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Biomedical subjects

K Svanes

Publications and source records attributed to K Svanes.

At least 73 records · Page 4Linked to original sources
PubMed1989

A multifactorial analysis of factors related to lethality after treatment of perforated gastroduodenal ulcer. 1935-1985.

One thousand one hundred and twenty-eight patients treated for perforated gastroduodenal ulcer during the years 1935-1985 were studied at the Haukeland University Hospital. The majority of patients (97.7%) were treated surgically. The data was analyzed by contingency tables and chi square testing, and a stepwise logistic regression analysis was performed in order to reveal interactions between variables and to elucidate time trends in lethality rates. The total postperforation lethality was 7.4%, the postsurgical death rate was 6.6%, and the death rate among conservatively treated patients was 42.3%. Lethality was significantly influenced by year of hospital admission and increased markedly with the age of the patients. For all age groups, the lethality decreased markedly with time. Treatment delay was associated with a moderate but significant increase in lethality. In patients with gastric ulcer the lethality was 3.6 times higher than in those with duodenal ulcer. The death rate was similar in the duodenal and pyloric ulcer groups. Death rate decreased with time in both stomach ulcer, duodenal, and pyloric ulcer patients. There was no sex difference and no difference between patients treated with simple suture or gastric resection.

Duodenal Ulcer↗
PubMed1988

Epithelial restitution and cellular proliferation after gastric mucosal damage caused by hypertonic NaCl in rats.

Hypertonic NaCl enhances gastric cancer in rats induced by N-nitroso compounds. This study was designed to examine the structural changes and alterations in mitotic activity occurring after mucosal exposure to hypertonic NaCl. Wistar rats were given one ml of 4.5 M NaCl by gastric tube and groups of 4-5 animals were sacrificed at different time intervals up to 120 h. An i.p. injection of thymidine was given 1 h before death. Samples of antral and corpus mucosa were prepared for microscopy and autoradiography. Hypertonic NaCl caused uniform destruction of surface mucous cells and pits in the corpus and antrum. Epithelial restitution with the formation of a thin epithelial layer occurred within one h of damage. The mucosa changed towards normal within 24-48 h. The distance between mucosal surface and the replicating cells decreased during the first 2 h. The proliferation zone remained in the middle of the glandular layer throughout the experiment. The proliferative activity increased during the first 24 h after mucosal damage. The number of labelled cells per unit area of mucosa was somewhat larger in the corpus than the antrum, but in the corpus the distance between proliferating cells and mucosal surface was double that of the antrum. Hypertonic NaCl causes a series of changes in the gastric mucosa. The increased mitotic activity can only partly explain the cocarcinogenic effect, since N-nitroso-induced adenocarcinomas occur predominantly in the antrum while the mitotic activity is maximal in the corpus.

Analysis of Variance↗
PubMed1988

Gastric mucosal repair in the cat: role of the hyperemic response to mucosal damage.

This study concerns the significance for the mucosal repair process of the gastric mucosal hyperemic response after mucosal damage caused by 2 M NaCl. Celiac artery blood flow was measured by Doppler ultrasound and stomach arterial inflow was either left undisturbed or reduced in a controllable fashion by tightening a vessel loop around the celiac artery immediately after mucosal exposure to 2 M NaCl or 150 mM NaCl. The stomach lumen was perfused with saline at pH 1.00 before and after exposure to 2 M NaCl. Gastric mucosal blood flow increased after exposure to 2 M NaCl, and 90 min after mucosal exposure to 2 M NaCl the mucosal surface showed nearly complete restitution of the surface epithelium. In all animals in which mucosal hyperemia was restricted by reducing celiac artery blood flow by 60% after mucosal damage, extensive gastric erosions were present. Similar reduction of celiac artery blood flow in control animals without mucosal damage did not produce visible lesions, and the stomachs proved to be normal by microscopy. These findings show that the gastric mucosal hyperemic response after damage is important for protection of the damaged mucosa during restitution of the gastric surface epithelium.

Animals↗
PubMed1987

Gastric epithelial restitution at low luminal pH during influence of pentagastrin or cimetidine in the cat.

This study examines restitution of the gastric surface epithelium at luminal pH 1 after damage to the gastric mucosa by instillation of 2 M NaCl for 10 min. After mucosal damage, potential difference decreased to zero and H+ back-diffusion increased. Gastric blood flow increased after exposure to 2 M NaCl, irrespective of the secretory state of mucosa. Neither pentagastrin nor cimetidine showed any protective effect against mucosal damage produced by 2 M NaCl. Ninety minutes after mucosal exposure to 2 M NaCl there was an almost complete restitution of the gastric surface epithelium in pentagastrin-stimulated and cimetidine-treated animals, whereas about 15% of the gastric surface still showed damage in animals in which acid secretion was not interfered with. These findings show that restitution of the surface epithelium, in vivo, is a rapid and resistant process even at a very low luminal pH. The secretory state of mucosa may have some influence on this process.

Animals↗
PubMed1987

Regional blood flow and acid secretion associated with damage and restitution of the gastric surface epithelium in cats.

The gastric mucosa of anesthetized cats was exposed to 2 M NaCl for 10 min. After returning to gastric perfusion with 150 mM NaCl and pH 7.40, with and without pentagastrin stimulation, transmucosal potential difference decreased to zero and then gradually increased to approximately half the original value during the following 90 min. H+ secretion decreased and remained close to zero after exposure to 2 M NaCl in nonstimulated cats, whereas pentagastrin-stimulated secretion gradually increased to nearly half the preexposure level. Mucosal blood flow increased, and the vascular resistance decreased in the posterior wall of the stomach corresponding to epithelial damage, as observed by light microscopy after 15 min. Blood flow during pentagastrin stimulation was initially high in fundus and corpus and did not increase further after exposure to 2 M NaCl, but showed similar changes as without pentagastrin in the antrum. Epithelial restitution occurred within 90 min during both nonstimulated conditions and pentagastrin stimulation. In control animals subjected to 150 mM NaCl there were no changes in transmucosal potential difference, H+ secretion, or blood flow throughout the experiment and epithelial damage was not found. In conclusion, damage caused by 2 M NaCl to the gastric surface epithelium was associated with decreased acid secretion and increased mucosal blood flow. These factors may contribute to creating favorable conditions for the epithelial restitution, indicated by restoration of transmucosal potential difference and observed by light microscopy.

Animals↗
PubMed1986

Microsphere method in measurement of blood flow to wall layers of small intestine.

Microspheres of 10.90 +/- 0.65 micron (SD) were injected in the superior mesenteric artery of cats and their intramural distribution and diameter in the small intestine were studied microscopically under basal conditions and after vasodilation by isoproterenol. Approximately 2% of the spheres were shunted through the small intestinal vasculature and could be recovered in the liver. Analysis of the tissue distribution suggested that all spheres arrested in villi represented villous blood flow, spheres arrested in the crypt layer represented flow to the crypts, and the majority of microspheres trapped in the submucosa also represented crypt flow. Nutritive blood flow to the submucosa constituted only 1.5% of total intestinal flow. Log-linear analyses identified factors responsible for sphere distribution, including effects of sphere size, isoproterenol treatment, and local blood flow or vascular resistance. Spheres with diameters greater than 11.08 micron had 1.35 times larger odds than smaller spheres to embolize in the muscularis rather than in the mucosa, but no consistent difference between diameter profiles in the crypts and villi was found. With this reservation, 11-micron spheres seem to be appropriate for measuring blood flow to the muscle, crypt, and villous layers of the small intestine.

Animals↗
PubMed1984

Gastric blood flow determination: intramural distribution and arteriovenous shunting of microspheres.

Total and regional gastric blood flows were measured in 23 anesthetized cats by labeled 10-micron (range 8-12 microns) and 15-micron (range 12-20 microns) microspheres. Total blood flow correlated closely with the gastric venous outflow. Flow estimates by 10-microns spheres were 2.95% lower than simultaneous 15-micron estimates. Approximately 2% of the 10-micron spheres and 0.1% of the 15-micron spheres were shunted through the gastric vasculature. The diameter distribution of 6,245 embolized spheres, measured by microscopy, corresponded to that of the injectate, except for a lack of the smallest spheres. Within the mucosa, the 10-microns spheres predominantly lodged in the glandular layer, whereas larger spheres gradually lodged more basally; 50% of the 15-microns population appeared in the lamina propria below the gland bases. Vasodilation did not alter the intramucosal distribution. Spheres in the subglandular lamina propria represented blood flow mainly to the glandular layer. It is therefore essential for reliable estimation of blood flow to the glandular layer of the mucosa that the lamina propria is completely included in the specimens. The submucosa contained only 0.5% of the 10-microns and 2.2% of the 15-micron embolized spheres. Spheres of 10.5-17 microns in diameter are considered the most suitable for determination of gastric blood flow.

Animals↗
PubMed1983

Regional gastric blood flow and acid secretion during histamine H2 receptor blockade in cats.

Experiments were performed in anesthetized cats. Tissue blood flow and cardiac output were measured by means of labeled microspheres. Cimetidine did not affect gastric blood flow at basal conditions. Pentagastrin stimulation more than doubled corpus-fundus mucosal blood flow (MBF). Cimetidine reduced pentagastrin-stimulated corpus-fundus MBF and acid output towards basal level. Recovery of acid secretion after inhibition by a bolus dose of cimetidine occurred without a corresponding restoration of MBF. Neither pentagastrin nor cimetidine significantly altered antrum MBF or muscularis blood flow. The study demonstrates that cimetidine reduces the ratio between pentagastrin-stimulated acid secretion and corpus-fundus MBF by lowering secretion considerably more than the corresponding MBF.

Animals↗
PubMed1983

Effect of luminal pH and nutrient bicarbonate concentration on restitution after gastric surface cell injury.

Frog fundic mucosas whose surface layers were severely injured by exposure to 1 M NaCl for 10 minutes in an Ussing chamber uniformly recovered both physiologically and anatomically within 4 to 6 hours. The purpose of the present study was to examine the effects of luminal H+ and nutrient HCO-3 concentrations on this process of reconstitution. With 18 mM HCO-3, return of the transmucosal potential difference, tissue electrical resistance, and short-circuit current toward normal and anatomic recovery occurred at luminal pH of 7.4, 5.0, and 4.0 but not at 3.0. An inhibitor of pepsin did not favorably affect the outcome of luminal pH 3.0, but a nutrient HCO-3 concentration of 47.8 mM completely prevented the adverse effects of luminal pH 3.0. Reconstitution of epithelial integrity did not occur in the absence of HCO-3 at luminal pH 4.0. Thus, low luminal pH inhibits and high nutrient HCO-3 concentration supports the epithelial restitution after mucosal damage caused by hyperosmolar NaCl.

Animals↗
PubMed1982

Restitution of the surface epithelium of the in vitro frog gastric mucosa after damage with hyperosmolar sodium chloride. Morphologic and physiologic characteristics.

Frog fundic mucosas mounted in Ussing chambers between HCO-3-buffered nutrient and unbuffered secretory solutions were exposed to 1 M NaCl on the mucosal surface for 10 min. After washing and return to control solutions, transmucosal potential difference, short-circuit current, and tissue electrical resistance decreased markedly, but within 6 h these measurements had gradually returned to almost control values. A net luminal alkalinization occurred during the first 4 hours, changing into a net acid secretion of approximately 1.1 mumol . cm-2 . h-1 at 6 h. Histamine increased H+ secretion in all tissues at 8 h. In seven metiamide-treated tissues, an average alkaline flux of approximately 0.75 mumol . cm-2 . h-1 was obtained during the first 4 h after damage, decreasing to approximately 0. 40 mumol . cm-2 . h-1 during the ensuing 4 h. With HCO-3-free nutrient solution (n = 7) luminal alkalinization was decreased by about 80% 2-4 h after injury. After 1 M NaCl, the surface epithelium and gastric pit cells were destroyed and partially lifted from the gastric glands. The lamina propria between the remaining intact glands was open to the lumen or contiguous with the damaged mass of cells and mucus. During the 6 h after damage, there was a gradual process of restitution of epithelial integrity, beginning with squamous-shaped cells that appeared to be migrating from the glands and ultimately concluding with complete epithelialization by cuboidal and columnar cells. Typical junctional complexes were present between adjacent epithelial cells. The uniformity of the restoration process was such that it was possible to predict blindly in toluidine blue-stained semithin sections whether the recovery stage was short (30 min or less), intermediate (1-2 h), or advanced (4-6 h). These observations indicate that there is a very intimate correlation between the restoration of epithelial continuity and the reestablishment of secretory and electrical activity of frog gastric mucosa damaged by hypertonic NaCl in Ussing chambers.

Animals↗
PubMed1982

The significance of gastric mucosal blood flow and acid secretion in erosive gastritis following hemorrhagic shock in cats.

Gastric acid secretion was stimulated in 21 anesthetized cats by infusion of pentagastrin for 45 min. Thirty minutes later the arterial blood pressure in two groups of the cats was lowered by bleeding to 75 mmHg for two hours, during which time one group was infused with cimetidine and the other with Ringer's solution. The tapped blood was then reinfused and normotension was maintained for two hours. In the third group the cats received pentagastrin and Ringer's solution but were kept normotensive throughout the experimental period. Blood flow was determined with the microsphere distribution technique. The volume and pH of the gastric juice were measured. In the cats with hemorrhagic hypotension, mucosal erosions developd in the corpus/fundus and antrum regions irrespective of cimetidine administration. In the normotensive cats there were few erosions. The gastric mucosal blood flow decreased markedly when the arterial pressure was lowered and returned to control levels and reinfusion of blood. The volume of gastric juice was fairly constant in the experimental period, but the concentration of H+ showed a gradual fall in the three test groups. The study showed that gastric mucosal erosions may develope in cats subjected to hemorrhagic hypotension when the stomach contains gastric acid without bile.

Animals↗
PubMed1981

Effects of hemorrhagic shock on gastric blood flow and acid secretion in cats.

Anesthetized cats were cannulated and successively bled to arterial pressures of 100, 75 and 50 mmHg. The pressure was maintained at each level for 20 min. One group of animals was given 16 mu . kg-1 . h-1 of pentagastrin and another group 2 mg . kg-1 . h-1 of cimetidine throughout the experiment. Blood flow was determined by means of the microsphere distribution technique using spheres 14 +/- 1 micrometer in diameter. At each pressure level 15 min sample of gastric juice were collected. Twenty ml of saline was instilled into the stomach and withdrawn together with the gastric juice. Adenosine triphosphate (ATP) content and enzymatic activity (LD, ASAT) of the gastric mucosa and blood pH, pCO2 were determined at 140 and at 50 mmHg. In both pentagastrin and cimetidine treated cats gastric mucosal blood flow decreased and the vascular resistance increased markedly when the pressure was lowered by bleeding from 140 to 100 mmHg. On further bleeding to 50 mmHg only slight additional flow reduction occurred and the vascular resistance remained constant. Under shock blood flow was higher and the resistance lower in pentagastrin than in cimetidine treated animals. In pentagastrin treated animals a parallel decrease in acid secretion and mucosal blood flow occurred under shock. Cimetidine inhibited acid secretion both at normal blood pressure and under shock. The ATP content of the mucosa did not decrease, no morphological changes of the mucosa occurred and there was no leakage of cellular enzymes during the period of hypotension.

Adenosine Triphosphate↗
PubMed1981

The effect of hyperbaric oxygenation on experimental Bacteroides fragilis infection in the rat liver.

An experimental intra-abdominal model for producing Bacteroides fragilis abscesses in the rat liver was used to evaluate the therapeutic effect of hyperbaric oxygenation (HO) at 3 ATA (atmospheres absolute). Two different experiments were performed. In the first experiment one half of the animals were inoculated with B. fragilis, and the other half were sham-operated. Whether the inoculated or sham-operated animals were given single or repeated HO treatment at 3 ATA for 90 min, the bacteriological pattern was about the same. In the second experiment all the animals were inoculated with B. fragilis; half of the animals were given HO at 3 ATA for 90 min as single or repeated treatments, and the other half acted as controls receiving no HO. Even if the HO treatment was given every day during 21 days, B. fragilis could be recovered in all inoculated animals 22 days after inoculation.

Animals↗
PubMed1980

Changes in gastric mucosal morphology, capillary permeability and blood flow during the first 3 days of acute gastritis in cats.

In the present investigation gastric morphology, blood flow, vascular permeability and water content were studied in cat stomachs with acetic acid-induced gastritis at different time intervals up to 3 days after induction of gastritis. The morphological changes including mucosal erosions, edema and hemorrhage showed normalization within 3 days. The mucosa and muscularis blood flow remained essentially unchanged compared with pre-gastritis values and with the control group. Gastritis was associated with leakage of circulating albumin into the stomach wall most pronounced 4 h after the induction of gastritis. The water content was high at 4 and 24 h after induction of gastritis with almost normalization at 3 days. The morphologaical characteristics of our model are very similar to those observed in man. Leakage of circulating albumin into the gastric wall seems to be the best parameter for quantifaication of the inflammatory changes found in acute gastritis, while blood flow seems to be a less important parameter.

Acute Disease↗
PubMed1980

The effect of intragastric pressure on gastric blood flow after partial devascularization of the stomach in cats.

The influence of intragastric pressure (IGP) on gastric blood flow was studied in cats with regional ischemia due to partial gastric devascularization, and in sham-operated cats. IGP was controlled by intragastric installation of saline. Blood flow was determined by means of the microsphere distribution technique. Increment of IGP reduced mucosal and muscularis blood flow in all areas of the stomach, both in sham-operated and devascularized cats. In areas with reduced mucosal blood flow due to devascularization, blood flow became further reduced by IGP to an extremely low flow level. The present results are pertinent to the pathogenesis of early lesser curvature ulcer or necrosis sometimes ll areas of the stomach, both in sham-operated and devascularized cats. In areas with reduced mucosal blood flow due to devascularization, blood flow became further reduced by IGP to an extremely low flow level. The present results are pertinent to the pathogenesis of early lesser curvature ulcer or necrosis sometimes ll areas of the stomach, both in sham-operated and devascularized cats. In areas with reduced mucosal blood flow due to devascularization, blood flow became further reduced by IGP to an extremely low flow level. The present results are pertinent to the pathogenesis of early lesser curvature ulcer or necrosis sometimes occurring after proximal gastric vagotomy in man.

Animals↗
PubMed1980

Transient intestinal ischaemia induced by degradable starch microspheres. Experiments in the cat.

Temporary ischaemia was induced in cat small intestine by degradable starch microspheres. Regional arterial and tissue blood flow immediately fell by 85 per cent with subsequent normalization within 26 min after microsphere injection. Degraded 99Tcm-labelled microspheres were exponentially removed from intestinal vessels and accumulated in the liver. Provided near-total arteriolar obstruction is induced, external isotope detection may permit assessment of the duration of the induced ischaemia, which implies a selection of the appropriate time for radiation therapy.

Animals↗