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Regulation of gastric mucosal calcium channel activity by an antiulcer agent, ebrotidine

100%

Slomiany B. L., Liu J., Piotrowski J., Czajkowski A., Yotsumoto F., Slomiany A.

Journal of Physiology and Pharmacology

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1994

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tom 45

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nr 1

2

The presence of Helicobacter-like microorganisms in the gastric mucosa in dogs

86%

Sapierzynska R., Malicka E., Bielecki W., Sendecka H.

Polish Journal of Veterinary Sciences

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2003

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tom 06

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nr 4

3

Role of sulfation in the processing of gastric mucins

86%

Liau Y. H., Murty V. L. N., Slomiany A., Bielanski W., Slomiany B. L.

Journal of Physiology and Pharmacology

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1991

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tom 42

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nr 4

The role of sulfation in the processing of mucus glycoprotein in gastric mucosa was investigated. Rat gastric mucosal segments were incubated in MEM at various medium sulfate concentrations in the presence of [³⁵S]Na₂ SO₄ [³H] glucosamine and [³H]proline, with and without chlorate an inhibitor of PAPS formation. The results revealed that the mucin sulfation attained maximum at 300 µM medium sulfate concentration. Introduction of chlorate into the incubation medium, while having no effect on the protein synthesis as evidenced by [³H]proline incorporation, caused at its optimal concentration of 2 mM a 90% decrease in mucin sulfation and a 40% drop in mucin glycosylation. Evaluation of mucin molecular forms distribution indicated the predominance of the high molecular mucin form in the interacellular fraction and the low molecular mucin from in the extracellular fraction. Increase in medium sulfate caused an increase in the high molecular weight mucin form in both fractions, and this effect was inhibited by chlorate. Also, higher medium sulfate concentrations led to a higher degree of sulfation in the high molecular weight mucin form, the effect of which was inhibited by chlorate. The results suggest that the sulfation process is an early event taking place at the stage of mucin subunit assembly and is required for mucin polymer formation. Hence, the disturbances in mucin sulfation process could be determinal to the maintenance of gastric mucus coat integrity.

4

Apoptosis in H.pylori infected gastric mucosa

86%

Stachura J., Bobrzynski A.

Journal of Physiology and Pharmacology. Supplement

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1997

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tom 48

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nr 1

5

Protective effect of gastric acid secretion in ammonia induced gastric lesions

86%

Warzecha Z., Dembinski A., Brzozowski T., Ceranowicz P., Niemiec J., Pajdo R., Walocha J., Konturek S. J.

Journal of Physiology and Pharmacology. Supplement

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1997

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tom 48

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nr 1

6

Influence of central and peripheral administration of pancreatic polypeptide on gastric mucosa growth

86%

Dembinski A., Warzecha Z., Ceranowicz P., Pawlik M., Dembinski M., Kabat K., Konturek S. J., Kownacki P., Hladki W., Pawlik W. W.

Journal of Physiology and Pharmacology

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2004

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tom 55

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nr 1,2

Previous studies have shown that pancreatic polypeptide (PP) inhibits exocrine pancreatic secretion. The aim of present study was to determine the influence of PP administration on gastric growth and blood flow. Methods: Study was performed on regularly fed, fasted or fasted and subsequently refed rats. Rats were treated with saline (intraperitoneally - i.p.), caerulein (0.24 nmol/kg/dose, i.p.), pentagastrin (0.38 µmol/kg/dose, i.p.) or PP (5 nmol/kg/dose, i.p. or 10 pmol/dose intracerebroventricularly - i.c.v.). Saline, caerulein, pentagastrin and PP were administered alone or in combination, 3 times daily during last 48 h of experiment. Results: Treatment with pentagastrin increased gastric mucosa weight, mucosal DNA synthesis and gastric blood flow in all group tested. Intraperitoneal and i.c.v administration of PP alone reduced mucosal DNA synthesis in regularly fed and refed animals, and decreased gastric blood flow in refed animals. Combination of PP i.p. or i.c.v plus pentagastrin significantly reduced the pentagastrin-evoked increase in gastric mucosa weight, gastric DNA synthesis and gastric blood flow in fasted animals, as well as regularly fed animals. In refed animals, influence of PP administration on the pentagastrin-evoked increase in gastric mucosa weight was weak and statistically insignificant, but still i.p or i.c.v administration of PP significantly reduced gastric blood flow and mucosal DNA synthesis in this group of animals. Administration of caerulein caused weak, but significant increase in gastric DNA synthesis, gastric mucosa weight and gastric blood flow in fasted rats. In regularly fed animals, caerulein significantly increased only gastric DNA synthesis and gastric blood flow. In fasted animals with subsequent refeeding, caerulein was without effect on parameters tested in the stomach. Neither i.p. nor i.c.v administration of PP affected the caerulein-evoked effects in the stomach. Conclusions: Peripheral and central administration of PP inhibits food- and pentagastrin-stimulated growth of gastric mucosa. Similar effects of low central doses of PP as the high peripheral doses of PP suggests a crucial role of the central nervous system in the inhibitory effect of PP on gastric mucosa growth.

7

Effects of indomethacin and rofecoxib on gastric mucosal damage in normal and Helicobacter pylori - infected Mongolian gerbils

86%

Kanatani K., Ebata M., Murakami M., Okabe S.

Journal of Physiology and Pharmacology

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2004

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tom 55

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nr 1,2

This study examined the effects of indomethacin and rofecoxib on normal and Helicobacter pylori (H. pylori)-infected gastric mucosa of Mongolian (M.) gerbils. M. gerbils (6-wk-old) were orally administered H. pylori (ATCC43504, 2×108 CFU/ml) after fasting for 24 hours. Beginning 3 mo after inoculation, indomethacin (2 mg/kg, s.c) or rofecoxib (10 mg/kg, p.o.) was administered once daily for 2 wk to the gerbils. At autopsy, gastric mucosal ulcer area, myeroperoxidase (MPO) activity, prostaglandin (PG) E2 synthesis, and H. pylori viability were determined. Histamine-stimulated gastric acid secretion was measured with the acute gastric fistula method. Histological study was performed with H&E staining. H. pylori infection caused severe mucosal damage and production of lymphoid follicles in the gastric submucosa. In H. pylori-infected gerbils, indomethacin aggravated the gastric mucosal damage induced by H. pylori infection. Furthermore, indomethacin by itself induced gastric ulcers at an incidence of 6/10. In contrast, rofecoxib did not aggravate the H. pylori-induced mucosal damage. Indomethacin and rofeocoxib significantly reduced H. pylori viability. MPO activity was significantly increased in H. pylori-infected gerbils compared with H. pylori-uninfected gerbils. Indomethacin and rofecoxib reduced MPO activity in H. pylori-infected gerbils. PGE2 synthesis was markedly increased in H. pylori-infected gerbils (approximately 3-times) compared with the normal gerbils. Indomethacin significantly inhibited PGE2 synthesis in the gastric mucosa, both in normal and H. pylori-infected gerbils. Rofecoxib did not reduce PGE2 synthesis in normal gerbils, however, PGE2 synthesis was reduced to normal levels in H. pylori-infected gerbils. In H. pylori-infected gerbils, histamine-stimulated gastric acid secretion was reduced compared with normal gerbils. Indomethacin significantly increased histamine-stimulated gastric acid secretion and rofecoxib tended to increase secretion in H. pylori-infected gerbils. It was concluded that indomethacin enhances development of gastric mucosal damage in normal gerbils and aggravates H. pylori-induced gastric damage, resulting in gastric ulcers. Rofecoxib did not induce gastric damage in normal gerbils and did not aggravate damage in H. pylori-infected gerbils, suggesting that rofecoxib is less damaging to the stomach than indomethacin.

8

The electrolyte barrier of the gastric mucosa and the barrier breakers

86%

Szlachcic A., Dziadus-Sokolowska A.

Biophysics of Membrane Transport

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1994

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tom 12

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nr 2

9

Heat shock protein 70 (HSP70) in gastric adaptation to aspirin in Helicobacter pylori infection

86%

Konturek J. W., Fischer H., Konturek P. C., Huber V., Boknik P., Luess H., Neumann J., Brzozowski T., Schmitz W., Hahn E. G., Domschke W., Konturek S. J.

Journal of Physiology and Pharmacology

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2001

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tom 52

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nr 1

10

Helicobacter pylori infection in patients with rosacea

86%

Ciesla B., Raszeja-Kotelba B., Klincewicz H., Majewski P.

Journal of Physiology and Pharmacology. Supplement

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1997

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tom 48

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nr 1

11

Modulation of gastric mucosal calcium channels activity by platelet-derived growth factor

86%

Slomiany B. L., Liu J., Fecete Z., Piotrowski J., Slomiany A.

Journal of Physiology and Pharmacology

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1992

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tom 43

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nr 4

A dihydropyridine-sensitive gastric mucosal calcium channels were isolated from the solubilized epithelial cell membranes by affinity chromatography on wheat germ agglutinin. The channels following labeling the calcium antagonist receptor site with [³H]PN200-100 were reconstituted into phospholipid vesicles which exhibited active ⁴⁵Ca²⁺ uptake as evidenced by La³⁺ displacement assays. The uptake of calcium was independent of sodium and potassium gradients indicating the electroneutral nature of the process. The channels responded in a dose dependent manner to dihydropyridine calcium antagonist, PN200-110, which at 0.5/zm exerted maximal inhibitory affect of 66% on ⁴⁵Ca²⁺ uptake, while a 52% enhacement in ⁴⁵Ca²⁺ uptake occurred with a specific calcium channel activator, BAY K8644. On platelet-derived growth factor (PDGF) binding in the presence of ATP, channel protein showed an increase in tyrosine phosphorylation of 55 and 170 kDa calcium channel proteins. Such phosphorylated channels following reconstitution into vesicles displayed a 78% greater ⁴⁵Ca²⁺ uptake. The results demonstrate the importance of PDGF in the regulation of gastric mucosal calcium uptake.

12

Ghrelin - a new gastroprotective factor in gastric mucosa

86%

Konturek P. C., Brzozowski T., Pajdo R., Nikiforuk A., Kwiecien S., Harsch I., Drozdowicz D., Hahn E. G., Konturek S. J.

Journal of Physiology and Pharmacology

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2004

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tom 55

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nr 2

Ghrelin, a novel peptide expressed in the gastrointestinal tract, especially in the gastric mucosa, exerts several biological activities including the stimulation of appetite and food intake, the stimulation of intestinal motility and the release of growth hormone. The aim of this study was to examine the expression of ghrelin in gastric mucosa after its exposure to ethanol and its effects on gastric lesions induced by ethanol with and without pretreatment with indomethacin. Acute gastric lesions were induced by intragastric administration of 75% ethanol in rats pretreated with saline-vehicle or ghrelin injected intraperitoneally (i.p.) without or with i.p. pretreatment with indomethacin. At the end of experiments, the rats were anesthetized, the stomach was exposed to measure gastric blood flow (GBF), to determine the area of gastric lesions and to take biopsy samples from the oxyntic mucosa for determination of transcripts of ghrelin, tumor necrosis alpha (TNF-alpha) and transforming growth factor alpha (TGFalpha) using RT-PCR and to assess the generation of PGE2 by RIA. Exposure of gastric mucosa to 75% ethanol resulted in numerous mucosal lesions of an area of about 115 mm2 and in the increase of mucosal expression of TNF-alpha, PGE2, TGFalpha and ghrelin with concomitant decrease in GBF. Exogenous ghrelin reduced dose-dependently acute gastric lesions with simultaneous attenuation of GBF and a decrease in the expression of TNF-alpha but not TGFalpha. Pretreatment with indometahcin, which suppressed the generation of PGE2 by about 85%, augmented ethanol-induced gastric lesions and eliminated the ghrelin-induced protection of mucosa against ethanol. We conclude that ghrelin, whose mucosal expression is enhanced after exposure to ethanol, exhibits a strong gastroprotection, at least in part, due to its anti-inflammatory action mediated by prostaglandins.

13

Effects of prostaglandins on [Ca2] and adenylate cyclase activity in isolated porcine gastric mucous cells

86%

Heim H. K., Bersimbaev R. I., Gandjour A., Beil W., Sewing K. F.

Journal of Physiology and Pharmacology

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1994

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tom 45

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nr 2

14

Actions and interactions of endothelins, prostacyclin and nitric oxide in the gastric mucosa

86%

Whittle B. J. R., Lopez-Belmonte J.

Journal of Physiology and Pharmacology

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1993

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tom 44

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nr 2

15

Mucosal adenosine deaminase activity and stump ulcer healing

86%

Namiot Z., Namiot A., Stasiewicz J., Marcinkiewicz M., Jaroszewicz W., Gorski J.

Journal of Physiology and Pharmacology

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1995

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tom 46

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nr 2

16

Melatonin and its precursors L-tryptophan prevent acute gastric mucosal damage induced by aspirin in humans

86%

Konturek P. C., Celinski K., Slomka M., Cichoz-Lach H., Burnat G., Naegel A., Bielanski W., Konturek J. W., Konturek S. J.

Journal of Physiology and Pharmacology. Supplement

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2008

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tom 59

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nr 2

Melatonin (MT) and its precursor L-tryptophan (Trp) are implicated in the protection of gastric mucosa against noxious agents. However, the role of MT and Trp on the gastric mucosal injury induced by aspirin (ASA) in human has not been investigated. Studies in animals showed that both MT and Trp given intragastrically prevents the formation of gastric mucosal lesions induced by ASA. The aim of the present study was to determine the influence of MT and Trp given orally to healthy humans on gastric mucosal lesions induced by ASA. The present study included 21 healthy, Hp-negative male volunteers with intact gastro-duodenal mucosa aging 20-50 yr. They were divided in 3 groups; group1: 7 volunteers receiving daily 2 x 1g ASA (Polfa, Rzeszow) during 11 days; group 2: 7 healthy volunteers receiving 2x1g ASA and MT (Lekam, Zakroczyn) (5 mg 30 min prior to ASA) during 11 days and group 3: 7 healthy volunteers receiving 2x1g ASA and Trp (Ardeytropin, Germany) (0.5 g 30 min prior to ASA) during 11 days. Mucosal damage was evaluated at 3rd, 7th and 11th days of ASA administration by endoscopy using Lanza score. Plasma melatonin was measured using RIA and gastric mucosal generation of PGE2 was assessed also by RIA. ASA caused marked mucosal injury at all days of its administration except day 11th when only moderate lesions were evident. Pre-treatment with MT or Trp alone was accompanied by a significant decrease in gastric mucosal lesion score. Gastric mucosal generation of PGE2 was suppressed by about 90% in subjects treated with ASA without or with MT or Trp. We concluded that: MT and its precursor Trp significantly attenuate gastric mucosal lesions induced by aspirin. The action of Trp may be be mediated by MT produced in gastrointestinal tract from Trp. The gastroprotective action of MT and Trp is independent on gastric mucosal PGE2 generation.

17

Helicobacter pylori inhibits expression of heat shock protein 70 (HSP70) in human epithelial cell line. Importance of Cag A protein

86%

Targosz A., Pierzchalski P., Krawiec A., Szczyrk U., Brzozowski T., Konturek S. J., Pawlik W. W.

Journal of Physiology and Pharmacology

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2006

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tom 57

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nr 2

Heat shock proteins (HSP) are crucial for the maintenance of cell integrity under normal cell growth and at pathophysiological conditions such as colonization of gastric mucosa by Helicobacter pylori (Hp). The effect of Hp on mRNA expression for HSP70 in the gastric epithelial cells in vitro has been little studied and remains inconclusive. In this study we attempted to determine the alterations in gene expression for HSP70 induced by two live strains of Hp in the epithelial MKN7 cells. The following Hp strains were employed; 1) Hp strain expressing cagA and vacA, and 2) cagA and vacA negative Hp strain without or with addition of exogenous recombinant protein CagA. MKN7 cells were incubated in a standard medium RPMI 1640 supplemented with 10% fetal bovine serum at 37°C with 5% CO2 and humidified atmosphere under basal condition or in a presence of Hp (1x109 CFU per dish) without or with the recombinant CagA (10 µg/ml of RPMI 1640 medium). After 3h, 24h and 48 h of incubation with Hp and in some experiments with the prolonged incubation time up to 72 h, the cells were harvested, the total cellular RNA was isolated and the expression of mRNA for HSP70 was determined by RT-PCR. The incubation of the MKN cells with CagA protein alone failed to affect significantly the expression of HSP70. In contrast, the strain Hp (cagA+, vacA+) inhibited in time-dependent manner the expression of mRNA for HSP70. When the MKN7 cells were coincubated with Hp (cagA+, vacA+) and exogenous CagA, the significant inhibition of the signal intensity for HSP70 mRNA was observed at 3 h and 24 h of incubation and these effects were followed by complete disappearance of the signal for HSP70 mRNA at 48 h. The incubation of MKN7 with Hp (cagA-, vacA-) also significantly attenuated the expression of HSP70 mRNA with the most pronounced inhibitory effect observed at 72 h of incubation with this Hp strain. Addition of the recombinant CagA to Hp (cagA-, vacA-) completely suppressed the expression of HSP70 at 48 h and 72 h after the end of incubation periods. We conclude that 1) both, Hp (cagA+, vacA+) and Hp (cagA-, vacA-) inhibit expression of HSP70 in MKN7 human gastric epithelial cells independently of the presence or absence of cagA gene, and that 2) recombinant CagA protein may exert biological activity in vitro via acceleration of inhibitory effect of Hp negative for Cag A and VacA on HSP70 expression in epithelial cells infected with this bacteria.

18

Vitamin A deficiency alters the bioelectric parameters and RNA content of rat gastric mucosa in vitro

86%

Ventura U., Ceriani T., Montini E., Romano M., Ricci V.

Journal of Physiology and Pharmacology

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2003

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tom 54

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nr 4

The present study was aimed to investigate the mechanisms by which vitamin A plays a role in maintaining the efficiency of gastric mucosal barrier. Particularly, we measured electrical parameters and the RNA/DNA ratio of gastric mucosa isolated in vitro from the stomach of rats in which vitamin A-deficiency was induced by means of a vitamin A-free diet and then abolished by means of a massive vitamin A supplementation. Pair-fed vitamin A-nondepleted rats and normal rats fed ad libitum on a standard diet served as controls. Vitamin A status was assayed for each group of rats by measuring the hepatic content of vitamin A. We found that in gastric mucosa vitamin A-deficiency induced: 1) a decrease in both transmucosal potential difference and short-circuit current; 2) an increase in transmucosal electrical resistance; 3) a decrease in RNA content resulting in a decreased RNA/DNA ratio. Abolishment of vitamin A-deficiency restored both electrical parameters and RNA content of rat gastric mucosa. Our results stress the role of vitamin A in maintaining the efficiency of the gastric mucosal barrier. Vitamin A seems to act by stabilizing gastric electrical parameters and by controlling the protein synthesis/turnover in the surface gastric mucosal cells.

19

Venous outflow system in rabbit gastric mucosa

86%

Moskalewski S., Biernacka-Wawrzonek D., Klimkiewicz J., Zdun R.

Folia Morphologica

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2004

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tom 63

|

nr 2

The purpose of this work was to compare the organisation of the gastric mucosal venous system in larger animals, exemplified by rabbits, with that of the rat and the hamster which we have described previously. Rabbits were given atropine and hexamethonium followed by intravital ligation of all veins draining the stomach, causing strong hyperaemia. The distribution of vessels was studied in the non-mounted mucosa, in mounts of mucosa cleared in light mineral oil and in paraffin or semi-thin plastic sections. We found that blood from rabbit gastric mucosa is drained by collecting venules, running from the subepithelial layer towards the muscularis mucosae. The collecting venules join the paramuscular vessels parallel and adjacent to the muscularis mucosae. Neighbouring venules form numerous arcade-like connections and gradually enlarge. Two venules and an arteriole form triplets initially situated at the luminal face of the muscularis mucosae and gradually passing onto its abluminal surface. In rats vascular triplets were absent and the collecting venules drained into paramuscular vessels joining submucosal veins. In hamsters both connections between paramuscular vessels and submucosal veins and the passing of vascular triplets across muscularis mucosae were observed. Contraction/relaxation of the muscularis mucosae may regulate the amount of blood in the venous system of the mucosa and change the intramucosal pressure, affecting movement of the tissue fluid and, indirectly, the function of the gastric cells.

20

Influence of the stimulation of central chemoreceptors on the gastric mucosal blood flow in artificially ventilated and spontaneously breathing rats

86%

Sinski M., Kowalczyk P., Stolarczyk A., Sawionek L., Przybylski J.

Journal of Physiology and Pharmacology

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2003

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tom 54

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nr 4

Respiratory failure coincides frequently with the occurrence of gastric ulceration. In advanced respiratory insufficiency hypoxemia is often accompanied by hypercapnia, which is the stimulus for central chemoreceptors as well as for carotid body chemoreceptors. The purpose of the work was to investigate the reflex effect of stimulation of central chemoreceptors on gastric mucosal blood flow (GMBF) in the rat. Central chemoreceptors were stimulated by a gas mixture composed of 10% carbon dioxide, 50% oxide and 40% nitrogen. In artificially ventilated and spontaneously breathing animals, the stimulation of central chemoreceptors caused a significant increase in gastric mucosal vascular resistance, accompanied by a marked decline in blood flow. We hypothesize that in patients with respiratory insufficiency accompanied by hypercapnia, the reflex impairment of GMBF may contribute to gastric ulceration.

Ograniczanie wyników

Regulation of gastric mucosal calcium channel activity by an antiulcer agent, ebrotidine

The presence of Helicobacter-like microorganisms in the gastric mucosa in dogs

Role of sulfation in the processing of gastric mucins

Apoptosis in H.pylori infected gastric mucosa

Protective effect of gastric acid secretion in ammonia induced gastric lesions

Influence of central and peripheral administration of pancreatic polypeptide on gastric mucosa growth