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Biomedical subjects

L Olbe

Publications and source records attributed to L Olbe.

At least 55 records · Page 3Linked to original sources
PubMed1992

Defective inhibition of gastrin release by antral distension in duodenal ulcer patients.

The gastrin response to a low and a high dose of gastrin-releasing peptide infusion was studied in healthy volunteers and in patients with duodenal ulcer disease. In duodenal ulcer patients, the gastrin response was exaggerated. Cholinergic blockade did not change the gastrin release in healthy volunteers. Antrum distension during neutralization of the gastric lumen was unable to stimulate gastrin release, also under cholinergic blockade. However, in healthy volunteers distension of the antrum significantly inhibited the gastrin response to gastrin-releasing peptide infusion. This inhibitory influence was most pronounced in patients given the lower dose of the neuropeptide. Cholinergic blockade counteracted the inhibitory effect exerted by antral distension. On the other hand, antral distension did not alter the gastrin response to gastrin-releasing peptide in patients with duodenal ulcer disease. These results suggest an additional defective inhibitory mechanism in duodenal ulcer patients.

Adult↗
PubMed1992

Comparison of once-daily intravenous and oral omeprazole on pentagastrin-stimulated acid secretion in duodenal ulcer patients.

The effect of 5 days of once-daily dosing with 20 mg p.o. and 40 mg i.v. omeprazole on pentagastrin-stimulated acid secretion was studied in 8 patients with duodenal ulcer. In addition they also received a 10-mg i.v. dose on day 6 during the oral treatment period. The antisecretory effect was measured 6-7 h after dose at a time point when maximal inhibition during the dosing interval is anticipated. The median percent inhibition of peak acid output (PAO) markedly increased from 43% on day 1 to 100% on day 5 during treatment with 20 mg p.o. The first 40-mg i.v. dose produced a median inhibition of 98% of PAO already on day 1. After 5 days of dosing, the inhibition had increased to 100%. On the other hand, a 10-mg i.v. dose could essentially maintain the degree of PAO reduction reached after 5 days of oral treatment. Plasma omeprazole concentrations increased during repeated dosing both with 20 mg p.o. and 40 mg i.v.

Administration, Oral↗
PubMed1991

Omeprazole in elderly duodenal ulcer patients: relationship between reduction in gastric acid secretion and fasting plasma gastrin.

The effect of omeprazole on acid secretion and gastrin levels has been investigated in 10 elderly duodenal ulcer patients in remission. Doses of 5, 10, 20 and 40 mg omeprazole were given once daily for 7 consecutive days and the basal (BAO) and peak (PAO) acid output and fasting plasma gastrin concentration were measured 24 h after the seventh dose. Omeprazole suppressed PAO significantly and dose-dependently after doses of 10, 20 and 40 mg, the suppression being 42%, 75% and 85%, respectively. No patient showed complete inhibition of PAO and at least 20 mg had to be given to obtain a marked inhibitory effect in all patients. Increasing the dose to 40 mg had only a slight additional effect compared to 20 mg. There was a relationship between degree of acid inhibition and the increase in fasting plasma gastrin. PAO had to be suppressed by more than 80% before a moderate increase in fasting plasma gastrin was observed. The optimal once-daily oral dose of omeprazole for inhibition of acid secretion in elderly patients appears to be 20 mg. Omeprazole 20-40 mg may cause a moderate increase in fasting plasma gastrin.

Aged↗
PubMed1991

Effects of some gastrointestinal peptides on isolated human and rabbit gastric glands.

The isolated gastric gland preparation, with aminopyrine accumulation as an index of the parietal cell response, has been used to study the effects of somatostatin (S-14), gastrin-releasing peptide (GRP), cholecystokinin (CCK-8), vasoactive intestinal peptide (VIP), and peptide YY (PYY) on the in vitro acid secretion in human and rabbit oxyntic mucosa. Somatostatin was able to inhibit the parietal cell response to histamine in both human and rabbit isolated gastric glands (maximal inhibition, 22% and 34%, respectively) but failed to inhibit the parietal cell response to db-cAMP. However, other peptides capable of inhibiting gastric acid secretion in vivo, such as CCK, VIP, and PYY, were unable to induce any inhibition of the parietal cell response to db-cAMP or histamine in the isolated gastric gland preparation irrespective of the species studied. GRP was not able to induce a parietal cell response, a finding that is in accord with the assumption that the stimulatory effect of GRP on gastric acid secretion in vivo is by releasing gastrin from antral G-cells.

Animals↗
PubMed1991

Factors influencing the release of cholecystokinin induced by gastrin-releasing peptide in man.

We have studied the basal release of cholecystokinin (CCK) and the CCK response to gastrin-releasing peptide (GRP) in man. GRP infusion was followed by a substantial and immediate release of CCK. Pancreatico-duodenectomy or antrectomy with or without duodenal exclusion or antrectomy with truncal vagotomy did not significantly change the basal release of CCK or the GRP-induced CCK release. These results indicate that both basal and GRP-induced release of CCK predominantly originate from the small intestine below the duodenum and the upper part of the jejunum and is unchanged by duodenal exclusion and vagal denervation of the small intestine.

Cholecystokinin↗
PubMed1991

Inhibition of gastrin release induced by fundic distension. Evidence of a defective inhibition in duodenal ulcer patients.

The serum gastrin response to an infusion of gastrin-releasing peptide (GRP), with or without simultaneous fundic distension, was studied in healthy volunteers and in patients with duodenal ulcer disease before and after a complete proximal gastric vagotomy (PGV). We also studied the effect of fundic distension alone on gastrin release and intraluminal gastric pressure in healthy volunteers and in patients after PGV. We observed an increased intraluminal pressure in patients after PGV compared with healthy subjects. During fundic distension with 600 ml of air no significant increase in gastrin values was observed in healthy subjects or in duodenal ulcer patients. In healthy subjects fundic distension significantly inhibited the gastrin response to the higher dose of GRP. This inhibitory effect exerted by fundic distension was counteracted by cholinergic blockade. In contrast, fundic distension did not alter the gastrin response to GRP in duodenal ulcer patients, suggesting a defective inhibitory mechanism in duodenal ulcer patients. After PGV, GRP infusion resulted in an enhanced gastrin response, and fundic distension seemed to facilitate the gastrin-stimulatory effect of GRP. This supports the concept of a vagally dependent inhibitory oxyntopyloric mechanism and that fundic distension can elicit both inhibitory and stimulatory secretory mechanisms.

Adult↗
PubMed1991

24-hour intragastric acidity and plasma gastrin during long-term treatment with omeprazole or ranitidine in patients with reflux esophagitis.

The reduction in intragastric acidity and the subsequent increase in plasma gastrin were compared during long-term treatment with either omeprazole or ranitidine in 19 patients with erosive reflux esophagitis. The patients received 40 mg omeprazole in the morning or 300 mg ranitidine twice daily. After healing, half the dose was given as maintenance treatment for 1 year. Intragastric acidity and plasma gastrin were measured 24 h before entry and monthly with the high dose and after 1, 6, and 12 months with the low dose. Omeprazole reduced intragastric acidity more effectively than ranitidine (p less than 0.001). This difference in efficacy was more pronounced during the daytime. Plasma gastrin increased more after omeprazole than after ranitidine (p less than 0.01), and both drugs showed a normal postprandial response and approached fasting levels before the next dose. During long-term treatment with 20 mg omeprazole in the morning no progressive alterations were observed in 24-h intragastric acidity or plasma gastrin.

Adult↗
PubMed1991

Colonic interposition for reconstruction after resection of cancer in the esophagus and gastroesophageal junction.

In 26 patients with carcinoma of the esophagus or gastroesophageal junction, intestinal interposition was performed in post-resection reconstruction, using left colon in 21 cases, right colon in one and a long jejunal segment in four cases. The tumor involved the gastric cardia in 16 patients with colonic interposition and five underwent palliative resection. Infectious pulmonary and abdominal complications were common. Three patients required reoperation, for empyema, ischemic colonic segment and subphrenic abscess, respectively. Ischemia of the interposed segment occurred in two patients, necessitating removal of the segment in one. There was no anastomotic dehiscence and no tumor in the margins of the resected tissue. The 30-day postoperative mortality was 1/22 and the mean postoperative hospital stay 24 days, with 11 patients discharged directly to their homes. The functional results 6 months postoperatively were favorable in most survivors, and only three complained of dysphagia.

Adenocarcinoma↗
PubMed1991

Reservoir function after subtotal or total gastrectomy with or without gastric substitute.

Volume and pressure characteristics as a measure of reservoir function were studied in three patient groups greater than 1 year after gastrectomy for cancer, one group with straight Roux-en-Y esophagojejunostomy, one with an s-shaped gastric substitute after total gastrectomy, and the third group with subtotal gastrectomy. A large latex balloon was introduced into the proximal jejunum, gastric substitute or gastric remnant and then filled with water at a constant, slow rate. The maximal volume capacity was 400 ml at basal pressure 13.9 cmH2O in the remnant after subtotal gastrectomy and 475 ml at 10.4 cm in the gastric substitute, but only 180 ml at basal pressure 40.4 cmH2O in the proximal Roux limb of the straight esophagojejunostomy. Maximal basal pressure and maximal pressure amplitudes throughout the study period were significantly higher in the patients with straight Roux-en-Y esophagojejunostomy. The results suggest that a gastric substitute constructed as an s-shaped pouch is characterized by pressure and volume typical of a low-pressure reservoir, similar to that achieved by leaving the proximal part of the stomach intact.

Adult↗
PubMed1990

Somatostatin release induced by gastrin-releasing peptide in man. Effect of proximal gastric vagotomy and cholinergic blockade.

The influence of intragastric pH on the basal release of somatostatin has been studied in healthy controls and in duodenal ulcer patients. In addition the somatostatin response to gastrin-releasing peptide infusion has been evaluated both regarding the effect of intragastric pH and the influence of vagal innervation and muscarinic blockade. No difference was found in basal blood levels, when changing the intraluminal pH, although a slightly higher basal somatostatin concentration was noticed in patients with duodenal ulcer disease. Neither proximal gastric vagotomy nor cholinergic blockade had any effect on basal somatostatin concentrations. GRP infused in stepwise increasing doses from 20 pmol/kg/h to 400 pmol/kg/h induced a small but significant response. This effect of GRP was most evident, when the stomach was perfused with 0.1 M HCl. The small, somatostatin response to GRP infusion was not influenced by vagal denervation of the parietal cell area, neither by cholinergic blockade. Despite the previously observed effects of vagotomy and cholinergic blockade on gastrin release induced by GRP, a corresponding inverse effect on somatostatin is not apparent.

Adult↗
PubMed1990

Histamine metabolism in human gastric mucosa. Effect of pentagastrin stimulation.

The metabolism of histamine in the human gastric mucosa was studied in the basal state and during pentagastrin stimulation. Studies were made in healthy volunteers and in patients with peptic ulcer disease. Mucosal biopsies were taken from antral and oxyntic gland areas whereupon histamine content, histidine decarboxylase activity, and histamine methyltransferase activity were simultaneously assayed. Histamine content of the oxyntic gland mucosa was decreased as a consequence of pentagastrin administration in all groups studied, and this decrease was numerically largest in patients with duodenal ulcer disease. Pentagastrin induced a significant increase in histidine decarboxylase activity of the oxyntic gland mucosa with the most profound increase seen in patients with duodenal ulcer. The highest rates of histamine formation were present in the oxyntic mucosa of patients with Zollinger-Ellison syndrome. The activity of histamine methyltransferase was the same in all groups studied and was not changed by pentagastrin. In conclusion, pentagastrin administration in humans is followed by a significant mobilization of histamine only from the oxyntic gland mucosa, an effect that is more pronounced in patients with duodenal ulcer disease.

Adult↗
PubMed1990

24-hour intragastric acidity and plasma gastrin after omeprazole treatment and after proximal gastric vagotomy in duodenal ulcer patients.

The relationship between suppressed gastric acidity and the increase in plasma gastrin levels after pharmacological and surgical treatment of peptic ulcer disease were compared in this study. Eight patients with chronic duodenal ulcer and referred for proximal gastric vagotomy were studied. 24-hour intragastric acidity and plasma gastrin levels were investigated in the same patients on three consecutive occasions: preentry without any treatment; after 4 weeks of administration of 20 mg of omeprazole daily, and 4-6 months after proximal gastric vagotomy. Intragastric acidity was slightly more reduced by omeprazole (94%) than after proximal gastric vagotomy (78%), with no difference found during the day or night with either. Plasma gastrin levels increased slightly more after proximal gastric vagotomy [284% (median, 2120 pmol.h/L; range, 733-2831 pmol.h/L)] than after omeprazole administration [186% (median, 1586 pmol.h/L; range, 495-2573 pmol.h/L)]. There is strong evidence that the increased plasma gastrin concentration following omeprazole treatment is caused by the reduced intragastric acidity. The slight increase in plasma gastrin concentration following proximal gastric vagotomy despite a lesser reduction in intragastric acidity may be the result of additional effects on gastrin release by the vagotomy. Both treatments resulted in a modest increase in plasma levels of gastrin that were far below the gastrin levels observed in achlorhydric patients, e.g., patients with pernicious anemia.

Adult↗
PubMed1990

Metabolism of adipose tissue in intraabdominal depots in severely obese men and women.

In groups of obese men and women with an abdominal type of fat distribution, we measured fat cell size, lipoprotein lipase (LPL) activity and lipolysis stimulated by norepinephrine (NE) or isoproterenol (ISO) or inhibited by insulin, in subcutaneous abdominal and retroperitoneal (nonportal), as well as in omental and mesenteric (portal) adipose tissues. Both men and women had large intraabdominal adipocytes. No differences were found between the two groups of obese subjects in fat cell size or LPL activity in the different adipose tissue regions. Women had as high NE- or ISO-stimulated lipolysis in the portal as in nonportal fat tissues, equally high as that found in men. In comparisons with a previous study in nonobese men and women, these results show an increased fat cell size in all tissues in obese women and an increased lipolysis in portal tissues in obese women and in nonportal tissues in obese men. Taken together, these results might mean that obese men and abdominally obese women have a large potential to release free fatty acids (FFA) from intraabdominal depots. This might be followed by metabolic derangements seen in such groups of obese subjects.

Abdomen↗
PubMed1990

Effects of histamine H2-receptor blockade on the cardiovascular reflex response to lower-body negative pressure in man.

The role of histamine H2-receptors in cardiovascular control is unknown. In seven healthy volunteers, we studied how histamine H2-receptor blockade affected the reflex response to hypovolaemia induced by lower-body negative pressure (LBNP). In placebo-treated individuals, LBNP down to -40 mmHg did not change systolic pressure but increased diastolic pressure, heart rate, forearm vascular resistance, plasma noradrenaline concentration and plasma renin activity. After pretreatment with ranitidine, a specific histamine H2-receptor antagonist, the diastolic pressure rise no longer sufficed to maintain a constant systolic pressure during LBNP. Ranitidine pretreatment also attenuated the heart rate response and the rise in plasma renin activity induced by LBNP, but did not significantly change the reflex forearm vasoconstriction or the forearm plasma noradrenaline response. The results suggest that histamine H2-receptor blockade attenuates the reflex vasoconstrictor response to lower-body negative pressure. The mechanism behind this effect remains unknown, but the data do not support the idea that the effect is exerted in the skeletal muscle vascular bed.

Adult↗
PubMed1990

Effect of parietal cell vagotomy and cholinergic blockade on gastrin release in man induced by gastrin-releasing peptide.

The influence of cholinergic blockade as well as vagal denervation of the oxyntic gland mucosa on the gastrin response to gastrin-releasing peptide (GRP) have been studied in patients with duodenal ulcer disease. The gastric luminal content was neutralized during the experiments. GRP induced a substantial increase in gastrin levels with a peak response already after 15 min of infusion. Vagal denervation of the parietal cell area induced a significant increase in basal gastrin concentrations and a significant enhancement of the GRP response. Two different doses of benzilonium bromide were studied and neither influenced the basal concentrations of gastrin. A significantly increased gastrin response to GRP was, however, observed after administration of both a high and a very low dose of the anticholinergic drug. Our results delineate a vagal, noncholinergic inhibitory influence on the basal gastrin release. In addition a vagally dependent oxyntopyloric mechanism inhibits the gastrin release stimulated by GRP. This inhibitory mechanism may hypothetically be a cholinergic reflex mechanism.

Bombesin↗
PubMed1990

Attenuation of gastric sham feeding response during reflex sympathetic activation in man.

In six human volunteers we studied the effects of hypovolemia on the secretory activity of the gastric mucosa. The secretion of acid and HCO3 from the stomach was calculated from continuous measurements of pH and Pco2 in gastric effluent. Gastric secretion was stimulated by sham feeding (SF), and cardiac filling pressure was decreased by pooling blood in the lower extremities (lower body negative pressure (LBNP]. LBNP at -20 mmHg had no significant effects on systemic arterial pressure or heart rate but increased plasma norepinephrine concentration by 48 +/- 6% (p less than 0.001). Both the acid and the alkaline responses to SF were significantly attenuated during LBNP (-38 +/- 8%, p less than 0.01, and -55 +/- 14%, p less than 0.05, respectively). Analysis of the relationship between acid and HCO3 secretion in individual experiments suggested a relatively more pronounced inhibition of HCO3 secretion. The results imply that a decreased responsiveness of the gastric mucosa may be one component of the cardiovascular reflex adaptation to hypovolemia. A downregulation of active secretion will lead to smaller metabolic demands from the secreting cells and may thereby help to maintain a vasoconstriction in the gastric mucosa.

Adult↗