Different ways to damage and protect gastric mucosa.
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Biomedical subjects
Publications and source records attributed to V Rovati.
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The pharmacokinetics of cimetidine after an oral dose of 400 mg were measured in 18 patients with duodenal ulcer, 9 refractory and 9 responders. The peak plasma concentration of cimetidine (2.13 +/- 0.17 micrograms/ml vs 1.43 +/- 0.04 micrograms/ml), the area under the plasma concentration curve (A.U.C.) between 0 to 8 hours after cimetidine (8.49 +/- 0.29 micrograms/ml/h vs 5.83 +/- 0.25 micrograms/ml/h), and the time span in which cimetidine was above 0.5 micrograms/ml (I.C.50) (401 +/- 8.86 min vs 296 +/- 20 min) were all found to be greater in responding patients than in non-responders to the therapy. No differences were detectable between the two groups in urinary excretion, T 1/2 of cimetidine or percentage inhibition (1%) of maximal pentagastrin-stimulated acid output (MAO). The results indicate that clinical healing of duodenal ulcer after cimetidine is related principally to the drug's pharmacokinetics, i.e. to its absorption from the small bowel, and that some other therapeutic approaches might be tried before surgery in cases of duodenal ulcer refractory to cimetidine.
Gastric cytoprotective effects of vagotomy, PGE2 and antimuscarinic compounds (pirenzepine, atropine) were studied in the rat. Both pharmacological and surgical treatment prevented the gastric damage induced by intragastric administration of acetylsalicylic acid plus hydrochloric acid. The mechanisms of action are discussed.
The colonizing ability of Streptococcus faecium strain SF 68 at different levels of the gastrointestinal tract was assessed in ten patients. They were orally treated with a preparation containing the bacteria in lyophilized form for three days. During an abdominal surgical operation a sample of bacterial content of jejunum, ileum and colon was taken and cultured. The Streptococcus faecium was detected in all treated patients in a quite high concentration compared to the counts of both aerobic and anaerobic germs. These data confirms the rapid growth of SF 68 after oral administration in the gastrointestinal human tract.
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