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Biomedical subjects

M Rokkjaer

Publications and source records attributed to M Rokkjaer.

28 records · Page 2Linked to original sources
PubMed1979

Bile-induced chronic gastric ulcer in swine with excised oxyntic gland area.

After excision of the oxyntic gland area in seven miniature pigs and cholecystogastrostomy in six of them, two developed chronic gastric ulcers in the gastric remnant. No parietal cells were found in the two pigs with ulcers, whereas small areas with polypoid oxyntic mucosa were found in four pigs without ulcer. The study indicates that bile-induced chronic gastric ulcer can occur in the pig despite the absence of oxyntic cells.

Animals↗
PubMed1977

Quantitative determination of pyloric regurgitation in response to intraduodenal bolus injection.

Employing 99m Tc-colloid and external scanning, a test has been developed to measure duodeno-gastric regurgitation quantitatively. The test is relatively simple and its reproducibility is good. Thirty-two patients with type I gastric ulcer had a median reflux of 14%, significantly higher than nine controls and nine duodenal ulcer patients with a median reflux of 4% and 5%, respectively.

Adult↗
PubMed1977

Influence of parietal cell vagotomy and selective gastric vagotomy on gastric emptying rate and serum gastrin concentration.

Gastric emptying of a solid meal and serum gastrin concentration were studied in 26 patients with duodenal ulcer disease before and after parietal cell vagotomy (PCV), selective gastric vagotomy with drainage (SGV + D), or parietal cell vagotomy with drainage. PCV had no significant effect on gastric emptying rate, whereas emptying was significantly delayed after SGV + D. The integrated gastrin output 60 to 300 min after the test meal was insignificantly altered after PCV, but significantly increased after SGV + D. It is concluded that the drainage procedure did not normalize the disturbed gastric emptying after SGV. The prolonged hypergastrinemia period after food stimulation may reflect stasis.

Adult↗
PubMed1977

On the cause of the increased Heidenhain pouch secretion and serum gastrin concentration after gastrojejunostomy in dogs. With a statistical appendix.

In 10 dogs with Heidenhain pouches (HP) a gastrojejunostomy (GEA) was constructed and later converted into a Roux en-Y anastomosis in order to abolish or reduce transstomal reflux. Next, duodenal inhibition was abolished by duodenal transection, and finally the duodenal bulb was excised. Twenty-four hour HP acid output increased after GEA, some 70% of the increase being attributable to transstomal reflux, the rest to decreased duodenal inhibition. Abolished duodenal inhibition caused a new rise, not significantly different from that caused by the combined effect of reflux and decreased duodenal inhibition after GEA. Twenty-four hour fasting HP acid output and 5 hr food-stimulated HP acid output rose after GEA by the same amount as that caused by abolished duodenal inhibition. A significant correlation was found between integrated gastrin and total HP acid output after food stimulation. Both fasting and food-stimulated gastrin concentration rose after GEA, the latter caused by reflux alone. Elimination of duodenal inhibition caused an unexpected rise in both fasting and food-stimulated gastrin concentration.

Animals↗
PubMed1976

Jejunal inhibition of pentagastrin-induced gastric acid secretion in man and Heidenhain pouch dogs.

The administration of hypertonic glucose and saline and of fat intrajejunally in man caused a marked and almost identical inhibition of pentagastrin-stimulated gastric acid secretion. Hypertonic glucose administered intrajejunally in Heidenhain pouch dogs resulted in an equal inhibition of pentagastrin-induced acid secretion from the pouch and the main stomach, whereas hypertonic saline had no effect. The study demonstrates the existence of potent jejunal inhibitors of gastric secretion, which seem to operate independently of vagal innervation.

Adult↗