Production and action of local mediators in the rat gastric mucosa.

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Aston University. Department of Pharmaceutical Science , Birmingham
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Production and action of local mediators in the rat. Production and action of local mediators in the rat gastric mucosa. (Thesis) Brown JF. Publisher: University of Aston in Birmingham [] Metadata Source: The British Library Type: Thesis. Abstract. Highlight Terms No biological terms identified No abstract supplied.

Abstract. A technique for examination of the rat gastric mucosa by the use of a flexible endoscope was described. The procedure does not require prior surgery and can be repeated over long time periods making it specifically useful for evaluation of chronic : G.

Salmon. A technique for the close‐arterial administration of substances to the rat stomach in vivo has been developed. Intra‐arterial infusion of platelet‐activating factor (Paf, 10–50 ng kg −1 min −1 for 10 min) induced macroscopically assessed damage in the corpus mucosa, characterized as Cited by: Matsubara, Y., Ichinose, M., Tatematsu, M.

et al. () Stage specific elevated expression of the genes for hepatocyte growth factor, keratinocyte growth factor and their receptors during the morphogenesis and differentiation of rat stomach mucosa. Biochem. Biophys. Res. Commun.– PubMed CrossRef Google ScholarCited by: 2.

Abstract. Prostaglandins play an important role in preventing gastric mucosal injury, referred to as “gastric cytoprotection”. Although PGE 1 and PGE 2 inhibit gastric secretion, cytoprotection is considered independent of the antisecretory mechanism. PGE 2 and PGI 2 in gastric mucosa, have prevented gastric mucosal injury from various noxious stimuli.

This mucosal cell protection is. Morris GP, Keenan CM, MacNaughton WK, el al: Protection of rat gastric mucosa by s of luminal stasis and inhibition of prostaglandin synthesis. Am J Med 86(suppl 6A)–16, This paper describes the ability of sucralfate to maintain a pH gradient over the surface of the gastric mucosa at sites to which it is bound.

The effects of chronic mild restraint on the susceptibility of the rat gastric mucosa to ethanol or cold-restraint injury were studied. Gastric mucosas of animals subjected to chronic mild. The main aim of this review article has to summarize the ulcerogenic mechanisms of various mediators involved in Peptic ulcer disease.

the rat gastric mucosa is not action of solcoseryl in. RESULTS As is shown in Fig. 2, the gastric mucosa of several spe- PROSTAGLANDINS AND THE GASTRIC MUCOSA TABLE 1 FORMATION OF 6-oxo-PGF,a AND PGE, BY STRIPS OF GASTRIC MUCOSA FROM RAT AND RABBIT 6-oxo-PGF.a ng/g tissue PGE, Rat Rabbit 91 14 12 4 l 30 16 The tissue was incubated in vitro by vortex-mixing for l min and the levels of.

Description Production and action of local mediators in the rat gastric mucosa. FB2

CONCLUSION: The rat gastric mucosa responds to chronic superficial injury by down-regulation of acid secretory cells and gastrin secreting cells and an up-regulation of proliferating cells.

The appearance of a prominent layer of mucous neck-like cells may indicate a new secretory function for these cells. Starlinger M, Jakesz R, Matthews JB, et al: The relative importance of HCO-3 and blood flow in the protection of rat gastric mucosa during shock.

Gastroenterology –, One of the clearest in vivo demonstrations of the critical importance to the gastric mucosa of bicarbonate delivery via mucosal blood flow. Also notable is the in vivo demonstration that carbonic anhydrase activity. Characterization of labelled material secreted by a suspension of cells isolated from the rat gastric mucosa and preincubated with d-[6- 3 H]glucosamine Article Feb Within the subgroups of eicosanoids, one can also find examples of mediators that have opposing actions on a target tissue as well as examples in which there appears to be a redundancy of actions.

The biological actions of PGs in the gastrointestinal tract are diverse, including effects on blood flow, motility, and secretion. The role of endogenous prostaglandins (PGs) in adaptation of the rat gastric mucosa to chronic stress was examined.

After 10 days of chronic mild restraint (CMR), gastric mucosal damage induced by. The mechanisms through which NSAIDs produce damage in the stomach can be subdivided into local (topical) actions and systemic actions Prostaglandins as endogenous mediators of interleukin 1 production.

J Immunol –, PubMed Ito S. Rapid epithelial restitution of the rat gastric mucosa after ethanol injury. NO synthase activity could also be detected in the supernatants from homogenates of the underlying gastric muscle and also in the muscular forestomach ().The rate of formation of NO by extracts of rat gastric muscle and forestomach was ± and ± nmol min –1 g –1 tissue, respectively (n = 5).

The gastric mucosal formation of NO was inhibited in a concentration dependent. In contrast, SC potently inhibited PGE 2 production in stomach mucosa (ED 50 = mg/kg), as expected because COX-1 is the primary source of gastric mucosa PGs.

The results with SC indicated that COX-2 is responsible for PG production in the LPS-induced rat air pouch. Gastric acid is required for recurrence of gastric ulcers caused by IL-1beta, and gastric acid stimulates the inflammatory process in scarred mucosa during ulcer recurrence.

Discover the world's. Cells expressing IL-8 and iNOS were detected at the rat gastric mucosa as early as 1 h after indomethacin ingestion. The frequencies and intensities of these cells increased with time. Figure 4 shows the expression of IL-8 and iNOS in the serial sections of rat gastric mucosa 9 h after administration of indomethacin.

The isolated stomach was ligated at both ends, filled with ml of 2% formalin, and immersed in 2% formalin for 15 min. Then, the stomach was cut along the greater curvature, and the lengths of lesions on the stomach wall were measured using a millimeter scale with a magnifying glass.

The total length of lesions was used as a lesion index. Cyclooxygenase (COX), the key enzyme for synthesis of prostaglandins, exists in two isoforms (COX-1 and COX-2). COX-1 is constitutively expressed in the gastrointestinal tract in large quantities and has been suggested to maintain mucosal integrity through continuous generation of prostaglandins.

COX-2 is induced predominantly during inflammation. On this premise selective COX-2 inhibitors not. The stomach mucosa’s epithelial lining consists only of surface mucus cells, which secrete a protective coat of alkaline mucus.

A vast number of gastric pits dot the surface of the epithelium, giving it the appearance of a well-used pincushion, and mark the entry to each gastric gland, which secretes a complex digestive fluid referred to as gastric juice.

In humans, a variety of mediators/hormones and cell types are involved in acid production and regulation. 8 The stomach of a premature infant, let alone that of a term infant, produces gastric acid upon birth.

9–14 The physiological management of gastric acid, however, depends on age. Direct evidence of the presence of a surface pH gradient on top of gastric mucosa comes from numerous demonstrations of a pH gradient across the mucus layer.

This has been shown for human, rabbit, and amphibian gastric mucosa in vitro (, ) and for rat (,), canine, and human stomach in vivo (, ). Shay H, Komarov SA, Fels D., Meranze D., Gruenstein H., Siplet H. A simple method for the uniform production of gastric ulceration in the rat.

Gastroenterology. ; – Brodie DA. The mechanism of gastric hyperacidity produced by pylorus ligation in the rat. Am J. The mechanism of gastric mucosal damage and protection is yet unclear.

NO, an important gas signaling molecule, is a gastric mucosal protective factor that contributes significantly to maintaining normal gastric mucosal integrity. Gastric mucosa is composed of gastric. Herein, we report expression of TGF alpha mRNA in normal gastric mucosa of the adult guinea pig, rat, and dog.

Details Production and action of local mediators in the rat gastric mucosa. FB2

TGF alpha mRNA was also detected in matched surgically resected gastric mucosa and adjacent gastric carcinoma from 10 patients, and in gastric mucosa adjacent to a benign ulcer from an additional patient. Additionally, endogenous production of H 2 S in gastric mucosa has been increased in rats pretreated with donor of this gaseous mediator.

We assume that elevated H 2 S bioavailability caused by the administration of NaHS releasing H 2 S enhanced gastric mucosal resistance to oxidative I/R-induced gastric mucosal damage.

Role of COX-1 products. Early experimental studies established that the endogenous metabolites of arachidonic acid, prostaglandins, formed via the cyclo-oxygenase enzyme, now called COX-1, were involved as local physiological mediators or modulators of gastric mucosal function.8 Prostaglandins of the E and I series, PGE 2 and prostacyclin, respectively, are formed by gastric mucosal tissue.

Gastric ulcer is a painful lesion of the gastric mucosa which can be disabling, or even more very serious in the case of a perforation of the stomach and internal hemorrhage.

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Traditional pharmacopeias have shown the efficacy of various plant extracts in the treatment of this pathology.

Some extracts from Opuntia ficus indica (OFI) have been proven to have medicinal therapeutic benefits.The “cytoprotective” action of prostaglandins in preventing gastric erosions and ulceration is mainly brought about by endogenously produced prostacyclin and PGE 2 which reduce gastric acid secretion, exert a direct vasodilator action on the vessels of the gastric mucosa, and stimulate the secretion of viscous mucus and duodenal bicarbonate.Capsaicin, the pungent ingredient of the hot chili pepper, is known to act on the transient receptor potential cation channel vanilloid subfamily member 1 (TRPV1).

TRPV1 is involved in somatic and visceral peripheral inflammation, in the modulation of nociceptive inputs to spinal cord and brain stem centers, as well as the integration of diverse painful stimuli.