Biomedical subjects

E Kivilaakso

Publications and source records attributed to E Kivilaakso.

At least 163 records · Page 9Linked to original sources

PubMed1977

Relative risk of stump cancer following partial gastrectomy.

The relative risk of stump cancer following partial gastrectomy for a benign gastroduodenal condition was estimated using an individually matched retrospective study design based on autopsy material. Data on all patients dying with gastric cancer and autopsied at the Central Laboratory of Pathology, University Central Hospital, Helsinki, during 1961-75 were collected. Matched pairs of the same sex and age were used as controls. Of the 464 patients dying with gastric cancer, 9 had undergone previous partial gastrectomy, while the respective number among the controls was 5. This result suggests that the risk of cancer in the gastric stump was not significantly increased as compared to the normal unoperated population.

Aged↗

PubMed1977

Ultrastructural changes in the gastric mucosa following hemorrhagic shock in pigs.

Ultrastructural changes in the gastric mucosa of 14 piglets subjected to transient hemorrhagic shock (3 hr duration; mean arterial pressure 40 mmHg) are described. After 30 min there was mucosal edema and extravasation of red blood cells. Microthrombi with degranulating thrombocytes and fibrin strands were seen in the capillaries. These changes were also seen in the antral mucosa where no subsequent ulceration usually occurs. At this stage the cells of the neck region of the gastric glands showed mitochondrial dilatation and their apical parts were seen to bulge into the lumen of the gastric glands. Other cell types were affected later and necrosis progressed from the surface into deeper parts of the mucosa. Mast cells and mucosal endocrine cells were relatively resistant, being mostly undamaged at the end of the shock period and later. The findings suggest that, during the shock, local formation of thrombi contributes to mucosal ischemia and ulcer formation, and that the cells at the neck region of the gastric glands form the locus of limited resistance to ulcerogenic effects.

Animals↗

PubMed1976

Modification of procine stress ulceration by methylprednisolone, vitaminA and methysergide treatment.

Using a swine shock ulcer model, three pharmacological agents, methylprednisolone, vitamin A and methysergide were evaluated, as they protect gastric mucosa against acute ulceration. Following haemorrhagic shock (3 h duration; mean arterial pressure 40 mm Hg) nine of the ten control animals (90%) developed gastric ulceration. Of the six test animals treated with intravenous methylprednisolone during the shock, only one (17%) developed gastric lesions (p less than 0.02; x2 = 5.76). Of the ten test animals pretreated with massive doses of parenteral vitamin A, only three (30%) developed lesions (p less than 0.05; x2 = 5.21). In contrast to this, treatment with methysergide, a serotonin antagonist, did not significantly effect the ulceration rate, since four of the six test animals (67%) had gastric lesions. The results suggest that methylprednisolone and vitamin A do protect the gastric mucosa from experiment stress ulceration, but their mechanism of action remain obscure and further investigation is needed to judge their value in clinical use.

Animals↗

PubMed1976

Electron microscopic and histological findings on urinary bladder epithelium in interstitial cystitis.

Urinary bladder epithelium was studied with electron microscope in 50 patients with interstitial cystitis (IC) and 9 controls. In addition, biopsies of 14 patients with IC were studied with special stains for the presence of bacteria or viral inclusions in the epithelium. No bacteria or viral inclusions could be demonstrated. On the basis of these and earlier negative findings it appears that simple infection of the epithelium is ruled out as the aetiology in IC. Electron microscopy demonstrated an increase in large swollen epithelial cells with decreased amount of lateral processes in half of the IC samples and inflammatory changes in the mucosa. The similarity of the ultrastructure of epithelial cells in controls and IC patients makes it improbable that the disease process originates in the epithelium. In this study special attention was paid to large cytosomes (diameter 0.4--6.0 mum) in the epithelial cells. These contained small vesicular bodies (diameter 0.04--0.2 mum) and lipid droplets, and were found in controls as well as in IC patients.

Basement Membrane↗

PubMed1976

Duodenogastric reflux of lysolecithin in the pathogenesis of experimental porcine stress ulceration.

The role of duodenogastric reflux of lysolecithin, a normal constituent of duodenal juice, in the pathogenesis of gastric stress ulcerations was investigated with a swine shock-ulcer model. Twenty-seven piglets, weighing 8 to 12 kilograms, were used. In an intact animal, the average concentration of intragastric lysolecithin before shock was 138 mug per milliliter (median, N = 6). At the end of the shock period, the average concentration of lysolecithin was 540 mug per milliliter and the over-all amount in the gastric juice was 14.3 mg. (median, N = 6). Following hemorrhagic shock (3 hours duration; mean arterial pressure, 40 mm. Hg), all six control animals with normal gastroduodenal continuity got gastric ulcerations. Interruption of duodenogastric reflux by duodenal exclusion and gastrojejunostomy completely abolished the development of these ulcerations in six test animals. When the interrupted duodenogastric reflux was replaced artificially by intragastric instillation of lysolecithin (500 mug per milliliter; 25 ml.), all six animals developed lesions. Intragastric lysolecithin without shock had no effect. The results provide further support to the concept that regurgitation of duodenal juice into the stomach is an essential factor in the pathogenesis of gastric stress ulceration. The results also suggest that, in this respect, one of the active components in duodenal juice is lysolecithin.

Animals↗

PubMed1975

Role of pyloric reflux in experimental stress ulceration during haemorrhagic shock.

The significance of pyloric reflux of bile and duodenal juice in experimental gastric stress ulceration was studied using a swine shock ulcer model. Following a haemorrhagic shock of 3 h duration, nine of the ten control piglets (90%) with normal bile flow have gastric mucosal lesions. None of the five piglets with permanent bile diversion (ligation of common bile duct; cholecystojejunostomy) has gastric lesions. Intragastric instillation of pure bile prior to the shock in piglets with permanent bile diversion induced gastric lesions in only one of the five test animals (20%). If duodenal juice was used instead, four of the six test animals (67%) have lesions. The results indicate that, in the pig, an uninterrupted flow of bile into the duodenum is a prerequisite for the development of gastric mucosal lesions following haemorrhagic shock. They also suggest that duodenal juice containing both bile and pancreatic juice has a stronger ulcerogenic influence on shocked porcine gastric mucosa than bile alone.

Animals↗

PubMed1975

Surface electron microscopical changes of the gastric mucosa in experimental porcine stress ulceration.

Gastric mucosal changes in 8 piglets subjected to a transient hypovolaemic shock were studied using scanning electron microscopy (SEM). The mucosal lesions during the shock were characterized by progressive degenerative changes in the mucous membrane of the stomach. These surface changes included flattening or swelling of the individual cells. The flattening of the mucous membrane was later connected with red cell diapedesis through it. These changes were most typical in the areas of haemorrhagic gastritis and preceded the ulcer formation. Following retransfusion, the affected epithelial lining appeared greatly distended over the oedematous lamina propria, with almost complete loss of structural detail. Masses of red blood cells were seen to emerge through the epithelium as an indication of subepithelial haemorrhage. It is possible that the injured epithelium is actually broken down by the pressure of the underlying mucosal haemorrhage and oedema. At later stages, the ulcerated areas showed complete loss of epithelial cells and thus the underlying structureless lamina propria, covered by necrotic cell remnants, blood cells and fibrin, was denuded.

Animals↗

PubMed1974