PubMed Health⌕ Search

Biomedical subjects

H L Waldum

Publications and source records attributed to H L Waldum.

At least 19 recordsLinked to original sources
PubMed1995

[Bismuth. An old medicine of current interest].

Bismuth has been used to treat dyspepsia for more than a hundred years, and has now become an important element in the treatment of peptic ulcer disease. Less than 1% of ingested bismuth is absorbed in the gastrointestinal tract and is excreted in the urine. Bismuth forms a protective coating on the mucosa, it stimulates secretion of bicarbonate and has an effect on the G-cell and Helicobacter pylori. Bismuth gives equal ulcer healing rates as H2-receptor blocking agents, but causes significantly less relapses. Triple treatment with bismuth, tetracycline and metronidazole eradicates H pylori in 95% of patients. Bismuth accumulates in the body during treatment and is neurotoxic, and it cannot be excluded that even short-term treatment may cause subclinical damage to the central nervous system.

Bismuth↗
PubMed1995

[Damages to the large intestine induced by non-steroidal anti-inflammatory agents].

Non-steroidal anti-inflammatory drugs can cause side effects in the large bowel. We describe two cases which illustrate some of the aspects associated with this problem, and briefly outline the different types of side effects encountered, and possible pathogenetic mechanisms. It is emphasized that non-steroidal anti-inflammatory drugs can cause exacerbation of quiescent colitis in patients with inflammatory bowel disease. The use of these drugs in such patients should be very restrictive. Non-steroidal anti-inflammatory drugs can also precipitate de novo colitis. They are also associated with collagenous colitis, non-gangrenous ischemic colitis, complications to diverticular disease, and ulceration of the colon.

Adult↗
PubMed1995

Role of prostaglandins and histamine in hyperemic response to superficial and deep gastric mucosal injury and H+ back-diffusion in cats.

This study was undertaken to examine the role of prostaglandins and histamine in the hyperemic response to gastric mucosal damage followed by H+ back-diffusion. Cat stomachs were exposed to 2 mol/liter NaCl for 10 min followed by luminal perfusion at pH 1. Hypertonic saline caused extensive (microscopic) damage to the surface epithelium, increased gastric mucosal blood flow, and increased release of histamine, PGE2, and 6-keto PGF1 alpha (prostacyclin) into portal venous blood. The effect of indomethacin and histamine blockers (H1 + H2) on the hyperemic response to acid back-diffusion was related to the depth of the mucosal injury and the region of the stomach. In the corpus, indomethacin enhanced mucosal injury. In areas with superficial damage, the hyperemia was inhibited by indomethacin and antihistamines and eliminated by the combination of both. In corpus areas with indomethacin-induced deep lesions, the blood flow was very high, and this hyperemia was partly inhibited by antihistamines. In the antrum the hyperemic response was reduced by antihistamines. Indomethacin increased the release of histamine into portal venous blood (baseline recordings) and reduced basal gastric mucosal blood flow.

6-Ketoprostaglandin F1 alpha↗
PubMed1995

Differential expression and regulation of SSTR2 messenger RNA in rat gastric antrum and corpus.

Somatostatin modulates both endocrine and exocrine functions in the gastric mucosa, where three of the five cloned somatostatin receptors are present. This study examines changes in somatostatin receptor (SSTR) mRNA abundance during fasting, feeding, and profound acid inhibition with omeprazole. Serum gastrin as well as somatostatin and SSTR mRNA abundances were measured in antrum and corpus. In Northern blots of corpus RNA, the SSTR2 probe hybridized with two previously reported species of mRNA (2.4 and 2.8 kb); in addition, a weak previously unreported 1.6-kb band was detected. In antrum, the 1.6-kb band dominated. Fasting increased antral somatostatin mRNA from 100 +/- 8 to 161 +/- 24% and SSTR mRNA from 100 +/- 10 to 179 +/- 14% (P < 0.05). Omeprazole reduced antral somatostatin mRNA to 34 +/- 4% of control (P < 0.05) and elevated SSTR mRNA to 135 +/- 5% of control (P < 0.01). Omeprazole treatment reduced corpus somatostatin mRNA to 59 +/- 5% (P < 0.05), and elevated SSTR mRNA to 140 +/- 3% of control (P < 0.01). The results therefore indicate that a novel SSTR mRNA subtype exists in the stomach and predominates in the antrum. The abundance of this SSTR mRNA is upregulated by both fasting and achlorhydria; conditions that increase or decrease endogenous antral somatostatin, respectively.

Animals↗
PubMed1995

Role of histamine and calcitonin gene-related peptide in the hyperemic response to hypertonic saline and H+ back-diffusion in the gastric mucosa of cats.

BACKGROUND: The present study was undertaken to measure the output of histamine and calcitonin gene-related peptide (CGRP) from injured and restituting gastric mucosa into venous blood and to study the effect of acid back-diffusion on the release of these mediators and their role in the hyperemic response to injury. METHODS: Stomachs of cats were perfused with saline at pH 1.0 or 7.4. Gastric mucosal blood flow (GMBF) was determined with radioactive microspheres, and blood flow in the portal vein and celiac artery was determined by transit-time flowmetry. H+ back-diffusion/secretion was measured by pH-stat titration and by measuring the arteriovenous base excess difference. Mucosal injury was produced by exposure to 2 M NaCl. Histamine and CGRP in portal venous blood were measured by radioimmunoassay. RESULTS: During mucosal exposure to 2 M NaCl GMBF increased, and histamine (0.23 nmol/min) and CGRP (1.2 pmol/min) were released from the mucosa into blood. The hyperemic response was reduced by pretreatment with H1 and H2 blockers and still further by addition of the blocker CGRP8-37. After mucosal damage and luminal perfusion at pH 7.4, GMBF and output of CGRP and histamine decreased towards base-line levels within 30 min. During luminal perfusion at pH 1.0 associated with acid back-diffusion, GMBF and histamine output remained high, whereas the output of CGRP decreased to base-line level. Pretreatment with H1 and H2 blockers reduced the hyperemic response as measured 30 min after damage. CONCLUSIONS: The hyperemic response caused by 2 M NaCl is most likely mediated by histamine and CGRP and maintained by histamine released by back-diffusion of H+ through the superficially damaged gastric mucosa.

Animals↗
PubMed1995

Effect of the histamine-2 agonist impromidine on stem cell proliferation of rat oxyntic mucosa.

BACKGROUND: The trophic effect of gastrin on the histamine-containing enterochromaffin-like cell is pronounced but on the stem cell of the oxyntic mucosa it is only modest. In the rat, gastrin stimulates acid secretion mainly by releasing histamine from enterochromaffin-like cells. This study was designed to test the hypothesis that the trophic effect of gastrin on stem cells is also mediated by histamine released from the enterochromaffin-like cell. METHODS: We stimulated rats with the histamine-2 agonist impromidine. Impromidine, 0.2 mg/h, was given for 2 days by subcutaneously implanted osmotic minipumps, and the trophic effect on stem cells was assessed by incorporation of tritiated thymidine. RESULTS: The plasma gastrin concentrations were 33.9 (9.4) pM and 27.3 (6.0) pM, and the stem cell labelling index values were 5.92 (1.94) and 8.09 (3.78) in the controls and impromidine-stimulated animals, respectively (mean value (SD)). These differences were not statistically significant. CONCLUSION: The present study provides no evidence that histamine-2 receptors mediate a trophic effect on the stem cell of the rat oxyntic mucosa.

Animals↗
PubMed1994

[Symptomatic gallstones in a patient with heart transplantation. A serious and little observed adverse reaction of cyclosporine A].

A 53 year old male patient developed symptomatic cholelithiasis shortly after a heart transplantation following postinfarction heart failure. The patient was both initially cholecystectomized and later endoscopically treated for recurrent biliary pain and multiple concrements in the choledochus. He did not present any of the known predisposing risk factors for developing biliary stones. The possible role of cyclosporine in inducing biliary stones is discussed.

Cholangiopancreatography, Endoscopic Retrograde↗
PubMed1994

Immunoassays for measurement of chromogranin A and pancreastatin-like immunoreactivity in humans: correspondence in patients with neuroendocrine neoplasia.

Chromogranin A (CgA) is a useful marker of neuroendocrine tumors in humans. Here we describe and compare two immunoassay methods for determination of CgA, a radioimmunoassay (RIA) and an enzyme linked immunoassay (ELISA). The detection limit of the ELISA was lower than that of the RIA method (2 ng/ml versus 10 ng/ml, respectively), though the CgA RIA method covered a wider range than the CgA ELISA (10-920 ng/ml versus 2-500 ng/ml, respectively). There was no cross-reactivity with synthetic human and porcine pancreastatin (PST) in the two assays. There was a significant positive correlation between levels of CgA in sera from patients with carcinoid disease, measured by the two methods (r = 0.9, p < 0.0001), and the values were in the same range. Similarly, serum CgA levels in normal controls were also in the same range when assayed by the two methods. A commercially available porcine PST RIA method was evaluated, especially with respect to the influence of Sep-Pak extraction of serum on the levels of pancreastatin-like immunoreactivity (PST-LI). Ten sera from carcinoid patients were treated with Sep-Pak extraction, and levels of PST-LI were determined in non-extracted and extracted sera. There was a significant positive correlation between the concentrations of PST-LI measured in extracted and non-extracted carcinoid sera (r = 0.9, p < 0.002), and the levels were in the same range. There was also a significant positive correlation between levels of CgA and PST-LI in 49 carcinoid sera (r = 0.8, p < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

The effect of tripotassium dicitrato bismuthate on the rat stomach.

BACKGROUND: Bismuth has been used as symptomatic treatment of dyspepsia for many years. It promotes healing of peptic ulcers and reduces their recurrence. The beneficial effect of bismuth on duodenal ulcer disease is thought to be due to an effect on Helicobacter pylori, although it has a rather weak bactericidal effect on H. pylori in vitro. Eradication of H. pylori in duodenal ulcer patients by a combination of bismuth, tetracycline and metronidazole has been reported to increase the density of somatostatin-producing D cells in the antrum. A reduced D cell density in the antral mucosa of duodenal ulcer patients could explain their exaggerated gastrin release. AIMS/METHODS: To test the possibility that bismuth could affect the neuroendocrine cells independently of the presence of H. pylori or not, we gave rats a diluted tripotassium dicitrato bismuthate solution by gastric gavage for 14 days. RESULTS: Tripotassium dicitrato bismuthate treatment did not affect maximal pentagastrin-stimulated acid secretion or histamine release in isolated rat stomachs or the density of argyrophil cells in the oxyntic and antral mucosa. However, it significantly reduced the duodenal concentration of gastrin and calcitonin gene-related peptide, and the density of G cells in the antrum and duodenum. CONCLUSION: The effect of tripotassium dicitrato bismuthate on the G cell may be of significance for its beneficial effect on duodenal ulcer disease.

Administration, Oral↗
PubMed1994

Evaluation of the trophic effect of longterm treatment with the histamine H2 receptor antagonist loxtidine on rat oxyntic mucosa by differential counting of dispersed cells.

To evaluate whether the general trophic effect of gastrin on the oxyntic mucosa is an indirect effect mediated by histamine H2 receptors, sustained 24 hour hypergastrinaemia was induced in Sprague-Dawley rats by treatment with the long acting and potent histamine H2 antagonist loxtidine for five months. The trophic effect was assessed by weight, enumeration of total mucosal cells, parietal cells, and enterochromaffin like cells in smears stained for the actual cells after enzymatic dispersion of the mucosa, and by biochemical analysis of oxyntic mucosal homogenates. The weight of the whole stomach and the oxyntic mucosa increased by 12.7% (p = 0.016) and 27.5% (p = 0.006), respectively. Total oxyntic mucosal protein content increased by 28.7% (p = 0.058). Total numbers of mucosal cells and parietal cells increased by 11.9% (NS) and 24.1% (NS), respectively. The amount of the parietal cell specific enzyme H+,K(+)-ATPase was unchanged. On the other hand, the number of enterochromaffin like cells and related parameters, histidine decarboxylase activity and histamine content of the oxyntic mucosa, showed a pronounced and significant increase. It is concluded that the general trophic effect of gastrin on the oxyntic mucosa is not mediated by the histamine H2 receptor. The tropic effect of gastrin on the parietal cell seems, in contrast with that on the enterochromaffin like cell, not to be specific but only reflecting the general trophic effect on the oxyntic mucosa.

Animals↗
PubMed1994

Gastrin regulates histidine decarboxylase activity and mRNA abundance in rat oxyntic mucosa.

Gastrin release histamine from the oxyntic mucosa, stimulates the enzymatic activity of histidine decarboxylase (HDC), increases HDC mRNA abundance, and has a trophic effect on the enterochromaffin-like (ECL) cell. In the present study, we examined the effect of exogenous gastrin on HDC activity and mRNA and the time scale of increase and decline of HDC activity and mRNA. Rats received intravenous infusion of gastrin-(1-17) in different doses or periods of time. Oxyntic mucosal HDC activity and mRNA abundance increased significantly with serum gastrin concentrations in the physiological range. The onset of response was rapid and maximal for both parameters after 2 h. Poststimulatory decrease was maximal 2 h after cessation of gastrin infusion. Those observations suggest that HDC enzymatic activity and mRNA abundance are important in meal-to-meal regulation of gastric secretion. Furthermore, HDC enzymatic activity and mRNA abundance varied in parallel, indicating that HDC mRNA abundance is important in the overall regulation of gastric mucosal HDC activity.

Animals↗