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K Svanes

Publications and source records attributed to K Svanes.

At least 37 records · Page 2Linked to original sources
PubMed1997

Glutathione and N-acetylcysteine reduce gastric mucosal blood flow in rats.

Glutathione has been studied as a possible mediator in gastric mucosal protection and healing, but its extracellular function is not fully understood. This study evaluates blood flow changes in normal gastric mucosa secondary to glutathione modulation under stable central hemodynamic conditions. Thiol substances were quantified by reverse-phase ion-pair liquid chromatography and fluorescence detection. Central hemodynamics remained stable when glutathione and N-acetylcysteine were administered in a dose of 0.5 mmol/kg. Higher doses than 0.5 mmol/kg of glutathione and N-acetylcysteine caused unstable hemodynamics. Glutathione (0.5 mmol/kg intravenously) and N-acetylcysteine (0.5 mmol/kg intravenously) reduced corpus mucosal blood flow by 28% and 26% (P < 0.0005), respectively, and glutathione reduced antral mucosa blood flow by 22% (P < 0.01). L-Buthionine-[S,R]-sulfoximine (2 mmol/kg intravenously) did not effect gastric mucosal blood flow. Cysteine content in mucosa and plasma increased while mucosal glutathione levels were largely unchanged after administration of reduced glutathione and N-acetylcysteine. Plasma glutathione only increased after injection of glutathione. L-Buthionine-[S,R]-sulfoximine reduced the glutathione level in both plasma and mucosa. We conclude that glutathione and N-acetylcysteine reduce gastric mucosal blood flow and that the effect may be related to increased cysteine levels in plasma or mucosa.

Acetylcysteine↗
PubMed1997

Smoking and ulcer perforation.

BACKGROUND: The use of ulcerogenic drugs is the only well documented risk factor for peptic ulcer perforation, but accounts for only a quarter of the events. Smoking is a well known risk factor for uncomplicated ulcer disease, and patients with ulcer bleeding have increased death rates from smoking related disorders. AIM: To assess the role of smoking in ulcer perforation. SUBJECTS: A total of 168 consecutive patients with gastroduodenal ulcer perforation and 4469 control subjects from a population based health survey. METHODS: The association between ulcer perforation and smoking habits was analysed by logistic regression while adjusting for age and sex. RESULTS: Current smoking increased the risk for ulcer perforation 10-fold in the age group 15-74 years (OR 9.7, 95% CI 5.9 to 15.8) and there was a highly significant dose-response relationship (p < 0.001). The results were similar in men (OR 9.3, 95% CI 4.9 to 17) and women (OR 11.6, 95% CI 5.3 to 25), and for gastric (OR 10.5, 95% CI 4.5 to 25) and duodenal (OR 8.6, 95% CI 4.9 to 15.4) ulcer perforation. No increase in risk was found in previous smokers (OR 0.8, 95% CI 0.2 to 2.2). CONCLUSION: Our findings suggest that smoking is a causal factor for ulcer perforation and accounts for a major part of ulcer perforations in the population aged less than 75 years.

Adolescent↗
PubMed1996

Survival after peptic ulcer perforation: a time trend analysis.

The survival of 1098 patients with ulcer perforation in Norway during the period 1952-1990 was compared with expected survival. Cox regression models incorporating population mortality rates, were used to analyse effects of sex, age, year of birth, and year at risk on excess mortality. Survival was lower in patients than in the general population through a follow-up period of 38 years. Relative survival was lower in women as compared to men, due to more delayed treatment. Long-term survival was lower after praepyloric perforations than after the other perforation types. Relative survival was higher in patients treated 1952-1970 than in those treated more recently. However, adjustment for year of birth revealed a decline in short-term mortality with calendar time, which is in accordance with improved management during the study period. Relative mortality, particularly long-term mortality, was higher in younger birth cohorts, suggesting a shift towards more serious etiologies.

Cohort Effect↗
PubMed1996

Role of adenosine and nitric oxide in the hyperemic response to superficial and deep gastric mucosal injury and H+ back-diffusion in cats.

BACKGROUND: This study was undertaken to examine the role of adenosine and nitric oxide (NO) in the hyperemic response to H+ back-diffusion into superficially or deeply injured gastric mucosa, and the role of adenosine in mucosa when blood flow was reduced with indomethacin. METHODS: Cat stomachs were exposed to 2 M NaCl for 10 min followed by luminal perfusion at pH 1. Gastric mucosal blood flow was determined by radioactive microspheres, portal vein blood flow by transit-time flowmetry, and H+ back-diffusion/secretion by pH-stat titration, and concentrations of histamine in aortic and portal vein blood were measured. RESULTS: In the antrum pretreatment with the adenosine blocker 8-phenyltheophylline (8-PT) or with NG-methyl-L-arginine (L-NMMA), a specific inhibitor of NO formation, had no effect on the hyperemic response or mucosal injury. However, pretreatment with 8-PT in addition to indomethacin produced extensive deep lesions in the antrum. In the corpus/fundus 8-PT had no effect on the hyperemic response and did not increase indomethacin-induced lesions. L-NMMA significantly reduced the hyperemic response in corpus/fundus. In areas with deep lesions very high blood flow was observed in the vital part of the mucosa below the necrotic tissue. This hyperemia was reduced by L-NMMA but not by 8-PT. Indomethacin increased the release of histamine during base-line conditions, whereas 8-PT reduced histamine release after damage. CONCLUSIONS: This study indicates that usually adenosine is not involved in the hyperemic response to mucosal damage, but it appears to have important protective functions in the antral mucosa under marginal circulatory conditions. NO is one of the mediators of the hyperemic response to mucosal injury in the corpus/fundus.

Adenosine↗
PubMed1995

[Use of growth hormone during catabolic state in a patient in postoperative intensive care].

Patients in the intensive care unit often enter a catabolic state with significant protein loss, which may increase postoperative complications. Nutritional support alone usually does not reverse a catabolic state and thereby induce a positive protein balance. Recent studies suggest that recombinant human growth hormone (rhGH) stimulates protein synthesis and improves protein balance in critically ill patients. An increase in the level of growth hormone often fails to occur in critical illness and injury. We describe the case of a man aged 45 years who underwent laparoscopic fundoplasty for hiatus hernia repair. Because of complications, including perforation of the oesophagus, he entered a sustained catabolic state with negative protein balance and a weight loss approaching 20%. Therefore, on the 29th day after operation we started treatment with rhGH, Norditropin 24 IE/day im. The protein balance became positive three days later. This parameter maintained positive, also after the growth hormone therapy was discontinued 12 days later. The further course was uneventful and the patient was transferred to his local hospital 51 days after the fundoplasty. His condition was improving steadily.

Coma↗
PubMed1995

Incidence of perforated ulcer in western Norway, 1935-1990: cohort- or period-dependent time trends?

Previous reports have shown that peptic ulcer mortality follows birth cohorts. To the authors' knowledge, temporal variation in ulcer incidence has not been studied. Therefore, they present incidence data for a defined area of western Norway where 1,312 patients born between 1845 and 1975 were treated for ulcer perforation between 1935 and 1990. A rise and subsequent fall in incidence was observed in successive birth cohorts for both sexes, with the highest incidence observed for males born between 1900 and 1919 and females born between 1920 and 1929. Age-period-cohort analyses based on Poisson regression techniques were adapted to provide a statistical tool for testing specific cohort and period effects. Age-cohort models without period effects explained the variations in incidence for both sexes and all ulcer locations, suggesting cohort-dependent etiology. A cohort pattern in prevalence of smoking partly explained the cohort pattern in perforation risks for both sexes. No period effects were seen that could be attributed to the increase in the sale of non-steroidal anti-inflammatory drugs, to the introduction of antibiotics around 1950, or to World War II. Susceptibility to ulcer perforation seems to follow birth cohorts, and major etiologic factors should be sought in prenatal life, in childhood, or in life-style patterns that follow birth cohorts.

Adolescent↗
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

Blood flow and mucoid cap protect against penetration of carcinogens into superficially injured gastric mucosa of rats.

In this study we tested the influence of blood flow and the mucoid cap on the penetration of carcinogens to the proliferative cells in the injures rat gastric mucosa. Ten minutes after mucosal exposure to 4.5 mol/liter NaCl, N-[3H]methyl-N'-nitro-N-nitrosoguanidine was instilled intragastrically. Hypertonic saline caused superficial mucosal damage, formation of a mucoid cap, high gastric mucosal blood flow, and a large flux of fluid into the gastric lumen. The mean percentage of S-phase cells labeled with carcinogen (the cell population at risk for N-methyl-N'nitro-N-nitrosoguanidine-induced carcinogenesis) in the antrum and corpus was 0.2 and 0.2, respectively, in the injury control group, 10.1 and 2.0 after removal of the mucoid cap, 1.5 and 9.8 after celiac artery ligation, and 28.2 and 21.9 after removal of the mucoid cap and celiac artery ligation. These results show that both the mucoid cap and gastric mucosal blood flow protect against penetration of carcinogens into the superficially injured gastric mucosa.

Animals↗
PubMed1995

Role of blood flow in protection against penetration of carcinogens into normal and healing rat gastric mucosa.

The effects of intragastric capsaicin and gastric artery ligation on the penetration of the gastric carcinogen N[methyl-3H]-N'-nitro-N-nitrosoguanidine ([3H]MNNG) to proliferative cells were studied in normal and healing rat gastric mucosa. The percentage of S-phase cells labeled with [3H]MNNG in normal corpus mucosa was higher (7.0 +/- 2.0%) after gastric artery ligation than in controls with intact blood flow (2.7 +/- 1.0%) and in animals treated with capsaicin (1.8 +/- 0.5%). Corpus mucosal blood flow was correlated with the percentage of S-phase cells labeled with [3H] MNNG in normal controls and in capsaicin-treated animals. In healing corpus mucosa and in the antrum, capsaicin or gastric artery ligation did not affect carcinogen penetration. We conclude that blood flow protects against penetration of carcinogens to proliferative cells in normal corpus mucosa but not in the antrum. Low mucosal blood flow in the corpus could be a risk factor for initiation of gastric carcinogenesis.

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

Morbidity, ability to swallow, and survival, after oesophagectomy for cancer of the oesophagus and cardia.

OBJECTIVE: To study survival, morbidity, and ability to swallow, after oesophagectomy for cancer of the oesophagus and cardia. DESIGN: Prospective open study. SETTING: University hospital, Norway. SUBJECTS: 83 patients, 38 with squamous cell carcinoma and 45 with adenocarcinoma of the oesophagus and cardia. INTERVENTIONS: Transhiatal (n = 51) and transthoracic (n = 32) oesophagectomy. Oesophageal replacement was by either stomach (n = 80) or colon (n = 3). Cervical anastomosis was used in all but 2. MAIN OUTCOME MEASURES: Early and late morbidity and mortality, length of stay in intensive care unit and in hospital, and survival analysis. RESULTS: 30 Day and in hospital mortality were 0 and 4% for transhiatal, and 6% and 9% for transthoracic, oesophagectomy. Complications included recurrent nerve palsy (n = 7), anastomotic leaks (n = 5), and chylothorax (n = 4). 17 Patients (22%) needed dilatations for stenosis of the anastomosis, and 71 (85%) of the patients left hospital within four weeks of operation. Survival analysis showed a 5 year survival rate of 33% for patients with adenocarcinoma operated on for cure and a 2 year survival of 28% for patients with squamous cell carcinoma. CONCLUSIONS: Oesophagectomy for cure is worthwhile as some patients are cured and most of the remainder have prolonged relief of their dysphagia. Palliative resections should not be done in patients with distant metastases or invasion of adjacent organs by the tumour because of long stay in hospital, appreciable morbidity, and short life expectancy.

Adenocarcinoma↗
PubMed1994

[Gastrointestinal diseases--the place of endoscopy in examination, treatment and control].

Dyspepsia, defined as discomfort in the upper abdomen after a meal, is the most frequent indication for gastroscopy. Such dyspepsia was earlier considered to be an element of the ulcer disease, Moynihan's disease. Whether examination showed an ulcer or not was of minor importance as long as the treatment was the same. Similar opinions still contribute to a negative attitude towards the need to obtain a more specific diagnosis, especially in young patients where risk of cancer is low. We are of the opinion that dyspepsia is a non-specific symptom of several different diseases, and that curative therapy is often available today provided the diagnosis is correct. It is therefore necessary to make an active effort to diagnose the cause of the dyspepsia, also in younger persons. In practice, this means that there are many different indications for gastroscopy. We try, however, to practice a restrictive policy with respect to control gastroscopy.

Cost-Benefit Analysis↗
PubMed1994

Effect of salt on cell proliferation and N-methyl-N'-nitro-N-nitrosoguanidine penetration to proliferative cells in the forestomach of rats.

We have studied the effect of intragastric instillation of 4.5 M NaCl on cell proliferation and carcinogen penetration into the forestomach of Wistar rats at different time intervals after salt exposure. Cells in the S-phase were labelled by incorporation of bromodeoxyuridine and located after immunohistochemistry. N-[3H]Methyl-N'-nitro-N-nitrosoguanidine ([3H]MNNG) was used as the carcinogen and penetration of [3H]MNNG to proliferative cells was determined by autoradiography. The number of cells in S-phase per millimetre epithelium length 12 h and 24 h after salt exposure (32.2 +/- 11.9 and 20.6 +/- 7.4) was significantly higher than in the control animals (9.4 +/- 3.6). No increase in cell proliferation occurred during the first 2 h after salt exposure. Microscopy also revealed oedema in the lamina propia. The forestomach blood flow was not influenced by the application of hypertonic saline. [3H]MNNG at a concentration of 40 micrograms/ml did not penetrate to the proliferative cells in the forestomach and no effect of salt pretreatment on carcinogen penetration was seen. The low penetration of [3H]MNNG to proliferative cells in the forestomach epithelium may explain why this concentration of MNNG given in drinking water over several weeks usually does not induce squamous cell carcinomas in the forestomach. The previously observed cocarcinogenic effect of salt on squamous cell cercinogenesis in the upper gastrointestinal tract could be due to the observed increase in cell proliferation after salt exposure.

Animals↗
PubMed1994

Gastric carcinogenesis in rats given hypertonic salt at different times before a single dose of N-methyl-N'-nitro-N-nitrosoguanidine.

A 1-ml dose of 4.5 M NaCl was given intragastrically to male Wistar rats at 10 min, 1 h, 4 h, 12 h, 24 h or 48 h before a single intragastric dose of 250 mg/kg N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). After 52 weeks the incidence of forestomach squamous cell carcinoma was 21% in control animals receiving MNNG alone. The cancer incidence in the forestomach varied with the time elapsed between application of NaCl and MNNG, and was significantly increased in animals pretreated with NaCl 4 h (43%), 12 h (54%) and 24 h (41%) before MNNG. These results show that salt has a cocarcinogenic effect on initiation of forestomach carcinogenesis in rats, and that this effect depends on the time interval between pretreatment with NaCl and application of MNNG. Gastric adenocarcinomas occurred more frequently in the antrum (78%) than in the corpus (22%). The incidence of gastric adenocarcinoma in animals pretreated with salt before application of MNNG (11%-22%) was not significantly influenced by the time elapsed between pretreatment with salt and application of MNNG, and did not differ from animals receiving MNNG alone (18%). The lack of a cocarcinogenic effect of NaCl on glandular gastric carcinogenesis might be due to the use of dimethyl/sulfoxide as solvent for MNNG.

Adenocarcinoma↗
PubMed1994

Role of bicarbonate in blood flow-mediated protection and repair of damaged gastric mucosa in the cat.

BACKGROUND/AIMS: The hyperemic response after superficial gastric mucosal damage is essential for repair of the mucosa. Only indirect evidence suggests that this is caused by supply of bicarbonate. Therefore, this study tested the effect of maintaining the availability of bicarbonate after prevention of the hyperemic response after damage by 2 mol/L NaCl. METHODS: Celiac artery flow was reduced, as monitored by Doppler ultrasonography, by gradual constriction of the vessel after mucosal damage. Saline (pH 1.0) was perfused through the stomach lumen and thereafter through a closed chamber with pH and PCO2 electrodes. RESULTS: Exposure to 2 mol/L NaCl produced a marked increase of mucosal blood flow as measured by microspheres (P < 0.025) and a high degree of mucosal restitution 90 minutes after damage as judged by microscopy, whereas prevention of the hyperemic response caused extensive erosions and much less restitution (P < 0.001). The latter effect was completely counteracted by intravenous bicarbonate. High blood concentration of bicarbonate increased luminal release of bicarbonate, whereas high mucosal blood flow did not. CONCLUSIONS: These data show that bicarbonate is an important factor in blood flow-mediated protection and repair of damaged gastric mucosa and suggest that concentration gradients are the major determinants for transport of bicarbonate across the damaged and restituted mucosa.

Animals↗
PubMed1994

Effect of salt-induced mucosal damage and healing on penetration of N-methyl-N'-nitro-N-nitrosoguanidine to proliferative cells in the gastric mucosa of rats.

We have studied the effect of gastric exposure to 4.5 M NaCl on penetration of a carcinogen, N-[3H]methyl-N'-nitro-N-nitrosoguanidine (3H-MNNG) from the gastric lumen to proliferative cells in the gastric mucosa of Wistar rats at different time intervals after salt exposure. Cells in S-phase were labeled by incorporation of bromodeoxyuridine. Cells in S-phase labeled with 3H-MNNG (double-labeled cells) are the cell population at risk of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced gastric carcinogenesis. Ten minutes after salt damage the average percentage S-phase cells labeled with 3H-MNNG in pylorus was significantly decreased compared to control (1.2 +/- 0.6 and 9.5 +/- 0.7). Ten minutes after salt exposure a marked increase in gastric mucosal blood flow and leakage of fluid from the mucosa into the gastric lumen were observed, and the damaged gastric mucosa was covered by a thick mucoid layer. These factors may contribute to the reduced 3H-MNNG penetration into mucosa immediately after damage. Two hours after salt exposure the number of double-labeled cells (8.6 +/- 3.7/mm) and percentage S-phase cells labeled with 3H-MNNG (10.4 +/- 3.1) in pylorus did not differ from control (6.1 +/- 0.9/mm and 9.5 +/- 0.7). Twelve and 24 h after salt exposure the number of double-labeled cells (79.6 +/- 13.4/mm and 32.4 +/- 2.4/mm) and the percentage S-phase cells labeled with 3H-MNNG (29.7 +/- 2.8 and 18.9 +/- 1.3) in pylorus were significantly increased compared to control. Increased number of S-phase cells, a higher location of the proliferative zone in the glandular layer were observed 12-24 h after salt exposure and increased permeability of the mucosa to carcinogen was observed 12 h after salt exposure. These factors explain the increased number of double-labeled cells and the increased penetration of carcinogens to the proliferative cells, and may contribute to explain the previously described cocarcinogenic effect of salt on gastric carcinogenesis.

Animals↗
PubMed1994

Adverse effects of delayed treatment for perforated peptic ulcer.

OBJECTIVE: The authors assessed the consequences of delayed treatment for ulcer perforation with regard to short-term and long-term survival, complication rates, and length of hospital stay. SUMMARY BACKGROUND DATA: Important adverse effects of delayed treatment have not been studied previously. Conflicting results have been given with regard to short-term survival. METHODS: One thousand two hundred ninety-two patients operated on for perforated peptic ulcer in the Bergen area between 1935 and 1990 were studied. The effect of delay on postoperative lethality and complications adjusted for age, sex, ulcer site, and year of perforation was analyzed by stepwise logistic regression. The effect of delay on duration of hospital stay adjusted for potential confounding factors was analyzed by Cox proportional hazards regression. Observed survival was estimated by the Kaplan-Meier method, and expected survival was calculated from population mortality data. RESULTS: Adverse effects increased markedly when delay exceeded 12 hours. Delay of more than 24 hours increased lethality sevenfold to eightfold, complication rate to threefold, and length of hospital stay to twofold, compared with delay of 6 hours or less. The reduced long-term survival for patients treated more than 12 hours after perforation could be attributed entirely to high postoperative mortality. CONCLUSIONS: Delayed treatment after peptic ulcer perforation reduced survival, increased complication rates, and caused prolonged hospital stay. To improve outcome after ulcer perforation, an effort should be made to keep delay at less 12 hours, particularly in elderly patients.

Age Factors↗