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Biomedical subjects

H G Dammann

Publications and source records attributed to H G Dammann.

At least 163 records · Page 9Linked to original sources
PubMed1982

[Prevention of stress ulcer hemorrhage with H2-receptor blockade].

The prophylaxis of stress-induced gastrointestinal bleeding has gained particular clinical importance. The H2-receptor antagonist cimetidine as well as vigorous antacid treatment have been shown o be effective in preventing this complication. In six intensive care patients with an increased risk of gastrointestinal bleeding the new H2-receptor antagonist ranitidine in a dose of 0.125 mg/kg b.w./hr i.v. raised intragastric pH within two hours to values between 6.0 and 7.0. From these first data we may conclude that 200 mg i.v ranitidine daily may be at least as efficient as 1200 to 2000 mg i.v. daily cimetidine in inducing almost sustained anacidity. Its prophylactic use in high risk patients seems to be very promising.

Furans↗
PubMed1982

[Inhibition of acid secretion with substituted benzimidazole. A new principle in ulcer therapy?].

Substituted benzimidazoles inhibit gastric acid secretion stimulated by histamine, pentagastrin and vagal innervation. In contrast to anticholinergic agents and H2-receptor antagonists these compounds also block secretion induced by exogenous cyclic AMP suggesting a more peripheral site of action. Recent data show that these substances inhibit a H+/K+-ATPase which is localized at the secretory surface of the parietal cells and is generally regarded as the proton pump within the gastric mucosa. Because of the unique distribution of H+/K+-ATPase the inhibitory action of substituted benzimidazoles may offer a new therapeutic approach in hypersecretory states.

Adenosine Triphosphatases↗
PubMed1982

In vivo diagnosis of massive hepatic infarction by computed tomography.

A patient is presented with a postpartum hepatic artery thrombosis in association with presumed fibromuscular hyperplasia. Massive hepatic infarction developed characterized clinically by fever, coma, ascites, ileus, jaundice, and renal failure; and biochemically by markedly elevated SGOT and SGPT, alkaline phosphatase, total bilirubin levels, and decreased thromboplastin time. The diagnosis was made in vivo by computed tomography (CT). Angiography revealed thrombotic occlusion of the hepatic artery in association with presumed fibromuscular hyperplasia. Laparoscopy and biopsy confirmed the diagnosis.

Adult↗
PubMed1982

[Prognostic value of computed tomography in acute pancreatitis (author's transl)].

A prospective study was performed in 50 patients with acute pancreatitis to find out the value of computed tomography for an early prognosis. CT findings (retroperitoneal fluid collections with enlargement of the retroperitoneal space, intraperitoneal air-fluid levels and ascites), clinical (age, ileus) and laboratory tests (LDH, blood glucose, urea, creatinine and calcium) were taken into consideration. These data were collected during the first two days after hospitalisation and turned out to be of considerable prognostic value: About 70% of the patients died when 5 or more of these pathological findings existed. More than 90% of all patients who died belonged to this group.

Acute Disease↗
PubMed1982

[SKF 93479, a newly developed histamine H2-receptor antagonist. / Effect on gastric potential difference in the presence and absence of acetylsalicylic acid].

Acetylsalicylic acid (ASA) alters the gastric mucosal barrier as measured by the transmucosal potential difference (PD). The effect of the newly developed histamine H2-receptor antagonist 2-(2-(5-dimethylaminoethylfuran-2-ylmethylthio)ethylamino)-5-(6-methylpyrid-3-ylmethyl)pyrimid-4-one trihydrochloride (SKF 93479) on the ASA-induced drop in gastric PD was studied in 6 healthy volunteers. Mean basal PD was -38.5 to -39.5 mV. After 1000 mg of ASA PD decreased in 10-15 min to -25 mV. In subjects pretreated orally with 0.5 mg/kg SKF 93479, PD rose during 30-45 min to -53.5 mV. After ASA PD fell to -38.5 mV, but did not fall below normal.

Adult↗
PubMed1982

[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↗
PubMed1982

[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↗
PubMed1982

[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↗
PubMed1982

[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↗