Fluorescein angiography for evaluation of intestinal intramural haemorrhage in abdominal missile injury.
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Abdominal Injuries↗
Biomedical subjects
K Norrby
Publications and source records attributed to K Norrby.
Mesenterial-window hyperplasia in the lactating rat.
By examining the true mesentery adjacent to the small gut before and after weaning, as well as in age-matched controls, we found that the number of mesenteric windows, their total area, and their total DNA content increased significantly during lactation. Simultaneously, Feulgen-DNA absorption analysis in individual mesenteric cells showed that these had a normal DNA stemline, and a normal distribution within the G1-G2 range. The hyperplasia and growth developed and declined temporally somewhat parallel in the mesenterial windows and their adjacent small gut, suggesting that an as yet unknown common factor(s) governs the hyperplastic growth in both these tissues. The novel physiological, mesenterial-window hyperplasia in the lactating rat described in the present study may prove useful for studies of the mesenteric function and the regulation of cell proliferation.
Animals↗
Hyperplasia of the mesenterial windows precedes that of the small gut in the streptozotocin-diabetic rat.
Hyperplastic growth of the mesenterial windows abutting the small gut occurs in lactating rats (Bergström and Norrby 1988) and chronically diabetic rats (Norrby et al. 1983). In the present study, early events in the mesenterial windows and the small gut in streptozotocin-diabetic rats were examined. The area of the mesenterial windows had already increased significantly on day 1 and hyperplasia in terms of increased DNA content, as well as an increase in histamine content (a mast-cell marker), was established from day 2 of diabetes. The increase in total mesenterial window content of DNA, histamine and protein was roughly linear and parallel from day 2 to day 19. The small-gut circumference increased transiently on day 1, but the small-gut mucosal volume was unaffected on days 1 and 2. The small-gut wet weight increased significantly from day 5, whereas elongation was not observed until day 19. The difference in time between the appearance of hyperplasia and the growth of the mesenterial windows and their adjoining gut and the rate with which the hyperplasia proceeds in the two tissues indicate that the regulatory mechanisms of early hyperplastic growth in these tissues are not identical. The factor(s) causing mesenterial window growth and hyperplasia is/are as yet unknown.
Animals↗
Mitogenesis in wound-healing cells in diabetic rats.
The healing of perforated mesenterial window is delayed in insulin-deficient rats after 4 weeks of streptozoticin-induced diabetes. In the present study we investigated the mitogenic capacity of the two predominating cell types in the healing mesenterial window in such rats. The labelling index (LI) in fibroblasts and mesothelial cells, normally constituting approximately 96% of all tissue-bound cells, was estimated in early and later phases of healing within (a) a 1 mm-wide zone surrounding the perforation and (b) centrally in wounds after healing by closure. The mitotic index (MI) of these cells was estimated at various distances from the perforation. Adjacent unperforated control mesenteric windows served as internal controls. Proliferation increased on days 1 and 2 post-perforation, whereafter it gradually diminished, fibroblasts showing a higher LI than mesothelial cells days 3-7 after closure. On day 1 post-perforation the relative increase of LI was greatest in diabetic mesenteries. During the period just preceding healing by closure. LI of both fibroblasts and mesothelial cells was, however, significantly reduced in diabetic animals. The impaired mitogenesis in these wound-healing cells in diabetic rats may thus be of pathogenic significance in the delayed healing in such animals.
Animals↗
Histologic changes in the gastroduodenal mucosa after long-term medical treatment with cimetidine or parietal cell vagotomy in patients with juxtapyloric ulcer disease.
Biopsy specimens were collected during endoscopy from pre-established sites in the corpus (n = 60), antrum (n = 53), and the duodenal bulb (n = 54) from the same patient before and 2-3 years after parietal cell vagotomy (PVC) or after a similar period of treatment with cimetidine. There was a significant increase in scores of chronic body gastritis after PCV (p less than 0.001) even in comparison with the cimetidine group (p less than 0.01), for which the scores of chronic body gastritis remained essentially unchanged. The scores of chronic antral gastritis and the incidence of intestinal metaplasia of the antrum increased significantly (p less than 0.05) in both the PCV and the cimetidine groups when the two treatment groups were analyzed together. The degree of polymorphonuclear infiltration in the body and antral mucosa, the incidence and severity of duodenitis, and the incidence of gastric metaplasia in the duodenal cap were unaffected by the treatment. In contrast to maintenance treatment with cimetidine PCV seems to accelerate the development of chronic body gastritis. The kappa statistics, as indicator of the reproducibility of histopathologic scoring, were acceptable.
Adult↗
Are endoscopic and/or histologic findings in gastroduodenal mucosa a predictor of clinical outcome in peptic ulcer disease? A 1-year follow-up study after initial healing with either cimetidine or medium-dose antacid.
Patients with duodenal ulcer (DU; n = 79) or prepyloric ulcer (PPU; n = 39) received cimetidine, 400 mg twice daily, or Novaluzid, 10 ml four times daily (acid-neutralizing capacity, 340 mmol/day), in a multicentre, randomized, double-blind trial. Ulcer healing was almost identical with the two treatments at 4, 6, and 12 weeks in the DU group. Cimetidine was significantly more effective than antacids in alleviating symptoms in PPU disease, with no significant difference in ulcer healing. In the PPU group the symptomatic improvement was inferior irrespective of treatment, and there was a significantly lower healing rate at 4 weeks (p less than 0.05) than in the DU group. The relapse rate over a 1-year follow-up period with no therapy did not differ between the two treatment groups or between the two ulcer groups. No factors in history of disease or endoscopic or histologic variables were of predictive value with regard to delayed healing. The macroscopic appearance of the duodenal and antral mucosae improved significantly when ulcers had healed. In the subgroup of about 50% DU patients who experienced a relapse during the 1-year follow-up period, the histologic scoring of duodenitis remained basically unchanged, contrary to the significant improvement seen in the non-relapsing subgroup. The microscopic changes of the antral mucosa from the time of inclusion to healing seen in the PPU patients were of no predictive value with regard to relapse rate.
Adult↗
Age-dependent mast-cell-mediated angiogenesis.
In maturing male rats of approximately 5.5,10.5, and 15 weeks of age (groups I, II, and III), the mast-cell-mediated angiogenesis in the mesenterial windows was quantitatively assessed on days 14,21,28, and 35 after the start of intraperitoneal treatment using the mast-cell secretagogue 48/80, and using the saline vehicle. The number of blood vessels per unit length of the central part of the mesenterial window was virtually unaffected by age as well as by the saline treatment. The number of vessels at the mesenterial-window circumference was, however, increased in the older, untreated animals. The postpubescent animals in groups II and III showed a marked mast-cell-mediated angiogenic response lasting until day 28. The relative angiogenic response over the period of 14-28 days clearly increased with advancing age. The highest mean value in group II was about 8 times (p less than 0.001), whereas the highest mean value observed in group III was about 24 times (p less than 0.001) greater than in corresponding saline-treated controls. In contrast, no statistically significant mast-cell-mediated angiogenesis appeared in the prepubescent rats of group I.
Aging↗
The influence of remnant size, antithyroid antibodies, thyroid morphology, and lymphocyte infiltration on thyroid function after subtotal resection for hyperthyroidism.
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Adult↗
Histamine and mucosal mast cells in gluten enteropathy.
Coeliac disease is a malabsorptive disorder caused by intolerance to gluten and is characterized by a remodelling of the intestinal mucosa including villus atrophy, crypt hyperplasia and net increase of mucosal volume. Changes of the number of mucosal mast cells (MMCs) in coeliac mucosa has recently been reported, suggesting that the mast cell activity could have a pathogenetic role in gluten enteropathy. MMCs located solely in the lamina propria are the main repository for small-gut mucosal histamine. A consecutive prospective study was designed to study the histamine content, MMC numbers, and the relative volume of lamina propria in intestinal biopsies from adult patients suffering from unexplained diarrhea and/or malnutrition. Histamine was measured by a HPLC-method, the number of MMC was counted after long toluidine-blue staining, and the relative volumes of lamina propria and epithelium were estimated morphometrically. The findings were correlated to the histopathological appearance of the mucosa. As compared to controls the histamine content increased by 80% and MMC numbers by about 60% in the coeliac mucosa. There was also a correlation between MMC numbers and histamine content for both normal and coeliac mucosae (r = 0.81). The morphometric estimation of the relative volumes of epithelium and lamina propria revealed that the lamina-propria compartment was increased by approximately 40% in coeliac mucosa. Taking the changes in compartmental volumes of the remodelled coeliac mucosa into account, our results suggest that the histamine content and MMC population were significantly increased. MMC and MMC-associated histamine may therefore be involved in the pathogenesis of gluten enteropathy.
Celiac Disease↗
Mast-cell-mediated angiogenesis: a novel experimental model using the rat mesentery.
The angiogenic effect of autogenous secreting mast cells (MCs) was studied using a novel experimental approach. The virtually avascular membranous rat mesentery was used as test tissue. The activation of MCs was elicited by repeated intraperitoneal injections of the MC-secretagogue compound 48/80, which per se appears inert from the proliferogenic and angiogenic point of view. Angiogenesis was quantitated histologically and expressed the number of vessels/unit length of mesentery. The smallest vessels recognized had a luminal area of approximately 7-8 microns 2 (corresponding to a circular diameter of 3.0-3.2 microns). Seven to ten days after MC-activation ended, the number of blood vessels had increased 7- to 6-fold. A retrogressive reaction occurred between days 21 and 38 after treatment, when the number of vessels had essentially normalized, as compared to vehicle-treated controls. The present study, introducing the membranous mesentery as a model for quantitative angiogenetic studies, provides evidence that MCs can induce angiogenesis, which is new. The possible therapeutic implication of this finding is noteworthy.
Animals↗
Evidence of mast-cell histamine being mitogenic in intact tissue.
We have reported previously that secretion by connective tissue mast cells (MCs) causes mitogenesis in adjacent cells in diverse rat tissues. In cultured rat mesentery there was a spontaneous release of about 45% of the histamine in 2 days, and a spontaneous marked increase in basal proliferation of the mesentery. The MC secretagogues, compound 48/80 and polymyxin B, released additional histamine and stimulated mitogenesis further. In contrast, 48/80 added to cultures of guinea-pig mesentery, the MC of which are unresponsive to the drug, did not affect the basal proliferation. However, exogenous histamine at 10(-10) M mitogenically stimulated the cultured guinea-pig mesentery. A histamine H2-receptor antagonist, which itself was mitogenically inert, significantly suppressed the 48/80-induced MC-mediated mitogenesis in rat mesentery in vivo and in vitro. On the other hand, a histamine H1-receptor antagonist did not affect this MC-mediated mitogenesis in rat. Our findings indicate that histamine is one of possibly several mitogens which are released or activated by the secreting MC.
Animals↗
Acute hyperglycaemia and mast-cell-dependent mitogenesis in rat.
Hyperglycaemia is considered to be of possible aetiological significance for proliferative lesions in diabetes. We recently found that mast-cell-mediated proliferation in mesentery and skin is augmented in hyperglycaemic rats with longstanding diabetes. We now report a study to examine whether acute hyperglycaemia affects the proliferative response of fibroblasts and mesothelial cells that follows local mast-cell secretion in healthy rats. Hyperglycaemia was achieved by continuous intravenous infusion of glucose over a period of 2.5 h preceding and 9.5 h following administration of the mast-cell secretagogue compound 48/80. The 48/80 was given intraperitoneally which causes rapid mast-cell secretion and prompt subsequent mesenteric mitogenic stimulation. Hyperglycaemia thus persisted throughout the prereplicative period, during which stimulated cells are recruited into the cell cycle from a quiescent state. Because the ensuing mesenteric mitogenic response, estimated by specific DNA activity and mitosis counting, was unaffected by glucose infusion, acute hyperglycaemia itself appears to be of no aetiological significance for the accelerated mast-cell-dependent mesenteric mitogenesis in the diabetic rat.
Animals↗
Enterogastric reflux after gastric surgery. A comparison between gastroduodenostomy and Roux diversion.
Reflux of upper intestinal content to the gastric remnant after gastric resection is common and may cause damage to the gastric mucosa, resulting in gastritis, gastric ulcer, and possibly dysplasia. Different surgical procedures have been proposed to prevent reflux, among them Roux-en-Y diversion. In this study we have compared antrectomy followed by gastroduodenostomy (BI) with antrectomy followed by Roux-en-Y anastomosis with regard to enterogastric reflux. Reflux was recorded by cholescintigraphy, using a new method for quantification. In all patients biopsy specimens were taken for histopathological evaluation at gastroscopy. Twenty-seven patients were studied, 11 with gastroduodenostomy and 16 with Roux-en-Y diversion. All patients in the gastroduodenostomy group had reflux, compared with four in the Roux group (p less than 0.001). Under the light microscope all patients in the BI group showed a moderate to severe degree of inflammation compared with only seven in the Roux-en-Y group (p = 0.028). Our results show that Roux-en-Y drainage effectively diminishes reflux and may be an explanation for the lower extent of mucosal damage in these patients.
Adult↗
Cellular and extracellular changes following mast-cell secretion in avascular rat mesentery. An electron-microscopic study.
Mast cell (MC) secretion induces local cell proliferation lasting 48-72 h in fibroblasts and mesothelial cells in the almost avascular true mesentery of the rat. We studied this membranous tissue by transmission electron microscopy with regard to cellular and extracellular features occurring during the first 72 h following MC secretion. After MC secretion elicited by compound 48/80, apparently all individual tissue-bound cells (i.e. fibroblasts, mesothelial cells, and macrophages) show signs of accelerated metabolic activity. In fibroblasts, conspicuous increases in the volume of Golgi apparatus and rough endoplasmic reticulum and in the amount of plasmalemmal indentations suggest an increased production and secretion of the extracellular matrix. Released MC granules lying close to projections of nearby phagocytosing cells cause areas free from electron-dense material in the extracellular matrix. MC secretion therefore appears to produce a remodelling of extracellular matrix. Most of the activities initiated by MC secretion start to subside within (48-)72 h. The findings indicate a close functional relationship between the tissue MC and all its neighbouring cells and the surrounding extracellular matrix. The striking chain of events that it induces emphasizes strongly that the secreting MC plays a prominent although as yet in many respects enigmatic role in normal tissue.
Animals↗
On disturbance of homeostasis in organ-cultured tissue.
The intact membranous rat mesentery was cultured in Eagle's minimum essential medium containing no serum or only low concentrations of serum. The procedure is in some important respects superior to previous organ culture techniques. To estimate the extent of disturbance of homeostasis of the tissue in culture, the spontaneous mast-cell histamine release was quantitated after preculture preparation of the specimens and after different intervals in culture. Also, the proliferation of fibroblasts and mesothelial cells that predominate in the mesentery was assessed at 48 h by cytofluorometric quantitation of DNA in single-tissue cells. Spontaneous histamine release was time dependent during cultivation, amounting to ca. 50% at 48 h, and was affected by the medium used for moistening the tissue before cultivation. Culturing also brought about great spontaneous increase in the proliferation of fibroblasts and mesothelial cells, the rate being related to the concentration of serum. Addition of the mast-cell secretagogues 48/80 or polymyxin B at 1 h caused rapid release of 50 to 60% of the histamine and was followed by augmented proliferation in the serum-containing media. The spontaneous increase of cell proliferation in tissue culture may be causally related to mast-cell secretion. Further studies are needed to define factors influencing the spontaneous mast-cell secretion and the mast-cell-dependent mitogenesis in normal tissue cells.
Animals↗
Further studies on the delayed mast-cell-mediated mitogenesis in diabetic rat.
We have investigated whether the delayed augmented mast-cell-dependent mitogenesis that we recently demonstrated in the true mesentery of diabetic rats may occur also in a tissue which is essentially different both functionally and structurally. Cutaneous proliferation in insulin-deficient rats following a single intradermal injection of compound 48/80 was assessed by the specific DNA activity and mitotic index, on days 7 and 28 after giving streptozotocin. The proliferation variables, which ran parallel, indicated that mast-cell secretion was not followed by proliferation on day 7, whereas there was markedly augmented proliferation on day 28. Mitosis counting showed that cell production following mast-cell secretion was significantly increased not only in the entire cutis but also in epithelial structures (epidermis and epidermal appendages). These findings are closely similar to the delayed augmentation of mast-cell-dependent mesenteric mitogenesis in diabetic rats. It is concluded that there may be a general pattern of delay in the appearance of augmented mast-cell-mediated mitogenesis in rats with chemically induced diabetes. It is questioned whether or not this delayed mitogenesis may be connected with the postponed proliferation in a variety of tissues and organs (such as arteries, eyes, and kidneys) that occurs in experimental and clinical diabetes.
Animals↗
On the role of arachidonic acid metabolites in mast-cell mediated mitogenesis in the rat.
We investigated whether the mitogenic response induced by local mast-cell secretion in the rat mesentery was affected by suppression of phospholipase A2, lipoxygenase, or cyclooxygenase in arachidonic acid metabolism. Enzyme inhibitor was given in a single intravenous dose 5 min before intraperitoneal injection of the mast-cell secretagogue 48/80. Mepacrine, a phospholipase A2 inhibitor, suppressed the generation of both leukotrienes (SRS) and prostaglandins (PG), whereas the lipoxygenase inhibitor BW 755C reduced the generation of SRS, and the cyclooxygenase inhibitor indomethacin significantly suppressed the generation of PG. None of the enzyme inhibitors affected the basal mesenteric histamine content or histamine release in the mesentery after exposure to 48/80, and none of them affected mast-cell-mediated mitogenesis in the mesentery as judged by specific DNA activity and mitosis counting. The stimulation of DNA synthesis and mitosis initiated by secreting mast cells is apparently not mediated or modulated by synthesis of leukotrienes, prostaglandins, or other known arachidonic acid metabolites.
4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
Tumor-bearing depresses distant mast-cell-mediated mitogenesis.
A methylcholanthrene-induced sarcoma grafted subcutaneously in rats was used in early transplantation generations. Tumor-bearing rats showed weight loss compatible with cachexia. Healthy rats of the same age served as controls. In tumor-bearing rats the basal mesenteric proliferation was unaffected whereas the strictly mast-cell-mediated hyperproliferative reaction in the mesentery was significantly reduced after intraperitoneal injection of the mast-cell-secretagogue compound 48/80, as judged from specific DNA activity and mitosis counting. However, in mesentery and peritoneal lavage the number of mast cells, their histamine-releasing capacity, and their content of histamine, 5-hydroxytryptamine and heparin were unaffected by tumor-burden. The findings suggest the presence of a tumor-associated systemic factor of unknown nature which interferes with the biochemical events leading to the mast-cell-dependent mitogenesis. Since this mitogenic reaction may normally compensate for injury at the cellular level it is questioned whether the decreased mast-cell-dependent proliferation in tumor-bearing is a component of cachexia.
Animals↗