Prostaglandins production

Prostaglandins, through their effects on mucous cell secretion, basal bicarbonate secretion, and mucosal growth, are important factors in gastric healing and protection. Inhibition of prostaglandin production by NSAIDs compromises these important protective mechanisms. Finally, the antiplatelet effects of NSAIDs may worsen bleeding complications associated with PUD. 

Acetaminophen is a centrally acting analgesic that produces analgesia by inhibiting prostaglandin production in the brain and spinal cord. It is an effective and inexpensive analgesic with a favorable risk-benefit profile.9 It should be tried initially at an adequate dose and duration before considering an... 

Neutrophils, lymphocytes, and monocytes are attracted to the area, and monocytes are converted to macrophages.18,19 The macrophages then stimulate additional prostaglandin production. Phagocytic cells and other players in the immune system release cytokines, including interleukins, interferon, and tumor necrosis factor. 

Kubata, B. K., el al (2007). Molecular basis for prostaglandin production in hosts and parasites. Trends Parasitol 23, 325-31. 

FIGURE 26.10 Superoxide- and NO-mediated stimulation of prostaglandin production. 

Alterations in mucosal defense induced by HP or NSAIDs are the most important cofactors in peptic ulcer formation. Mucosal defense and repair mechanisms include mucus and bicarbonate secretion, intrinsic epithelial cell defense, and mucosal blood flow. Maintenance of mucosal integrity and repair is mediated by endogenous prostaglandin production. 

The mechanism of action of mesalamine (and sulfasalazine) is unknown, but appears to be topical rather than systemic, and it is possible that mesalamine diminishes inflammation by blocking cyclooxygenase and inhibiting prostaglandin production in the colon. 

A. 17,20 lyase is required for androgen synthesis, cyclooxygenase for prostaglandin production, 11- 3-hydroxysteroid dehydrogenase-2 acts as a reductase-converting cortisol to its inactive 11-keto derivative cortisone, whereas 18-hydroxylase is required for aldosterone production. 

Release of oxytocin at this stage of parturition promotes prostaglandin production, particularly of the E and F series, within the decidua these prostaglandins are powerful myometrial stimulants and thus further enhance uterine contractions. The prostaglandin concentration in maternal serum and amniotic fluid increases with the progression of labor. 

Evans. Isolation from Cannabis sativa L. of cannflavin—A novel inhibitor of CS040 prostaglandin production. Biochem Pharmacol 1985 34(11) 2019-2024-GS028 Barrett, M. L., A. M. Scutt and F. J. 

Mechanism of Action A 5-aminosalicylic acid derivative that changes intestinal microflora, altering prostaglandin production and inhibiting function of natural killer cells, mast cells, neutrophils, and macrophages. Therapeutic Effect Diminishes inflammatory effect in colon. 

Mechanism of Action A salicylic acid derivative that locally inhibits arachidonic acid metabolite production, which is increased in patients with chronic inflammatory bowel disease. Therapeutic Effect Blocks prostaglandin production and diminishes inflammation in the colon. 

Mechanism of Action Asalicylicacidderivativethat isconvertedtomesalamineinthe colon by bacterial action. Blocks prostaglandin production in bowel mucosa. Therapeutic Effect Reduces colonic inflammation in inflammatory bowel disease. Pharmacokinetics Small amount absorbed. Protein binding 99%. Metabolized by bacteria in the colon. Minimal elimination in urine and feces. Half-life 0.9 hr. 

The action of thiazides depends in part on renal prostaglandin production. As described for loop diuretics, the actions of thiazides can also be inhibited by NSAIDs under certain conditions. 

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