Search PubMed⌕ Search

Biomedical subjects

P Kirkegaard

Publications and source records attributed to P Kirkegaard.

At least 127 records · Page 7Linked to original sources
PubMed1982

Closure of terminal and loop colostomy.

The clinical course after closing of a temporary colostomy was studied in 56 patients, 26 with loop colostomy and 30 with terminal colostomy. No significant difference was found in the complication rate or hospital stay between the two groups. It is concluded that terminal colostomy is preferable, as a standard procedure, because it is more acceptable to the patient and gives a complete diversion of the fecal stream.

Adolescent↗
PubMed1982

Effect of naloxone on met-enkephalin-induced gastric acid secretion and serum gastrin in man.

It has previously been demonstrated that met-enkephalin, and endogenous opiate, stimulates gastric acid secretion in man, while naloxone inhibits meal-stimulated acid secretion. In seven healthy subjects the opiate receptor antagonist naloxone was infused in a dose of 10 microgram/kg/h during stimulation of gastric acid secretion with pentagastrin 100 ng/kg/h and met-enkephalin 0.1 microgram/kg/h. Naloxone had no effect on pentagastrin-induced acid secretion, whereas met-enkephalin-induced acid secretion was completely abolished in both studies without affecting serum gastrin levels, suggesting that the acid inhibitory effect of naloxone is specifically directed towards met-enkephalin-induced acid secretion. The results support the assumption that met-enkephalin participates in the physiological stimulation of gastric acid secretion.

Adult↗
PubMed1982

The mechanism of gastrin release in cysteamine-induced duodenal ulcer.

Duodenal ulcer can be induced in rats by a single dose of cysteamine. The ulcer formation is accompanied by acid hypersecretion and elevated serum gastrin levels. This study was performed to elucidate the mechanisms of gastrin release after an ulcerogenic dose of cysteamine. Cysteamine induced a rise in serum gastrin from 29 +/- 5 pg/ml to a maximum of 203 +/- 62 pg/ml after 3 h in unoperated rats, whereas no rise was seen in vagotomized or antrectomized rats. The beta-adrenergic blocking agent propranolol strongly inhibited cysteamine-induced gastrin release, whereas atropine dependent on an intact vagus and may be mediated by beta-adrenergic receptors.

Animals↗
PubMed1982

Vagal control of glucagon-induced inhibition of gastric acid secretion in duodenal ulcer patients.

To study the vagal influence on the inhibitory effect of pancreatic glucagon on gastric acid secretion, the effect of exogenous pancreatic glucagon on pentagastrin-stimulated acid secretion was studied in duodenal ulcer patients before and after parietal cell vagotomy without drainage (PCV). Preoperatively, exogenous pancreatic glucagon inhibited gastric acid secretion, whereas no effect was found postoperatively. Plasma pancreatic glucagon was identical pre- and post-operatively and was within the physiological range. The study demonstrates that the inhibitory effect of pancreatic glucagon on pentagastrin-stimulated gastric acid secretion is dependent on an intact vagal innervation of the parietal cell area.

Adult↗
PubMed1982

Role of delayed gastric emptying in the pathogenesis of cysteamine-induced duodenal ulcer in the rat.

Cysteamine is a potent duodenal ulcerogen in rats. It has been demonstrated to inhibit gastric empyting, whose role in ulcer formation is unknown. In the present study the effect of cysteamine on gastric motility and emptying rate in rats was studied by direct fluoroscopic observation. The delayed gastric empyting was due to a pronounced relaxation of the stomach and a complete blocking of gastric peristalsis. These effects have their maximum within the first 4 h after administration of cysteamine. Thereafter peristalsis and gastric empyting slowly return. In controls contrast medium administered intragastrically was completely discharged from the stomach within 30 min. After cysteamine the first small amounts of contrast medium were discharged into the duodenum after 4 h, and contrast medium remained in the stomach for at least 12 h after administration. The size of the stomach reached a maximum after 3 h and approached normal values again after 12 h. Because of complete gastric retention the acid gastric secretions provoked by cysteamine probably accumulate in the stomach during the first 4 h after cysteamine administration, and because of the absence of peristalsis they are not mixed with gastric contents. After 4 h this pool of undiluted gastric secretions gradually is emptied into the duodenum, where the mucosal resistance is reduced by inhibition of the secretory activity of Brunner's glands, and ulceration rapidly develops. The time relationship is supported by histopathologic findings and measurements of gastric acid secretions after cysteamine. Vagotomy augmented the inhibitory effect of cysteamine on gastric motility. The relaxation was even more pronounced, and contrast medium was not discharged from the stomach within 24 h. In these rats cysteamine induced ulcerations in the stomach.

Animals↗
PubMed1982

Calcium and stimulus-secretion coupling in gastric fundic mucosa. Effect of inhibition of calcium transport by verapamil on gastric acid secretion in the isolated guinea pig fundic mucosa and in healthy subjects.

The effect on gastric acid secretion of blocking transmembrane Ca2+ influx into the parietal cells has been studied in the isolated guinea pig fundic mucosa and in healthy volunteers. Verapamil inhibited in a dose-related manner histamine-stimulated acid secretion in the guinea pig mucosa, whereas stimulation with theophylline and dibutyryl cyclic-AMP was unaffected. The effect of verapamil (Isoptin, 2.0 mg/h) on acid secretion stimulated by increasing doses (50, 200, 500 ng/kg-h) of 15-leucine synthetic human gastric I was studied in seven healthy volunteers, alone and in combination with infusion of calcium gluconate (1.0 meq Ca2+/kg-h). Verapamil inhibited the acid response to the lowest dose of gastrin, resulting in a significant increase of D50 of 15-leucine synthetic human gastrin I. This effect was partly reversed by calcium infusion. It is concluded that one of the mechanisms by which extracellular calcium concentration influences acid secretion is by transmembrane influx of Ca2+ during stimulation.

Adult↗
PubMed1981

Delorme's operation for complete rectal prolapse.

Twelve patients with a median age of 73 years were treated for complete rectal prolapse by Delorme's operation. The patients were mildly sedated, and local anaesthesia with lidocaine--adrenaline was administered submucously. No postoperative mortality or cardiopulmonary complications occurred. After a medial follow-up of 3 years, two recurrences were found. The Delorme procedure seems to be superior to the Thiersch operation, and the postoperative mortality and morbidity is equally low. Delorme's operation should be considered as an alternative treatment for complete rectal prolapse in patients who are not suitable for a transabdominal procedure.

Aged↗
PubMed1981

Bladder dysfunction after low anterior resection for mid-rectal cancer.

Twenty consecutive patients with carcinoma 7 to 12 cm from the anus underwent radical low anterior resection of the rectum; the anastomosis was performed by the EEA stapling instrument. One patient died from pulmonary complications. On urologic follow-up 6 to 8 months after the operation, five patients had significant symptoms from the urinary tract, and in three patients denervation of the bladder was demonstrated. The study establishes that bladder paresis, which is a well-known complication after extirpation of the rectum, also may follow very low anterior resection with anastomosis. The importance of careful follow-up is emphasized

Aged↗
PubMed1981

Effect of endogenous pancreatic glucagon on gastric acid secretion in patients with duodenal ulcer before and after parietal cell vagotomy.

The effect of endogenous pancreatic glucagon on submaximal pentagastrin stimulated gastric acid secretion was studied by infusion of 1-arginine in patients with duodenal ulcer before and after parietal cell vagotomy without drainage (PCV). Preoperatively infusion of 1-arginine resulted in a marked inhibition of acid secretion, whereas no effect was found postoperatively. Plasma glucagon concentrations were identical pre- and postoperatively, fasting as well as during arginine infusion. Serum gastrin concentration rose after PCV but not unaffected by arginine infusion both pre- and postoperatively. The study demonstrates that intact vagal innervation of the fundic glands is a condition of inhibition of pentagastrin induced acid secretion by pancreatic glucagon released by infusion of 1-arginine.

Adult↗
PubMed1981

Infusion of vasoactive intestinal polypeptide in man: pharmacokinetics and effect on gastric acid secretion.

Elimination and effect on acid secretion of vasoactive intestinal polypeptide (VIP) were studied in six healthy volunteers. On a background infusion of pentagastrin, 100 ng/kg-h, VIP was administered as stepwise intravenous infusions in doses of 0.5, 0.9, and 2.7 micro/g/kg-h, each dose being give for 1 h. Mean plasma VIP concentrations rose from 5.7 pmol/l to 28, 106 and 336 pmol/l during the VIP infusions. No significant changes in acid secretion occurred during VIP infusion as compared to infusion of pentagastrin alone, and no duodeno-gastric reflux was registered. Serum gastrin concentrations were unaltered during VIP infusion. Elimination of VIP was bi-exponential with half-lives of 2 and 21 min, respectively. Metabolic clearance rate was 42 ml/kg-min and the estimated volume of distribution 135 ml/kg.

Adult↗
PubMed1981

Brunner's glands of the rat during cysteamine ulceration.

Duodenal ulcers can be produced in rats by subcutaneous administration of cysteamine-HCl. The pathogenesis of these ulcers has not been fully explained. Increased acid secretion is necessary but not sufficient for ulcer production. In the present study we have observed pronounced alterations in the histologic appearance of the duodenal glands of Brunner during ulcer formation. The secretory cells became extremely flattened without mucus content and the lumina of the acini dilated. Changes became most pronounced between 4 and 8 h after administration of cysteamine. Repeated injections of pentagastrin in a dosage inducing an acid response equivalent to the one induced by cysteamine did not produce any histologic changes in Brunner's glands or any ulcerations. When cysteamine was administered to rats with chronic gastric fistulas draining the gastric secretions, no duodenal ulcerations were produced, but Brunner's glands still became depleted of mucus. These findings suggest that the histologic changes in Brunner's glands are not secondary either to the increased acid secretion induced by cysteamine or to ulcer formation. Together with our previous demonstration of a marked reduction duodenal secretion in the first 10 h after cysteamine administration, the results of the present study suggest an inhibitory effect of cysteamine on the synthetic activity of Brunner's glands rather than an impaired release mechanism. The effect of cysteamine on Brunner's glands may be an important factor in the pathogenesis of cysteamine-induced duodenal ulceration.

Animals↗