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Gastrointestinal tract, prostaglandins

Ulcer formation is the net result of a lack of homeostasis between factors within the gastrointestinal tract responsible for the breakdown of food (e.g., gastric acid and pepsin) and factors that promote epithelial defense and repair (e.g., bicarbonate, mucus secretion, and prostaglandins). [Pg.271]

Prostaglandins play critical roles in a number of physiological processes. These molecules regulate blood flow to organs, stimulate secretion of protective mucosal linings in the gastrointestinal tract, participate in the initiation of platelet aggrega-... [Pg.169]

Hormones transfer signals by migrating from their site of synthesis to their site of action. They are usually transported in the blood. In this case, they are said to have an endocrine effect (1 example insulin). By contrast, tissue hormones, the target cells for which are in the immediate vicinity of the glandular cells that produce them, are said to have a paracrine effect (2 example gastrointestinal tract hormones). When signal substances also pass effects back to the cells that synthesize them, they are said to have an autocrine effect (3 example prostaglandins). Autocrine effects are often found in tumor cells (see p. 400), which stimulate their own proliferation in this way. [Pg.372]

Wang D, Mann JR, DuBois RN The role of prostaglandins and other eicosanoids in the gastrointestinal tract. Gastroenterology 2005 128 1445. [PMID 15887126]... [Pg.416]

The effectiveness of ketoprofen at dosages of 100-300 mg/d is equivalent to that of other NSAIDs. In spite of its dual effect on prostaglandins and leukotrienes, ketoprofen is not superior to other NSAIDs in clinical efficacy. Its major adverse effects are on the gastrointestinal tract and the central nervous system (see common adverse effects above). [Pg.804]

Rofecoxib, a furanose derivative, is a potent, selective COX-2 inhibitor (Table 36-1). In the USA, rofecoxib is approved for osteoarthritis and rheumatoid arthritis, and it also appears to be analgesic and antipyretic—in common with other NSAIDs. This drug does not inhibit platelet aggregation and appears to have little effect on gastric mucosal prostaglandins or lower gastrointestinal tract permeability. At high doses it is associated with occasional edema and hypertension. Other toxicities are similar to those of other coxibs. [Pg.818]

Prostaglandins whose synthesis involves COX-1 are largely responsible for maintenance and protection of the gastrointestinal tract (inhibiting acid production and stimulating mucous production), while prostaglandins whose synthesis involves COX-2 are responsible for inflammation and pain. [Pg.223]

Indometacin is the best-known and most thoroughly tested indoleacetic acid derivative. It is one of the most effective NSAIDs, and most of its toxic and therapeutic effects appear to be due to marked inhibition of prostaglandin sjmthesis. Because of its potency, its clinical efficacy is comparable, if not superior, to any other NSAID, but for precisely the same reason its adverse effects on the gastrointestinal tract and the nervous system inevitably limit its use. However, patients who tolerate it reasonably well are naturally not anxious to exchange it for any newer drugs with fewer problems but less potency. A meta-analysis of patients preference in 37 crossover comparisons of indometacin with newer NSAIDs did not provide evidence of a trend to replace indometacin with newer NSAIDs (1). [Pg.1739]

The most prominent and frequent adverse effects of prostaglandins are those on the gastrointestinal tract. However, the most dangerous are likely to be the cardiovascular effects, which in predisposed patients can sometimes cause hfe-threatening collapse and heart failure. Hyperthermia and headache are frequent nervous... [Pg.2955]

Figure 14.2 The two isoforms of cyclooxygenase (COX1 and COX2) produce identical products but different effects. COX1 is constitutively produced in many tissues, such as the kidney and the gastrointestinal tract, whereas COX2 is an inducible enzyme produced primarily in inflammatory settings. The two isoforms are involved in production of eicosanoids that have various roles. PG, prostaglandin ... Figure 14.2 The two isoforms of cyclooxygenase (COX1 and COX2) produce identical products but different effects. COX1 is constitutively produced in many tissues, such as the kidney and the gastrointestinal tract, whereas COX2 is an inducible enzyme produced primarily in inflammatory settings. The two isoforms are involved in production of eicosanoids that have various roles. PG, prostaglandin ...
The mechanisms of ibuprofen-induced toxicity have not been clearly defined. Acute renal failure is postulated to result from decreased production of intrarenal prostaglandins via inhibition of the cyclooxygenase pathway. In turn, this will decrease the renal blood flow and glomerular filtration rate. Ibuprofen also interferes with prostaglandin synthesis in the gastrointestinal system that can contribute to its irritating effect on the mucosa of the gastrointestinal tract. [Pg.1377]

Pertwee RG (2001) Cannabinoids and the gastrointestinal tract. Gut 48 859-867 Pertwee RG, Ross RA (2002) Cannabinoid receptors and their hgands. Prostaglandins Leukot... [Pg.596]

Small doses of garlic are purported to increase the tone of smooth muscle in the gastrointestinal tract, while large doses decrease such actions (Tyler, 1993). An ethanol—chloroform extract of fresh bulb antagonized acetylcholine and prostaglandin E induced rat fundus smooth muscle contraction at a concentration of 0.002 mg/mL however, an ethanol extract of fresh garlic bulb caused rat fundus smooth muscle stimulation at a concentration of 0.016 mg/mL (Ross, 1998). [Pg.168]

Aspirin and the older nonselective NSAlDs inhibit both cyclooxygenase isoforms and thereby decrease prostaglandin and thromboxane synthesis throughout the body. Prostaglandins necessary for normal cell function are depleted, as well as prostaglandins involved in inflammation. Theoretically, the COX-2-selective inhibitors should have less effect upon the prostaglandins involved in normal cell function, particularly those in the gastrointestinal tract. [Pg.323]


See other pages where Gastrointestinal tract, prostaglandins is mentioned: [Pg.527]    [Pg.564]    [Pg.527]    [Pg.564]    [Pg.67]    [Pg.872]    [Pg.885]    [Pg.227]    [Pg.184]    [Pg.270]    [Pg.406]    [Pg.404]    [Pg.802]    [Pg.607]    [Pg.103]    [Pg.105]    [Pg.207]    [Pg.299]    [Pg.115]    [Pg.392]    [Pg.149]    [Pg.872]    [Pg.562]    [Pg.566]    [Pg.21]    [Pg.2957]    [Pg.823]    [Pg.1981]    [Pg.102]    [Pg.267]    [Pg.362]    [Pg.328]    [Pg.374]    [Pg.323]    [Pg.87]    [Pg.61]   
See also in sourсe #XX -- [ Pg.531 ]

See also in sourсe #XX -- [ Pg.531 ]




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Gastrointestinal tract

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