion, do protect the mucosa of the gastrointestinal tract against a great number of noxious agents. Similar effects could be shown recently in hepatic, pancreatic, renal, and myocardial tissue. The mechanism of cytoprotective action remains unclear. Since cytoprotection is quite ubiquitous, a common mechanism as for instance stabilisation of membranes seems to be effective. It remains to be seen, if this protective action of prostaglandins can be used in therapy.

Acute Disease↗

[Inhibition of nocturnal acid secretion by pirenzepine (author's transl)].

The effect of 50 and 100 mg of 5,11-dihydro-11-[(4-methyl-piperazin-1-yl)acetyl]-6H-pyrido]2,3-b][1,4]benzodiazepin-6-one dihydrochloride (pirenzepine), respectively, given p.o. at 6 p.m. on nocturnal acid secretion was tested in 6 healthy volunteers. Pirenzepine showed a long-lasting antisecretory activity. The total acid output between 0 a.m. and 6 a.m. was reduced with 50 mg of pirenzepine by about 32% and with 100 mg of pirenzepine by about 41%. It is assumed that pirenzepine (100 mg at bedtime) should be tested in the prevention of relapse in chronic duodenal ulcer disease.

Benzodiazepinones↗

[Effect of 16,16-dimethyl-PG E2 on the 24 hours intragastric acidity in man].

24 hours intragastric acidity was measured in 6 healthy volunteers in 4 separate 24-hours studies, during which the subjects ate Hipp-meals and had unrestricted physical activity. The medication consisted of 1.0 microgram/kg b.w.td p.o. and 0,5 micrograms/ kg b.w. td p.o. of 16,16-dimethyl-PG E2 or placebo. 1.0 microgram/kg b.w. of 16,16-dimethyl-PG E2 decreased mean 24 hours hydrogen ion activity from 9,81 +/- 1,85 mmol/l (+/- SEM) to 4,08 +/- 1,14 mmol/l (+/- SEM). The degree of inhibition with 0,5 micrograms/kg b.w. td was significantly smaller than that due to ten higher dose of this methylated PG-analogue. Our data reveal, that lower doses of 16,16-dimethyl-PG E2 as originally believed inhibit gastric acid secretion in man effectively.

16,16-Dimethylprostaglandin E2↗

[16,16-Dimethyl prostaglandin E2, human gastric potential difference and ethanol (author's transl)].

Experiments were performed in 8 healthy volunteers to determine the effect of graded doses of oral 16,16-dimethyl prostaglandine (PG) E2 on the ethanol-induced drop in gastric potential difference (PD). All doses of 16,16-dimethyl PG E2 between 1.0 and 20 micrograms did not prevent the initial fall in gastric PD induced by 48% ethanol. However, baseline PD-values recovered faster in the presence of 16,16-dimethyl PG E2. This effect was shown to be dose-dependent.

16,16-Dimethylprostaglandin E2↗

[16,16-Dimethylprostaglandin E2. Antisecretory and protective effects on human gastric mucosa].

The effect of graded oral doses of 16,16-dimethyl-prostaglandin E2 (PG E2) on basal acid secretion in healthy volunteers was tested over a time period of 6 h. In addition, studies were conducted to determine whether pretreatment with this methylated PG-analog could prevent the characteristic fall in human gastric potential difference (PD) associated with intragastric instillation of 50 ml of 4 mmol/l Na-taurocholate. Basal acid output was reduced by 80--90% after 0.5 microgram/kg b.w. 16,16-dimethyl-PG E2. Half maximum inhibition was achieved by 0.1 microgram/kg b.w., whereas a 10 fold lower dose of 16,16-dimethyl-PG E2 (0.01 microgram/kg b.w.) effectively protected human gastric mucosa against the injurious effects of Na-taurocholate. In analogy to findings in animals it is, therefore, concluded that 16,16-dimethyl-PG E2 has two distinct properties in human stomach, antisecretory and protective ones, which were independent of each other.

16,16-Dimethylprostaglandin E2↗

[Ranitidine and transmural potential difference. Results with sodium taurocholate (author's transl)].

The effect of different doses of the newly developed histamine H2 receptor antagonist ranitidine on the sodium taurocholate-induced decrease of the potential difference across the human gastric mucosa was investigated in 18 healthy persons. It was shown that ranitidine protects the human mucosal epithelium against this agent both in acid-inhibitory and non-acid-inhibitory dosages. The results suggest that besides the prostaglandins histamine H2 receptor antagonists possess cytoprotective properties at least against bile acids.

Adult↗

[Effects of magaldrate on circadian profile of gastric juice pH in medical intensive care patients (author's transl)].

The effect of the antacid magaldrate on intragastric pH behaviour was investigated in 9 medical intensive care patients. During the 24-hour test period 10 ml of this complex preparation induced pH increases to values between 6 and 7 when it was administered every two hours. However, three-hourly administration of 15 ml magaldrate did not result in a sufficient intragastric pH increase. Thus relatively small volumes of magaldrate are sufficient to neutralize gastric acid of these intensive care patients effectively.

Aluminum Hydroxide↗

[Ranitidine, a new histamine H2 receptor antagonist. First experimental and clinical data].

The new developed histamine H2-receptor antagonist ranitidine has proven to be a more potent and longer acting anti-secretory compound than cimetidine both after intravenous as well as oral administration. A daily dose of 200-300 mg ranitidine should correspond to 1.0-1.2 g cimetidine in the acute therapy of duodenal ulcer disease. Ranitidine acts neither as a dopamine receptor blocker nor as a dopamine agonist at the pituitary level. Antiandrogenic properties of ranitidine have not yet been described. Ranitidine a more powerful and more selective inhibitor of gastric acid secretion, provides an alternative to cimetidine for clinical situation in which blockage of histamine H2-receptors is useful.

Animals↗

[Fibrinolytic treatment of severe thrombosis of the basilar artery (author's transl)].

Thrombosis of the basilar artery occurred in a 27-year-old woman after physical exercise (bowling). She became deeply unconscious without change so that four days after onset urokinase was administered. The neurological status than markedly improved, with partial regression of the paresis and the cranial nerve deficits, and she became responsive again. Angiography after four-day urokinase administration demonstrated complete recanalisation of the basilar artery. Subsequent rehabilitative measures led to almost complete disappearance of all symptoms. Later neurological tests revealed merely very discrete left hemiparesis, mainly of the arm.

Adult↗