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Biomedical subjects

H Kather

Publications and source records attributed to H Kather.

At least 73 records · Page 4Linked to original sources

[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↗

The new histamine H2-receptor antagonist ranitidine. Duration of action.

The antisecretory effects of a new histamine H2-receptor antagonist, ranitidine hydrochloride, have been investigated on basal and pentagastrin-stimulated acid secretion in healthy volunteers 5 and 10 h after oral administration of 150 mg. In addition, the 24-h intragastric pH-profiles have been measured in patients undergoing parenteral nutrition after three doses of 150 mg ranitidine per day. A 40% inhibition of basal acid output has been noted even 10 h after drug intake. The intragastric pH-values were raised above 5 for at least 24 h. The new H2-antagonist ranitidine has been proven to be a potent and long-acting antisecretory compound.

Adult↗

Adrenoceptor of the alpha 2-subtype mediating inhibition of the human fat cell adenylate cyclase.

In an attempt to characterize the adenylate cyclase-coupled alpha-adrenoceptors of human fat cells the effects of various alpha-adrenergic agonists and antagonists were examined in the presence of 0.05 mmol/l of propranolol. The order of agonist potencies with respect to alpha-adrenergic inhibition was (-)-adrenaline greater than alpha-methyl-(-)-noradrenaline greater than (-)-phenylephrine with half-maximal inhibition occurring at 2 mumol/l of (-)-adrenaline and 7 mumol/l of alpha-methyl-(-)-noradrenaline respectively. The inhibition of adenylate cyclase induced by 0.05 mmol/l of (-)-adrenaline was reversed by the alpha-blocking agents yohimbine and prazosin, with the alpha 2-site-directed antagonist yohimbine being more than 100-times more potent than prazosin which is more active at alpha 1-sites. The results show that the cyclase-coupled alpha-adrenoceptors of human fat cells, which probably represent the physiologically relevant target of antilipolytic catecholamine effects, display characteristic features of the alpha 2-adrenoceptor subtype.

Adenylyl Cyclases↗