Acetic acid-induced gastritis in cats. Changes in blood flow and capillary permeability.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to K Svanes.
Explore the source record for details and available documents.
Gastric ulcer was induced in rats by application of acetic acid to the anterior wall of the stomach. Leakage of circulating albumin into the gastric wall was estimated by intravenous injection of radioactive albumin and determination of the radioactivity in different samples of the stomach wall. The protein leakage was found to be markedly increased in the anterior wall of the stomach, the increase being most pronounced close to the ulcer. The leakage remained fairly constant during the first 10 h of the experiment. The protein content of the posterior wall was about the same as in animals on which a sham operation had been performed. The protein leakage was associated with considerable oedema formation. The protein leakage indicates that inflammatory mediators are released in a wide area around the ulcer. The present experimental model offers an opportunity to find out which mediators are involved in the lesion.
Explore the source record for details and available documents.
Radioactive microspheres 15 mum in diameter were injected into the left ventricle of the heart of cats. Simultaneously a blood sample was drawn from the aorta. Standardized samples of the stomach wall were separated into mucosa and muscularis samples. For each sample the blood flow was calculated in terms of ml/minute/100 g tissue weight. The distribution of microspheres to different layers of the samples was determined microscopically. In the mucosa samples the majority of spheres were found in the propria and glandular layer, only a few persent in the submucosa. In the mscularis samples most of the microspheres were present in the muscle tissue, only 1--9% in the submucosa fraction. The present method is considered to give a good expression of the capillary blood flow in the glandular layer of the mucosa and the muscularis.
Ulcer was induced in the anterior wall of the antrum by a subserous injection of 0.3 ml of a 20% acetic acid solution. Carbonized microspheres 15 plus or minus 5 mu in diameter and labelled with 169Yb were used to measure blood flow in different regions and layers of the stomach. Approximately 2-3 million microspheres were injected into the left ventricle of the heart. Simultaneously a blood sample was drawn from the distal aorta at a flow of 1 ml/min. Standardized tissue samples were punched from the lesser curvature and the anterior and posterior walls of the antrum, corpus, and fundus. In each sample the mucosa was separated from the muscularis. The radioactivity of the blood and tissue samples was determined, and the blood flow was calculated for each tissue sample. Three groups of animals were examined: 1) anaesthetized control animals, 2) animals laparotomized one week before examination, 3) animals with a one-week ulcer. In the control animals the blood flow was found to be the same in corresponding regions of the anterior and posterior walls of the stomach. The flow was slightly lower in the antrum than the fundus. The flow was similar in the different regions of the muscularis. The muscularis flow was markedly lower than the mucosa flow. In the laparotomized animals the blood flow was found to be increased in the muscularis of the corpus. In the ulcer animals the mucosa flow was increased in the anterior wall of the antrum, and the muscularis flow was increased in the antrum and the anterior wall of the corpus.
A case of intestinal obstruction due to impaction of an enterolith in the distal ileum is reported. The patient had jejunal diverticulosis. One of the diverticula showed evidence of acute inflammation and another showed signs of fibrosis suggesting previous inflammation. Apparently the enterolith had been released from the acutely inflamed diverticulum. One of the diverticula contained a smaller enterolith. The impacted enterolith was removed by enterotomy and the smaller one milked into the intestine. Chemical analysis of the removed stone showed that it consisted of mainly cholic, desoxycholic and fatty acids.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
This study was performed to examine if the cytokines interleukin-1 (IL-1), interleukin-6 (IL-6) or tumor necrosis factor (TNF) are released from the gastric mucosa during acute mucosal damage, and if the generation of these cytokines is affected by indomethacin. 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. Concentrations of active cytokines and of histamine in aortic and portal vein blood were measured by bioassay and RIA, respectively. Active IL-6, but not IL-1 and TNF, is released from the gastric mucosa during acute mucosal damage by 2 M NaCl and acid back diffusion. Indomethacin increased mucosal injury and enhanced the TNF generation but reduced the release of IL-6 from the gastric mucosa. We conclude that IL-1 and TNF probably do not play an important modulating role during acute gastric mucosal damage. The generation of IL-6 may, however, contribute to mucosal protection.