Biomedical subjects
K F Sewing
Publications and source records attributed to K F Sewing.
Adenylate cyclase in human gastric mucosa: its activation by histamine in morphologically different biopsy specimens.
In morphologically different biopsy specimens from fundic, antral and duodenal mucosa of 134 persons, basal and histamine stimulated adenylate cyclase activity was studied: Basal and stimulated adenylate cyclase activities were log-normally distributed. Only in the fundic but not in the antral and duodenal mucosa adenylate cyclase was sensitive to histamine. The mean basal activity in the fundic gastric mucosa was 148, in response to 10(-5) mol/l histamine 292 pmol cAMP/mg protein/20 min. In human fundic biopsy specimens histologically identified as normal gastric mucosa, the stimulatory effect of histamine on adenylate cyclase decreased with the individual's age. In bioptic material from patients suffering from histologically proven chronic gastritis the histamine effect decreased with the degree of atrophy. A similar loss of histamine sensitivity was found in gastric mucosal biopsies of antrectomized individuals operated at least 5 years before by the Billroth I or II method, whereas in the mucosa of patients with gastric or duodenal ulcer no loss occurred. In contrast, the most pronounced stimulatory action of histamine was found in this latter group. Since a histamine sensitive adenylate cyclase is localized only in the glandular area of the fundic mucosa and the histamine sensitivity depends on a morphological intact structure of the mucosa, it can be concluded, that the effects of histamine on adenylate cyclase and on hydrochloric acid acid secretion have to be considered as a mechanism linked together.
Human gastric mucosal adenylate cyclase: activation by histamine-H2-receptor stimulation and inhibition by cimetidine in vitro and in peptic ulcer patients.
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Effect of histamine and NalphaNalpha-dimethylhistamine on gastric acid secretion and mucosal blood flow in Heidenhain-pouch dogs [proceedings].
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Robert Domenjoz for his 70th birthday.
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Determination of histamine and its metabolic products in the pig gastric mucosa.
This paper describes analytical techniques for quantitative and qualitative determination of histamine and its metabolites (N tau-methylhistamine, N alpha-methylhistamine and N alpha, N alpha-dimethylhistamine) in the pig gastric mucosa. These metabolites and N alpha-acetylhistamine, imidazolyl-4-acetic acid and N tau-methylimidazolylacetic acid were synthesized as reference compounds and analyzed by using the dansylation technique. TLC of dansylated mucosal extracts in various solvents (in situ fluorescence measurements) in combination with TLC/IR and TLC/MS transfer technique demonstrated the presence of histamine. The only metabolite was N tau-methylhistamine.
Anticholinergic effects of pirenzepine on the guinea-pig isolated atrium.
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[Gastrointestinal tract diseases as interfering factors in drug effects and kinetics].
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Enhancement of electrically stimulated guinea-pig gallbladder contraction by subthreshold concentrations of gastrointestinal hormones in vitro.
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[In-patient treatment of peptic ulcer with cimetidine. I. Effect on duodenal ulcer healing (author's transl)].
The effect of 300 mg cimetidine q.i.d. on ulcer healing was studied in a controlled double-blind clinical trial of 71 in-patients with duodenal ulcer. Healing occurred in 48.5% of patients in the cimetidine group after two weeks, and in 20.6% in the placebo group (P less than 0.05). The healing rate was 88% in the cimetidine group at four weeks, 79.4% in the placebo group. Only during the first day was ulcer pain significantly reduced in the cimetidine-treated patients. Neither basal nor pentagastrin-stimulated acid and pepsin secretions were affected by 17-day administration of cimetidine. The drug had to be withdrawn in two patients because of elevated serum-creatinine levels. There was no other untoward effect.
[In-patient treatment of peptic ulcer with cimetidine. II. Controlled double-blind trial on gastric ulcer patients (author's transl)].
In a controlled double-blind clinical trial of 39 in-patients with gastric ulcer the effect of cimetidine on ulcer healing, ulcer pain and pentagastrin-stimulated acid and pepsin secretion was measured. A faster healing rate in the cimetidine group was statistically not significant. Cimetidine had no effect on ulcer pain and pentagastrin-stimulated acid and pepsin secretion. There were no serious untoward reactions.
Effect of cimetidine on pentagastrin- and meal-stimulated gastric acid secretion and serum gastrin before and after one month of daily cimetidine treatment [proceedings].
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[Drug safety. Introduction to the topic].
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Effect of one-month treatment with cimetidine on gastric secretion and serum gastrin and pepsinogen levels.
The inhibitory effects of cimetidine on gastric acid and pepsin secretion were studied before and after 1 month of treatment with 300 mg of cimetidine four times a day in 15 male duodenal ulcer patients. Cimetidine inhibited both pentagastrin- and peptone meal-stimulated acid secretion significantly better before, than after, 1 month of treatment. Similarly cimetidine inhibited pentagastrin-stimulated pepsin secretion significantly better before treatment. Meal-stimulated serum gastrin concentrations were significantly higher after treatment. The mechanism(s) of these effects was not apparent.
Effect of cimetidine on gastric mucosal histamine and histidine decarboxylase activity in rats.
In conscious rats and in anaesthetized gastric fistula rats, the effects of low and high doses of the histamine H2-receptor antagonist cimetidine was studied on gastric mucosal histamine concentration and histidine decarboxylase activity with or without concomitant administration of pentagastrin. In conscious animals a singleinjection of pentagastrin reduced gastric mucosal histamine concentration and elevated histidine decarboxylase activity. This effect was not antagonized by low doses of cimetidine. High doses of cimetidine, like pentagastrin, reduced the histamine concentration and elevated the histidine decarboxylase activity. In anaesthetized rats low doses of cimetidine and reduced gastric acid secretion. The effects of cimetidine on gastric mucosal histamine and histidine decarboxylase were less pronounced than in conscious animals. The histidine decarboxylase stimulating activity of high doses of cimetidine was not abolished by gastric perfusion with acid suggesting that endogenously released gastrin is not involved. A feedback relationship between the blockade of the target organ and increased histamine biosynthesis is discussed.
Methylation of histamine in the gastric mucosa.
Methylation of histamine in the gastric mucosa of various species has been studied in vitro and in vivo. When gastric mucosal homogenates of rat, guinea pig, cat, dog, and pig were incubated with 14C-histamine in the presence of S-adenosyl methionine Ntau-methylhistamine was formed as the only methylated histamine derivative. Excessive concentration of Ntau-methylhistamine inhibited the formation of Ntau-methylhistamine. Pretreatment of guinea pigs with prednisolone, aminoguanidine, or pentagastrin neither influenced in vitro the formation of Ntau-methylhistamine significantly nor shifted the methylation reaction towards the side chain. Pretreatment of guinea pigs with the histamine H2-receptor blocker cimetidine significantly enhanced the formation of Ntau-methylhistamine in vitro. In pooled samples of guinea pig gastric mucosa histamine and Ntau-methylhistamine were found. Under none of these circumstances was Nalpha-methyl-or Nalpha,Nalpha-dimethylhistamine found. It is concluded that in rat (to a small extent), guinea pig, cat, dog, and pig gastric mucosa the formation of Ntau-methylhistamine is the only methylating pathway of histamine. In cases where other methylated histamine derivates (Nalpha-methyl- and/or Nalpha,Nalpha-dimethylhistamine) are found they must origin in sources other than the gastric mucosa.
[What is certain in the treatment of peptic ulcer using cimetidine?].
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