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Biomedical subjects

G Liedberg

Publications and source records attributed to G Liedberg.

At least 55 records · Page 3Linked to original sources
PubMed1978

Evidence for H2-receptor-mediated feed-back regulation of histamine release from endocrine cells in the rat stomach.

1. Pentagastrin reduces the concentration of gastric mucosal histamine in the rat. This effect is counteracted by large doses of histamine H2-receptor agonists which are particularly effective if infused I.V. 2. After blockade of histamine H2-receptors but not of H1-receptors, the pentagastrin-induced reduction of mucosal histamine is greatly augmented and H2-receptor agonists no longer inhibit the response to pentagastrin. 3. It is suggested that in the rat stomach, H2-receptors occur on the histamine storing endocrine cells as well as on parietal cells and that mobilized mucosal histamine inhibits further release of histamine by way of H2-receptor-mediated auto feed-back.

Animals↗
PubMed1977

Gastrin: obligatory intermediate in the postprandial mobilization of gastric histamine in the rat.

In unoperated fasted rats, feeding raised the serum gastrin concentration, reduced the gastric mucosal histamine content and activated the gastric histidine decarboxylase. The reduction of gastric histamine and activation of histidine decarboxylase was induced also by the injection of pentagastrin. In antrectomized rats, feeding failed to produce these effects. Injection of pentagastrin, however, still lowered gastric histamine and activated gastric histidine decarboxylase. Thus, antral gastrin seems to be an obligatory mediator of the postprandial activation of histidine decarboxylase and mobilization of histamine.

Animals↗
PubMed1977

Colchicine inhibits stimulated release of gastric histamine but not activation of histidine decarboxylase.

In the rat, gastric mucosal histamine is mobilized and histidine decarboxylase activated by treatment with insulin or pentagastrin. Colchicine pretreatment prevented the histamine release without preventing the enzyme activation. The results suggest a) that histamine release and histidine decarboxylase activation are independent events, and b) that microtubules are involved in the release of histamine.

Animals↗
PubMed1977

Suppression of rat stomach histidine decarboxylase activity by histamine: H2-receptor-mediated feed-back.

1. Gastrin activates rat stomach histidine decarboxylase. Exogenous histamine suppressed the basal enzyme activity in unoperated, in nephrectomized, in vagally denervated and in antrectomized rats, and counteracted the pentagastrin-induced enzyme activation in unoperated rats.2. Kinetic analysis of enzyme-catalysed histidine decarboxylation in extracts from untreated vagotomized and from histamine-treated vagotomized rats showed that the histamine-induced suppression of histidine decarboxylase activity probably reflects a reduced enzyme concentration. Moreover, the enzyme half-life in vagotomized rats after treatment with histamine was shorter than the half-life observed after inhibition of enzyme synthesis. These observations suggest that administration of histamine not only inhibits enzyme synthesis but also causes an accelerated rate of elimination of histidine decarboxylase.3. Intravenous infusion of histamine caused marked displacement of the pentagastrin dose-response curve, in a manner suggesting a reduced sensitivity to pentagastrin.4. After H(2)-receptor blockade, but not after H(1)-receptor blockade, histamine was less effective in suppressing the enzyme activity. Furthermore, H(2)-receptor blockade augmented the pentagastrin-induced enzyme activation.5. The results suggest that histamine (via H(2)-receptors) reduces the sensitivity of the histamine-storing cells to gastrin and that H(2)-receptor blockade induces the opposite effects.6. We propose that the histamine-storing cells in the rat stomach are endowed with H(2)-receptors and that exogenous histamine is capable of acting directly on the histamine cells. This may reflect a physiological control mechanism whereby mobilized endogenous histamine modifies its own synthesis and release.

Animals↗
PubMed1977

In vitro responsiveness of human gastric carcinoma to pentagastrin.

The influence of pentagastrin on thymidine incorporation of five human gastric carcinomas was studied by an in vitro short-term cell suspension technique. Two of the five tumours reacted with stimulation of incorporation to the treatment. Five tumours of other aetiology did not react to similar treatment. The possibility of gastric carcinoma as a hormone-sensitive tumour is discussed.

Breast Neoplasms↗
PubMed1976

Effects of antrectomy or porta-caval shunting on the histamine-storing endocrine-like cells in oxyntic mucosa of rat stomach. A fluorescence histochemical, electron microscopic and chemical study.

1. The argyrophil (enterochromaffin-like) cells in the oxyntic gland area of the rat stomach contain histamine, which can be demonstrated fluorescence microscopically after exposure to gaseous OPT. After administration of L-dopa (or L-5-hydroxytryptophan), these cells produce and temporarily store dopamine (or 5-hydroxytryptamine), demonstrable by its characteristic formaldehyde-induced fluorescence. Ultrastructurally, the enterochromaffin-like cells, which have the appearance of polypeptide hormone-secreting cells, comprise two main cell types, the most predominant one having vesicular type granules (EGL cells), the second most predominant one having smaller, uniformly electron dense granules (A-like cells). 2. Rats were subjected to the following surgical treatments: antrectomy; porta-caval shunting; antrectomy+porta-caval shunting; or sham-operation. Three to eight weeks after surgery the histamine-storing cells (enterochromaffin-like cells) of the oxyntic mucosa were analysed by fluorescence histochemistry, light and (quantitative) electron microscopy, and fluorometric determination of amines. 3. After antrectomy, fluorescence histochemistry and silver staining revealed a reduced number of enterochromaffin-like cells. The histamine content in the oxyntic mucosa was reduced by about 50%. As in unoperated injection of pentagastrin seemed to mobilize histamine. Feeding or injection of insulin failed to do so in antrectomized as opposed to control rats. Ultrastructurally, the cytoplasmic granules of both endocrine-like cell types were less numerous than in the unoperated rats. The reduction in cell number and granularity was particularly conspicuous with regard to the EGL cells. 4. After porta-caval shunting the number of enterochromaffin-like cells increased markedly. Chemical determination revealed a twofold increase in the histamine concentration of the oxyntic mucosa. Feeding or injection of insulin or pentagastrin lowered the histamine concentration. As judged by electron microscopy, the proliferation of endocrine-like cells induced by porta-caval shunting was restricted to the ECL cell type. Besides occurring in greater number, these cells were larger than those in unoperated controls, and their cytoplasm was densely packed with granules that were increased in size. 5. Following antrectomy of the porta-caval shunted rats the number of enterochromaffin-like cells and the oxyntic histamine concentration was reduced. 6. The results support the idea that gastrin exerts trophic as well as excitatory effects on oxyntic endocrine-like cells.

Animals↗
PubMed1976

Effect of bilateral nephrectomy on serum gastrin concentration, gastric histamine content, histidine decarboxylase activity, and acid secretion in the rat.

Nephrectomy caused a marked increase in the concentration of circulating gastrin immunoreactivity but did not increase basal acid secretion. In normal rats, both histamine and pentagastrin stimulated gastric acid output, but after nephrectomy only histamine was effective. Histidine decarboxylase in the oxyntic mucosa was greatly activated following nephrectomy. Thus, in the nephrectomized rat gastrin (and pentagastrin) no longer evoked acid secretion, whereas it retained its ability to activate gastric histidine decarboxylase. The results suggest that the kidney is important for metabolism and excretion not only of gastrin but of humoral antagonists of gastrin-induced acid secretion as well.

Animals↗
PubMed1975

Is the basal activity of rat stomach histidine decarboxylase affected by antrectomy?

The serum gastrin concentration and the gastric histidine decarboxylase activity are high in freely fed, unoperated rats but low in antrectomized rats. Following food deprivation the serum gastrin level and the enzyme activity are reduced simultaneously in the unoperated rats. After fasting for 36-48 h - but not before - the enzyme activity drops to the same low levels as in antrectomized rats.

Animals↗
PubMed1975

Activation of histidine decarboxylase by H2-receptor blockade: mechanism of action.

1 Treatment with histamine H2-receptor antagonists, which inhibit basal acid secretion was found to activate rat stomach histidine decarboxylase. At the same time the serum gastrin concentration was greatly increased. 2 In antrectomized rats neither the enzyme activity nor the serum gastrin concentration was affected by the treatment. 3 In analogy with previous observations on other inhibitors of acid secretion we suggest that the H2-receptor antagonists stimulate gastrin release through their effect on acid secretion and that the raised serum gastrin level is responsible for the enzyme activation.

Animals↗
PubMed1974

Correlation between serum gastrin concentration and rat stomach histidine decarboxylase activity.

After prolonged fasting the activity of histidine decarboxylase in the oxyntic mucosa of the rat stomach is low. Feeding or injection of gastrin or insulin rapidly raises the enzyme activity. It was earlier suggested that all enzyme-activating agents act through release of gastrin. This view has found experimental support in studies which show that in antrectomized rats the enzyme is activated by gastrin but not by gastrin-releasing stimuli like feeding or vagal excitation (insulin hypoglycemia). In the present investigation rats were subjected to a variety of treatments and serum gastrin concentrations and gastric histidine decarboxylase activities were measured. The main findings were as follows.1. Feeding raised the serum gastrin level and the enzyme activity in unoperated rats. In fasted antrectomized rats the serum gastrin concentration was low; in freely fed antrectomized rats it was at the same level as in fasted unoperated rats. In antrectomized rats the enzyme activity was low and not raised by feeding.2. Acid in the antrum inhibits the release of gastrin whereas an alkaline pH may facilitate such release. All treatments that blocked acid secretion, thereby raising the antral pH, also raised the serum gastrin concentration and concomitantly the histidine decarboxylase activity. Thus, vagotomy increased the serum gastrin level and the histidine decarboxylase activity in fasted rats. Treatment of fasted unoperated rats with atropine or hexamethonium had similar effects. Antral exclusion, which prevents HCl from reaching the pyloric glands, resulted in marked increase in the serum gastrin concentration and in the enzyme activity of fasted rats.3. Injection of insulin resulted in a rather slow, progressive increase in the serum gastrin concentration. The peak was reached after about 4 hr. The enzyme activity was also raised markedly and the peak response occurred about 1 hr later.4. An increase in the histidine decarboxylase activity was invariably preceded or accompanied by a raised serum gastrin level. With fasted or fed unoperated, vagotomized, antrectomized or antrally excluded rats, the correlation coefficient for the relation between enzyme activity and serum gastrin concentration was 0.69 (P < 0.05).5. Porta-caval-shunted fasted rats responded to feeding or injection of insulin with marked activation of gastric histidine decarboxylase. The response after feeding was at least 5 times higher in shunted than in nonshunted rats but serum gastrin was only slightly higher. Following antrectomy of porta-caval-shunted rats feeding no longer raised the enzyme activity. Thus, the enzyme-activating agent was of antral origin. In the shunted rats injection of pentagastrin induced an enzyme activation about 5 times that seen in intact rats. This response was not significantly reduced by antrectomy. In conclusion, we have observed a correlation between serum gastrin concentration and histidine decarboxylase activity. We have failed to obtain evidence for the existence of any physiological intermediate other than gastrin in the activation of histidine decarboxylase induced by feeding, vagal stimulation or inhibition of acid secretion.

Animals↗