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Biomedical subjects

K Svanes

Publications and source records attributed to K Svanes.

At least 55 records · Page 3Linked to original sources

Gastric mucosal repair and release of HCO3- after damage by 2 M NaCl in cat: role of systemic acid base status.

To study the influence of acid base balance on gastric mucosal repair, NH4Cl or NaHCO3 was given intravenously to anesthetized cats after mucosal damage induced by intraluminal 2 M NaCl. Saline at pH 5 or 1 was perfused via an oral tube through the stomach lumen and evacuated via a pyloric tube to a chamber with pH and PCO2 electrodes. Luminal bicarbonate (HCO3-) was markedly increased early after damage in both acidotic and alkalotic animals. In alkalotic animals mucosal blood flow increased about twofold in response to mucosal damage, whereas the early hyperemic response was either completely attenuated or blunted in acidotic animals. HCO3- release was correlated to availability of HCO3- by blood in alkalotic animals with luminal pH 5. Alkalotic animals showed improved repair compared with acidotic animals, and mucosal restitution was correlated to availability of HCO3- by blood. We conclude that luminal leakage of HCO3- or plasma after mucosal damage depends on availability by blood and consumption of HCO3- within the mucosa and that blood borne HCO3- has a major influence on gastric mucosal repair.

Acid-Base Equilibrium↗

Role of histamine in regulation of blood flow in the injured gastric mucosa of the cat.

Superficial mucosal damage caused by a mild irritant (2 M NaCl) results in release of histamine and probably prostaglandins giving increased GMBF. This hyperemic response contributes to protect the mucosa during the early phase of repair after damage by supplying the mucosa with bicarbonate and by eliminating back diffusing acid and other toxic substances such as ethanol. We conclude that histamine plays an important role in the blood flow regulation in the stomach.

Animals↗

Prognostic importance of radical lymphadenectomy in curative resections for gastric cancer.

OBJECTIVE: To evaluate the effect of extensive lymphadenectomy on survival in patients with gastric cancer. DESIGN: Retrospective analysis SETTING: University Hospital, Norway. SUBJECTS: 183 patients with stomach cancer resected for cure during the time period 1980-90. INTERVENTIONS: 78 patients had an R1- and 105 patients and R2 resection. 124 patients were treated by total gastrectomy, 5 by proximal--and 54 by distal resection. MAIN OUTCOME MEASURES: Morbidity, mortality and long term survival. RESULTS: The morbidity was 33% (60/183), of which 39 (21%) were general complications (pneumonia, thrombosis, or cardiovascular disease). 14 patients died postoperatively (8%). By logistic regression analysis we found that splenectomy was the only variable associated with both morbidity and immediate postoperative mortality. Five year survival was 39% for patients who had undergone curative resections, 30% for patients who had had an R1 resection, and 47% for those who had had an R2 resection. By multivariate analysis (Cox) we found that N-classification (TNM), tumour diameter of less than 45 mm, type of lymph node dissection (R2) and operation period (after 1984) correlated with improved survival. CONCLUSION: Extensive lymph node dissection improves survival without increasing morbidity or postoperative mortality.

Adult↗

Gastric mucosal injury and associated changes in mucosal blood flow and gastric fluid secretion caused by dimethyl sulfoxide (DMSO) in rats.

Dimethyl sulfoxide applied intragastrically for 10 min in rats caused extensive mucosal damage. In concentrations of 5%, 10%, or 100%, dimethyl sulfoxide caused superficial damage to 33%, 36%, and 97%, respectively, of the corpus mucosa, and 28%, 44%, and 96%, respectively, of the antral mucosa. Concentrated dimethyl sulfoxide also caused damage to the pits and glands in some areas of the mucosa. The amount of fluid in the stomach increased by 0.24 ml, 0.48 ml, and 2.07 ml during application of 5%, 10%, and 100% dimethyl sulfoxide. The 10% dimethyl sulfoxide increased mucosal blood flow by 0.57 ml/min/g in the antrum, and 100% dimethyl sulfoxide increased mucosal blood flow by 2.21 ml/min/g in the antrum and by 1.17 ml/min/g in the corpus. We conclude that dimethyl sulfoxide is a gastric irritant, which should be considered when it is used as an oxygen radical scavenger, as a drug or carcinogen vehicle, or as oral medication in patients. The protective effect of intragastric dimethyl sulfoxide against stress and various drug-induced gastric injury may be due to "adaptive cytoprotection" rather than an oxyradical scavenger effect.

Analysis of Variance↗

Release of bicarbonate from damaged and restituted gastric mucosa in the cat.

BACKGROUND: Gastric mucosal damage leads to luminal alkalinization, but its dependence on mucosal blood flow and acid secretory state of the mucosa is not known. This study examined release of bicarbonate to the gastric lumen and mucosal blood flow in cats after mucosal damage caused by 2 mol/L NaCl and during 90 minutes of epithelial restitution. METHODS: Bicarbonate was calculated from measurements of pH and PCO2 in the luminal perfusate. Mucosal blood flow was measured with microspheres. RESULTS: Luminal bicarbonate increased more than twofold after damage in pharmacologically nontreated, pentagastrin-treated, and omeprazole-treated animals (P < 0.001). Luminal bicarbonate thereafter decreased completely to pre-damage level in pentagastrin-treated, partly in nontreated, but remained elevated in omeprazole-treated animals. Mucosal blood flow increased about 100% 15 minutes after damage (P < 0.001), irrespective of secretory state. Bicarbonate availability (arterial [HCO(3-)] x mucosal blood flow) was significantly related to luminal release of bicarbonate from the newly damaged (P < 0.01) but not from the restituted mucosa. CONCLUSIONS: (1) From the newly damaged mucosa, the luminal release of bicarbonate is related to availability of blood-borne bicarbonate. (2) From acid-stimulated restituted mucosa, the bicarbonate produced by the parietal cells is not released to the lumen, but either consumed within the mucosa by back-diffusing H+ or distributed to the systemic circulation.

Animals↗

Penetration of N-methyl-N'-nitro-N-nitrosoguanidine to proliferative cells in gastric mucosa of rats is different in pylorus and fundus and depends on exposure time and solvent.

We have studied the penetration of a labeled gastric carcinogen, N-(3H)methyl-N'-nitro-N-nitrosoguanidine (3H-MNNG), from the gastric lumen to proliferative cells in the gastric mucosa of Wistar rats. 3H-MNNG was dissolved in deionized water or dimethyl sulfoxide (DMSO) and given intragastrically through a tube in the forestomach. Cells in the S-phase were labeled by incorporation of bromodeoxy-uridine. Penetration of the carcinogen was evaluated by light microscopy after immunohistochemistry and autoradiography. Cells in S-phase labeled with 3H-MNNG (double-labeled cells) are considered to represent the cell population at risk of MNNG-induced carcinogenesis. When deionized water was used as solvent for the carcinogen, the average percentage of double-labeled cells in the pylorus was 12.0, 22.4 and 32.5 respectively, after 10, 30 and 60 min of mucosal exposure to 3H-MNNG. The corresponding percentages for the fundus mucosa were 1.7, 3.1 and 3.4, which are significantly lower than the pylorus values. When DMSO was used as solvent for the carcinogen, the percentage of double-labeled cells was 0.3 and 1.1 in the pylorus and 0.1 and 1.3 in the fundus after 10 and 30 min exposure to 3H-MNNG. Dimethyl sulfoxide caused superficial mucosal damage to the gastric mucosa and increased secretion of fluid into the stomach. Our results strongly suggest that gastric cancer develops in the pylorus because the carcinogen penetrates more easily into pyloric than fundic mucosa. The results support the view that delayed gastric emptying is a risk factor in gastric carcinogenesis, and show that DMSO counteracts the penetration of MNNG into the mucosa.

Animals↗

Perforated peptic ulcer over 56 years. Time trends in patients and disease characteristics.

Perforated gastroduodenal ulcer was studied in 1483 patients in the Bergen area during the years 1935-90 to discover time trends in age and sex, disease characteristics, treatment, and outcome. The male:female ratio fell from 10:1 to 1.5:1, median age increased from 41 to 62 years. Most perforations were found in the duodenum in 1935-64, and in the pyloric and praepyloric area in 1965-90. There was a 10% occurrence of gastric ulcers throughout the study period. Ulcer site was related to age (more gastric and less duodenal perforations with increasing age) and sex (more pyloric and less duodenal ulcers among women). There were twice as many perforations in the evening compared with the early morning. The diurnal variation was more pronounced for duodenal and pyloric than for gastric and praepyloric perforations. Circadian and seasonal variation of ulcer perforation did not change during the 56 years studied. Treatment delay increased from median five hours to median nine hours. Infective complications and mortality fell with the introduction of antibiotics around 1950. General complications has increased in recent years because of the increase of elderly patients. Among patients who died, the proportion with associated disease rose from 27 to 85% during the study period.

Adult↗

Adaptive protection related to clearance of ethanol in gastric mucosa of cats.

This study was designed to test the hypothesis that hyperemia after exposure to 2 M NaCl protects the gastric mucosa against damage caused by absolute ethanol by removing ethanol diffusing from the gastric lumen into the mucosa. The stomach of anesthetized cats was perfused with saline at pH 1.0. Gastric mucosal blood flow was determined by radioactive microspheres, and portal vein blood flow was measured by Doppler ultrasound flowmetry. The concentration of ethanol in the corpus mucosa and the amount of ethanol transported away from the stomach in portal blood were measured by using absolute ethanol containing trace amounts of 14C-labeled ethanol. Pretreatment with 2 M NaCl for 10 min increased mucosal blood flow and prevented the development of deep mucosal lesions after subsequent application of absolute ethanol. An inverse correlation was found between mucosal blood flow and the degree of ethanol-induced damage. The mucosal content of ethanol was low in animals pretreated with hyperosmolar NaCl, and the degree of mucosal damage was related to the tissue concentration of ethanol. The amount of ethanol transported by blood from the stomach increased with increasing mucosal blood flow. We conclude that the mild irritant, 2 M NaCl, increases mucosal blood flow, which protects the mucosa by removing ethanol diffusing from the lumen. Thus, the mucosal ethanol concentration remains below a level that causes damage.

Animals↗

Tissue reaction to polypropylene mesh: a study of oedema, blood flow, and inflammation in the abdominal wall.

The purpose of the present work was to study the tissue reaction to polypropylene mesh (Marlex) implanted in three different layers of the abdominal wall, comparable to common clinical practices. The reaction to mesh was compared in terms of tissue oedema, blood flow, and histological appearance in rats. When mesh was placed between muscle layers, blood flow in the abdominal wall was high during the first 4 days after implantation but similar to flow in nonoperated rats 14 and 140 days after implantation. When mesh was placed under skin or on the peritoneum, there was no hyperaemia early after implantation, and flow rate was clearly lower than in non-operated controls 140 days after implantation. The operative procedure produced increased tissue water content, declining from the 1st to the 14th day after operation. Mesh induced additional oedema in adjacent muscle tissue irrespective of localization of the implant (p less than 0.01, vs. sham). Except when separated by peritoneum, mesh caused hyperaemia in muscle tissue in direct contact with mesh the 1st and the 4th day after implantation. After 14 and 140 days no mesh-induced hyperaemia was present. The inflammatory response to mesh was similar in the peritoneum and between muscles, less pronounced in the subcutis. It was characterized by the accumulation of macrophages and the formation of inflammatory granulation tissue in the subacute phase, later followed by the formation of fibrous tissue around mesh fibres. This study suggests that mesh implants should be placed in apposition to muscles in order to obtain well-vascularized healing.

Abdominal Muscles↗

The Effect of Gastric Banding on Weight Loss in Patients with Morbid Obesity.

The results following operation for morbid obesity in 41 patients (8 men and 33 women) during the period 1983-1989 are reported. The median preoperative body mass index (BMI) was 43.6 (median excess weight 81%). All patients were preoperatively evaluated at the Department of Internal Medicine, and they had all tried several conservative regimens in order to lose weight. They were all operated on with gastric banding, creating a gastric stoma of 15 mm. Pneumonia developed in 10 patients, one patient got a wound infection, and one patient died postoperatively from a massive coronary embolism. The immediate postoperative weight loss was satisfactory, median BMI being reduced from 43.6 preoperative to 30.5 after 9 months. Median BMI after 3 and 5 years was 34 and 32 (median excess weight 42 and 41%, respectively). Six patients were reoperated, four having their band removed, two being converted to vertical gastric banding. In conclusion, gastric banding gives satisfactory results for most of the patients. The reoperation rate is, however, high and the long-term result is not favorable for all patients

Journal Article↗

Gastric bicarbonate secretion, acid secretion, and mucosal blood flow during influence of pentagastrin and omeprazole in the cat.

In this study secretion of bicarbonate and acid and mucosal blood flow were determined simultaneously in cats. The gastric lumen of anesthetized cats was continuously perfused with isotonic saline. Secretion of HCO-3 and H+ was calculated from continuous measurements of pH and PCO2 in the perfusate. Mucosal blood was measured by means of radiolabeled microspheres. Under resting acid secretory conditions, bicarbonate secretion into the gastric lumen averaged 1.0 mumol/min. Somewhat surprising, both omeprazole (4 mg/kg as bolus) and pentagastrin (16 micrograms/kg.h intravenously) significantly reduced the HCO-3 secretion. Omeprazole did not influence mucosal blood flow, whereas corpus mucosal blood flow increased during pentagastrin stimulation. Under resting acid secretory conditions and during omeprazole treatment there was a close linear relationship between acid and bicarbonate secretion. No such relationship was found during pentagastrin stimulation of the mucosa. No consistent relationship was obtained between blood flow and bicarbonate secretion in normal gastric mucosa.

Animals↗

Ischaemic necrosis of lesser curve of stomach after proximal gastric vagotomy.

Of 483 patients treated by proximal gastric vagotomy (PGV) between 1972 and 1986 four (0.8%) developed lesser curve necrosis with perforation and one died of diffuse peritonitis. Gastroscopy 3-6 days after PGV in 26 patients between November 1985 and May 1987 showed that five had developed ischemic ulcers on the lesser curve (19%). One further patient developed lesser curve necrosis with perforation before endoscopy, giving a total of six lesser curve lesions after 26 vagotomies (23%). Endoscopy also showed that most patients had some gastric retention. Ulcers with maximal diameters of 0.4-2 cm were asymptomatic. One patient with a large ischaemic ulcer (3 cm) had an abrupt fall in haemoglobin concentration (from 148 to 73 g/l) as did two patients who developed lesser curve necrosis with perforation and peritonitis (143 to 93, and 159 to 71, respectively). We conclude that ischemic ulcers are relatively common after PGV, that small ulcers are asymptomatic and do not perforate, and that an upper GI bleeding after PGV strongly suggests that lesser curve necrosis has developed.

Aged↗

Role of blood flow in adaptive protection of the cat gastric mucosa.

This study was designed to test the hypothesis that adaptive cytoprotection is related to increased blood flow caused by mild irritants. The stomach of cats was perfused with saline at pH 1.0. Mucosal blood flow was determined by radioactive microspheres, and celiac artery blood flow was measured by Doppler ultrasound. Gastric blood flow was left undisturbed or reduced by tightening a vessel loop around the celiac artery. Mucosal exposure to absolute ethanol for 2 minutes caused extensive damage to the surface epithelium, the pits, and the upper half of the glands. Pretreatment of the mucosa with 2 mol/L NaCl for 10 minutes prevented the development of mucosal lesions after subsequent application of absolute ethanol. The mucosal blood flow increased markedly after treatment with 2 mol/L NaCl. When this hyperemic response was inhibited by reducing celiac artery blood flow, ethanol caused lesions of similar degree as in animals not pretreated with 2 mol/L NaCl. A highly significant correlation was obtained between mucosal blood flow, as determined just before the application of ethanol, and the degree of ethanol-induced damage. At a chosen level of blood flow, ethanol caused the same degree of damage with or without pretreatment with 2 mol/L NaCl. In conclusion, high mucosal blood flow caused by a mild irritant is an important factor in adaptive gastric protection. With the present experimental setup, the protection could be fully explained as a result of the hyperemic response caused by 2 mol/L NaCl.

Analysis of Variance↗

Proximal gastric vagotomy for peptic ulcer disease: follow-up of 483 patients for 3 to 14 years.

During the years 1972 to 1986, proximal gastric vagotomy was performed in 483 patients for management of duodenal, pyloric, or prepyloric ulcers. In 25 patients a drainage procedure was added because of pyloric stenosis. The operations were performed by 64 surgeons, most of whom were junior residents. After surgery four patients had lesser curve necrosis; one of the patients died. The 14-year cumulative ulcer recurrence rate was similar (about 13%) in patients treated for duodenal and pyloric/prepyloric ulcers. The cumulative recurrence rate was significantly higher in women (17%) than in men (12%). Twenty-three percent of female patients and 16% of male patients were considered Visick grade 4. Moderate dumping occurred in 29% and diarrhea in 7% of the patients. The diarrhea was moderate except in one patient who had disabling diarrhea. Women had more frequent nausea, epigastric fullness after meals, and food intolerance than men. Basal acid output, pentagastrin-stimulated peak acid output, and insulin-stimulated peak acid output were not found to be reliable tests for evaluating the completeness of vagotomy or predicting ulcer recurrence.

Duodenal Ulcer↗

Acute erosions of the gastric mucosa in burned rats: effect of gastric acidity and fluid replacement.

Early changes in the morphology of the gastric mucosa after the skin had been burned were studied using a standardised model in rats. A full thickness burn was inflicted by exposing about 20% of the total body surface area to hot water (99 degrees C) for 10 s. Intragastric acidity was kept at pH 1.0 or pH 7.4 in six experimental groups of eight rats. Rats were subjected to burns with the stomach irrigated at pH 1.0 or pH 7.4. Parallel groups received fluid replacement with a solution of human albumin, and two uninjured groups served as controls. Lesions of the gastric mucosa were measured by planimetry of photographs, and light microscopy was used for histological examination. At an intragastric pH of 1.0, the burned rats developed mucosal erosions covering an average of 13% of the total glandular mucosa; the remaining groups had only minimal mucosal lesions. Erosions of the gastric mucosa after the skin had been burned could be prevented in two ways--either by establishing an alkaline (pH 7.4) milieu in the gastric lumen, or by replacing sufficient fluid to maintain aortic blood pressure at the pre-experiment level. Fluid replacement prevented mucosal erosions even if the intragastric pH was kept at 1.0. Thus both luminal acidity and local tissue blood flow are possible mechanisms for gastric epithelial damage following burns of the skin.

Acute Disease↗

Trends in and value and consequences of radiologic imaging of perforated gastroduodenal ulcer. A 50-year experience.

The trends in and value and consequences of radiologic imaging in 1128 patients with perforated gastroduodenal ulcer have been studied over the 50-year period 1935-1985. The proportion of patients undergoing plain X-ray studies increased from 4% in the first 5-year period (1935-1939) to 94% in the last (1980-1985). Pneumoperitoneum was found in 77% of those undergoing X-ray studies. Water-soluble contrast studies were introduced in 1960, and in the three 5-year periods 1970-1985 from 8% to 13% underwent such imaging. Leakage was demonstrated in 60% of those undergoing contrast studies. Contrast studies have had a limited role in the pretreatment evaluation of these patients. The frequency of pneumoperitoneum was fairly constant over the 50-year period, and the only patient characteristic that influenced the occurrence of free gas in the abdominal cavity was age, with a higher proportion of patients with pneumoperitoneum in old patients. Any radiologic study increased treatment delay by at least 2 h.

Adult↗

Restituted gastric mucosa: tolerance against low luminal pH and restricted mucosal blood flow in the cat.

This study examined the tolerance of gastric surface epithelium allowed to restitute for 90 min after damage produced by mucosal exposure to 2 M NaCl for 10 min. Cats were subjected to gastric luminal perfusion with saline at pH = 1.0 and reduction of celiac artery blood flow for 90 min. A flow reduction of 55%, as assessed by Doppler ultrasound flowmetry, was obtained by constriction of the celiac artery. These interventions alone did not produce lesions in nondamaged control cats, whereas exposure to 2 M NaCl immediately before flow reduction evoked extensive erosions as judged by gross examination and microscopy. Stomachs exposed to 2 M NaCl 90 min before flow reduction showed lesions that were clearly less in extent and number than in animals in which an intervening restitution period was not allowed. Topical dimethyl-prostaglandin E2 (50 micrograms/kg) increased the rate by which restituted surface cells were transformed to apparently normal cells. This study shows that the restituted gastric mucosa possesses a remarkably high tolerance against lowered blood flow in the presence of high luminal acidity.

16,16-Dimethylprostaglandin E2↗

Acute gastric mucosal lesions, haemodynamic and microcirculatory changes in the thermally injured rat.

Early postburn changes in central haemodynamics, organ blood flow distribution and morphology of the gastric mucosa were studied using a standarized thermal skin injury model. Organ blood flow and cardiac output were determined using radioactive microspheres. In the control animals no marked changes in cardiac output or organ blood flow were observed, and the gastric mucosa remained essentially undamaged. After burn injury and no fluid resuscitation, cardiac output decreased by 78 per cent, and blood flow to the stomach, pancreas, spleen, muscle, skin and kidneys also decreased markedly and to about the same degree as the cardiac output, however the adrenal flow remained roughly unchanged at the baseline level. Gross and microscopic lesions developed in the stomach, especially in the corpus. In animals given fluid resuscitation after burn injury cardiac output decreased by 38 per cent during the experiment, but blood flow in the stomach, brain, kidneys and spleen remained fairly constant, while pancreatic and muscle blood flow decreased and adrenal blood flow increased markedly. The gastric mucosa showed only minor microscopic, but no macroscopic lesions at the end of the experiment. The results indicate that acute thermal skin injury induces profound changes in central haemodynamics and organ blood flow which can, however, largely be overcome by adequate fluid resuscitation. The data also suggest that, as in other examples of 'stress ulceration', impaired mucosal blood flow may underlie the stress ulceration which complicates severe burns.

Acute Disease↗