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Biomedical subjects

G Liedberg

Publications and source records attributed to G Liedberg.

At least 37 records · Page 2Linked to original sources
PubMed1982

Effect of vagotomy on gastric acid secretion in the rat.

The effects of pentagastrin, histamine or feeding on gastric acid secretion were studied in conscious rats with total gastric by-pass, achieved by transection of the cardia and pylorus, followed by an oesophago-duodenostomy. After closure of the cardia, the by-passed stomach was connected to the small intestine through a Roux-en-Y loop. A chronic gastric fistula was fitted into the rumen. Basal acid output was low in chronically vagotomized rats, being 6% of that in the innervated animals. A clear-cut stimulation was observed after both pentagastrin and histamine in innervated as well as denervated rats, although the maximal acid output in the denervated group was less than 10% of that in the innervated group. In previous studies on acid secretion in vagotomized rats with chronic gastric fistulas, neither basal nor stimulated acid secretion could be detected. Apparently, by-passing the stomach eliminates sources of error associated with the conventional gastric fistula technique (for instance, neutralization of acid gastric juice by swallowed saliva or regurgitated duodenal juice). Nonetheless, the greatly reduced acid output following vagotomy indicates that normal basal as well as normal stimulated acid secretion is dependent upon an intact vagus. Pentagastrin- and histamine-stimulated acid secretion was blocked by atropine and cimetidine in both the innervated and denervated rats. Feeding caused a significant inhibition of acid secretion in the by-passed, innervated stomach. In the denervated stomach feeding was without effect. The mechanism behind the postprandial inhibition of acid secretion in the innervated stomach is obscure. Direct vagal inhibition as well as humoral substances, liberated by vagal stimulation or by the presence of food in the intestine, may be responsible.

Animals↗
PubMed1982

Gastric cancer. Diagnosis, treatment and prognosis in clinical routine.

During 1972-1978, 235 cases of gastric cancer were diagnosed at the Central Hospital of Eskilstuna which serves 115 000 inhabitants. The diagnosis was histologically verified in 193 cases (82%). Only half of the cases were definitely diagnosed prior to exploratory laparotomy or death. More than one fourth of the patients had experienced symptoms consistent with gastric cancer for a period of 1-5 years prior to diagnosis. Gastric X-ray had been performed in 184 cases during the year preceding diagnosis. In 44 cases (24%) the examination gave no suspicion of cancer. One hundred and thirty-five patients were operated upon. Tumour resection was possible in 73, of which 12 (16%) died postoperatively. The crude 5-year survival rate after diagnosis was a mere 7% in the entire series and 19% after tumour resection. Only 14 patients were alive at the end of 1980, 13 after radical surgery. Eleven early gastric cancers (4.7%) were diagnosed, 9 prior to death. We conclude, that the symptoms of gastric cancer were regularly misinterpreted, that the diagnostic tools were dull and that the prognosis is still poor. Prompt recognition of the symptoms and liberal indications of gastroscopy might allow diagnosis at an earlier stage and thus, hopefully, an improved prognosis.

Adenocarcinoma↗
PubMed1982

Traumatic disruption of the axillary artery. Case report.

Total disruption of the axillary artery was caused by blunt trauma in a patient with two previous episodes of dislocation of the shoulder. The pathogenesis, diagnosis and treatment of injuries to the axillary artery by blunt trauma are shortly discussed together with a brief review of the literature.

Aged↗
PubMed1982

Gastrocolic fistula. Report on two cases healed by medical treatment.

Two cases of gastrocolic fistula secondary to benign gastric ulcer disease are described in two patients without any previous gastric surgery. Both cases were successfully treated medically with cimetidine. Implications of the successful outcome of the medical treatment and the possible causes of the symptom of diarrhea are discussed.

Aged↗
PubMed1981

Luminal gastrin does not activate rat stomach histidine decarboxylase.

Fasted rats have a low gastric histidine decarboxylase activity. I.v. infusion of heptadecapeptide gastrin for 2 h raised the enzyme activity. Intragastric perfusion with the same dose of gastrin and for the same period of time did not reproduce the effect of circulating gastrin. It is concluded that luminal gastrin, in contrast to circulating gastrin, does not activate rat stomach histidine decarboxylase.

Animals↗
PubMed1980

Gastrin cell proliferation after chronic stimulation: effect of vagal denervation or gastric surgery in the rat.

Chronic stimulation of the antral gastrin cells by elevated antral pH was achieved by fundectomy, antrum exclusion, fundectomy plus antrum exclusion, antrocolic transposition, and vagal denervation plus pyloroplasty. For comparison we studied also the effects of pyloroplasty alone and of portacaval shunting. All operations that elevated the antral pH resulted in high gastrin concentrations in serum. Particularly high concentrations were observed in fundectomized rats. Vagal denervation of fundectomized or antrum excluded rats reduced the serum gastrin concentration slightly compared with the corresponding innervated animals. Portacaval shunting reduced the gastrin concentration in serum. The antral gastrin concentration was raised or unchanged following fundectomy and vagal denervation, and reduced following antrum exclusion, antrum exclusion plus vagotomy, fundectomy plus antrum exclusion, fundectomy plus vagotomy, antrocolic transposition and portacaval shunt. The gastrin cell density in the antral mucosa was raised following fundectomy, vagotomy, and fundectomy plus vagotomy, unchanged following fundectomy plus antrum exclusion and antrocolic transposition, and reduced following antrum exclusion and portacaval shunting. Ultrastructurally the gastrin (G) cells in the excluded antrum and in the antrum of fundectomized rats showed signs of secretory activity in that the granule volume density or the number of granules per unit cytoplasm was lowered. In the fundectomized rats moreover, the endoplasmic reticulum of the G cells was increased, the Golgi area enlarged and the proportion and volume density of electron dense granules greatly increased. The granule profile diameter was not affected by either antrum exclusion or fundectomy. The results on the excluded antrum indicate that elevated antral pH per se is not sufficient to produce gastrin cell proliferation. In the fundectomized rats, where the hyperlasia of antral gastrin cells was considerable, there is the added stimulus of ingested food. In fundectomized plus antrum excluded rats this stimulus is eliminated and no proliferation ensues. The passage of intestinal material, as in the rats subjected to antrocolic transposition, did not elicit gastrin cell proliferation which seems to suggest that the character of the luminal material is important. We propose therefore that gastrin cell proliferation is due to the combined stimulation of high antral pH and passage of food. Vagal innervation is not required.

Animals↗
PubMed1980

Importance of the kidneys for gastrin elimination and gastric function.

1. The gastrin concentrations in serum were elevated after nephrectomy in rats and mice indicating the importance of the kidney for elimination of gastrin in these species. In guinea-pigs and rabbits nephrectomy did not cause increased serum gastrin concentrations. In rats there was a gradual rise in the serum gastrin level up to 48 hr after bilateral nephrectomy and also after ureteral ligation. After the latter operation the concentrations of gastrin in serum were lower than after nephrectomy. Significant elevation of the gastrin level 48 hr after ureteral ligation indicates that gastrin is eliminated at least partly through glomerular filtration. The gastric histidine decarboxylase activity after nephrectomy or ureteral ligation generally reflected the concentration of circulating gastrin.2. After bilateral ureteral ligation gastric acid secretion in conscious fistula rats was uniformly inhibited with no response to pentagastrin or histamine 24 or 48 hr after the operation. After nephrectomy basal acid secretion was reduced and there was no response to pentagastrin. The response to histamine was still present, although reduced at all dose levels. Linear transformation of the dose-response curve indicated mixed inhibition. The incidence of gastric ulcer was 75% 48 hr after nephrectomy and 30% after ureteral ligation. Since basal and pentagastrin-stimulated acid secretion were unaffected by nephrectomy in rats with the upper two-thirds of the intestine removed, the intestine appears to produce factors which are responsible for the inhibition of gastric secretion.2. On the whole, the gastrin concentration in serum and gastric histidine decarboxylase activity were not increased after five-sixths nephrectomy. Gastric ulcers were seen in the rats with the highest serum urea levels; one in addition had high serum gastrin concentration and gastric histidine decarboxylase activity. Basal, pentagastrin- and histamine-stimulated acid secretion were not affected by subtotal nephrectomy. It appears that in the rat about one sixth of the renal mass is the minimum required for handling gastrin degradation and excretion.

Animals↗
PubMed1980

Mechanisms of gastric acid secretion after pylorus and oesophagus ligation in the rat.

1. The effect of vagotomy on gastric acid secretion was studied in chronic gastric fistula rats at various times after denervation. In these rats basal and pentagastrin-induced acid output was permanently reduced. Thus, the magnitude of the acid response to pentagastrin in the conscious fistula rat is dependent upon an intact vagus. 2. The acid response to pylorus ligation in vagally intact rats was unaffected by drainage of the stomach and therefore not caused by distension. Bilateral vagotomy, performed simultaneously with the ligation, completely abolished acid secretion, while unilateral vagotomy reduced the acid output by half. Hence, in innervated rats, an intact vagal impulse flow appears to be essential for the acid response to pylorus ligation. When the pylorus ligation was performed 2-8 weeks after truncal vagotomy, the acid output showed a progressive return towards pre-denervation values. In the denervated rats the acid response to pylorus ligation was blocked by drainage of the stomach and therefore probably caused by distension, a mechanism which is independent of the vagal impulse flow. 3. The response to pylorus ligation in innervated rats was blocked by atropine and chlorisondamine but not by metiamide. In the denervated rats, the response to pylorus ligation was blocked by all three drugs. 4. Following ligation of both the pylorus and the oesophagus the acid response was poor. With drainage of the oesophagus the acid response was much enhanced, suggesting that oesophageal distension inhibits acid secretion. In the vagotomized rat the poor acid response to oesophageal + pyloric ligation could not be overcome by drainage of the oesophagus. In the innervated rat gastric distension could overcome the inhibition induced by oesophageal ligation. Also in chronically, but not in acutely vagotomized rats, gastric distension brought about a good acid response. Conceivably, gastric reflex mechanisms can activate acid secretion through vagal and/or intramural pathways. Both in innervated and denervated rats the response to gastric distension was inhibited by atropine, chlorisondamine and metiamide. 5. The results suggest that in the innervated rat vago-vagal reflexes are important for the gastric hypersecretion following ligation of the pylorus, and for the acid response to gastric distension following ligation of the pylorus and oesophagus. In the chronically vagotomized rat local intramural reflexes elicited by gastric distension are responsible for the acid response.

Animals↗
PubMed1980

Effects of various gastrointestinal peptides on parietal cells and endocrine cells in the oxyntic mucosa of rat stomach.

1. The effects of secretin, glucagon, cholecystokinin-pancreozymin (CCK-PZ), gastric inhibitory peptide (GIP), vasoactive intestinal peptide (VIP), somatostatin, neurotensin and enkephalin on basal, pentagastrin- and histamine-stimulated gastric acid secretion were investigated in the conscious fistula rat. 2. Glucagon and GIP were ineffective inhibitors of basal and pentagastrin-stimulated secretion. CCK-PZ stimulated acid secretion at a low dose level but at higher doses it inhibited both pentagastrin- and histamine-induced secretions. VIP was ineffective at low doses and at high doses its action was complicated by reflux of stimulated pancreatic and intestinal secretions into the stomach. Met-enkephalin inhibited histamine- but not pentagastrin-stimulated secretion. Neurotensin inhibited the response to pentagastrin but had no effect on histamine-stimulated secretion. Secretin and somatostatin were potent inhibitors of basal and pentagastrin-stimulated acid secretion with little or no effect on the response to histamine. 3. At doses completely inhibitory to pentagastrin-stimulated secretion secretin and somatostatin did not block the mobilization of gastric mucosal histamine by pentagastrin, although somatostatin caused partial competitive inhibition at lower doses of pentagastrin. Thus secretin and somatostatin inhibited pentagastrin-induced secretion neither by blocking gastric mucosal histamine mobilization nor by abolishing the direct action of histamine on the parietal cell -- findings which are inconsistent with the proposed role of histamine as the mediator of the action of gastrin on the parietal cell.

Animals↗
PubMed1979

Effect of antrum exclusion on endocrine cells of rat stomach.

1. Following antrum exclusion the serum gastrin concentration was raised and independent of the prandial state. The antral gastrin concentration and number of gastrin cells were greatly lowered. 2. The histamine content and the number of histamine-storing endocrine ('entero-chromaffin-like') cells in the oxyntic mucosa was almost doubled and the mucosal histidine decarboxylase activity was greatly elevated following antrum exclusion. 3. At the ultrastructural level both types of histamine-storing endocrine cells (ECL and A-like) were found to be enlarged and to have a reduced number of granules per unit cytoplasm. These changes are compatible with an increased secretory activity. The G (gastrin) cells were not increased in size but their granule volume density was lowered. 4. We propose that antrum exclusion results in uninhibited gastrin release causing profound changes in the histamine-storing endocrine cells of the oxyntic mucosa. The cells respond to the hypergastrinemia by an increase in functional activity (activation of histidine decarboxylase and reduction of granule volume density) as well as by an increase in number and size.

Animals↗
PubMed1979

Variated serum gastrin concentration: trophic effects on the gastrointestinal tract of the rat.

Gastrin is thought to be a trophic agent for the digestive tract and the pancreas. This concept was studied on rats subjected to various operations designed to create hyper- or hypo-gastrinemia. Elevated serum gastrin concentration resulted from vagal denervation, antrum exclusion and fundectomy. Reduced serum gastrin concentration resulted from antrectomy. Antrum exclusion but not vagotomy increased the weight and height of the oxyntic mucosa; antrectomy had the opposite effects. There were no trophic changes in the small and large bowel or pancreas, attributable to the serum gastrin concentration. In the bypassed duodenum (following antrum exclusion or antrectomy B II) the villus height was greatly lowered suggesting that in this location the passage of food acts as a trophic stimulant. Our results show that endogenous gastrin exerts a trophic effect on the oxyntic mucosa; there was no evidence for a similar effect on the extragastric gut and pancreas.

Animals↗