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Biomedical subjects

G Liedberg

Publications and source records attributed to G Liedberg.

At least 73 records · Page 4Linked to original sources
PubMed1973

Effects of prostaglandin E1 on acid secretion, mucosal histamine content and histidine decarboxylase activity in rat stomach.

1. Prostaglandin E(1) inhibits basal and pentagastrin-stimulated gastric acid secretion. The mechanism of this action is not clear. One possible explanation might be that prostaglandin E(1) interferes with the local release or synthesis of histamine which has been proposed as the mediator of the effects of gastrin on the parietal cell.2. A single injection of prostaglandin E(1) did not affect mucosal histamine content or histidine decarboxylase activity in the rat stomach. Pentagastrin lowered the histamine content and activated the histidine decarboxylase to the same extent in prostaglandin E(1)-pretreated and in control rats. We conclude therefore that the inhibitory effect of prostaglandin E(1) on basal and pentagastrin-stimulated acid secretion is not caused by inhibition of histamine release or histamine synthesis.3. Repeated injections of prostaglandin E(1) resulted in a significant elevation of the gastric histidine decarboxylase activity in normal but not in antrectomized rats. Conceivably, this increase in enzyme activity is secondary to prostaglandin E(1)-induced inhibition of acid secretion, which will stimulate release of gastrin due to the rise in intragastric pH.

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PubMed1973

Gastrin in portal and peripheral venous blood after feeding in man.

The concentrations of immunoreactive gastrin in serum from portal and peripheral venous blood were determined in 10 patients with indwelling portal catheters before and after feeding. No significant differences were found between the gastrin concentrations in portal and peripheral serum. Gel filtration studies of serum did not reveal any differences between the gastrin components of portal and peripheral venous serum. Since neither the concentrations of immunoreactive gastrin nor the four gastrin components differed between portal and peripheral serum it is suggested that the liver is without effect on gastrin metabolism.

Aged↗
PubMed1972

Effects of brocresine (NSD-1055) and cycloheximide on amino acid decarboxylase activities in gastric mucosa of normal and vagally denervated rats.

1. Histidine decarboxylase activity of rat stomach fluctuates depending upon the functional state of the stomach. This varying enzyme activity poses special problems in assessing the effectiveness of enzyme inhibitors. After vagal denervation gastric histidine decarboxylase is markedly activated and remains at a high, stable level, which is unaffected by the functional state of the stomach. Thus it appears that vagally denervated rats are well suited for studies on histidine decarboxylase inhibitors.2. In vivo, brocresine (NSD-1055) was found to be a more effective inhibitor of gastric DOPA decarboxylase than of gastric histidine decarboxylase. With the fairly high dose given (200 mg/kg) the inhibition of histidine decarboxylase was at most 75-85% and quite short-lasting. The DOPA decarboxylase activity, which was not affected by vagal denervation, was inhibited more than 95% by brocresine; this inhibition was longer-lasting.3. Cycloheximide, which probably lowers gastric histidine decarboxylase activity by inhibiting enzyme synthesis, was maximally effective at a dose level as low as 1 mg/kg. Gastric DOPA decarboxylase was not inhibited by cycloheximide. Vagotomized rats and control rats responded similarly.4. Combined treatment of vagally denervated rats with brocresine and cycloheximide resulted in a rapid and persistent reduction of the histidine decarboxylase activity. It is concluded that the failure of brocresine alone to induce a lasting inhibition of histidine decarboxylase is due to continuous, rapid synthesis of new enzyme.5. The calculated half-life of gastric histidine decarboxylase was 75 min in vagally denervated rats and 45 min in normal fasted rats. The results suggest that the increased enzyme activity after vagal denervation is caused by an increased rate of enzyme synthesis.

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