pgi2 การใช้

• It does not inhibit platelet aggregation, where PGI2 does.
• Prostaglandins, specifically PGE2 and PGI2, are important in inflammation and have been implicated in promoting apical resorption.
• More importantly, PGI2 ( and not nitrous oxide ) is also associated with an improvement in splanchnic perfusion and oxygenation.
• Apo A1 was also isolated as a prostacyclin ( PGI2 ) stabilizing factor, and thus may have an anticlotting effect.
• Thus, the protective anticoagulative effect of PGI2 is removed, increasing the risk of thrombus and associated heart attacks and other circulatory problems.
• Udvary E, Vegh A, Szekeres L . 7-oxo-PGI2 induced late protective action from arrhythmias due to local myocardial ischemia.
• Thus, the protective anti-coagulative effect of PGI2 is decreased, increasing the risk of thrombus and associated heart attacks and other circulatory problems.
• Inhibition of PTGS1 ( COX-1 ) reduces the basal production of cytoprotective PGE2 and PGI2 in the stomach, which may contribute to gastric ulceration.
• These metabolites contain two double bonds and are named series 2 prostanoids, i . e . PGD2, PGE2, PGF2?, PGI2, TXA2 and PGH2.
• There is indirect evidence for a second PGI2 receptor in BEAS-2B human airway epithelial cells but this finding has not been collaborated and the putative receptor has not been otherwise defined.
• Prostacyclin  PGI2, an arachadonic acid derived lipid mediator ( Epoprostenol, Flolan, Treprostenil )  is a vasodilator and, at the same time, the most potent inhibitor of platelet aggregation.
• Endothelial cells lining the microvasculature in the body are proposed to express PTGS2, and, by selectively inhibiting PTGS2, prostaglandin production ( specifically, PGI2; prostacyclin ) is downregulated with respect to thromboxane levels, as PTGS1 in platelets is unaffected.
• The underlying mechanism for the deleterious effect proposes that endothelial cells lining the microvasculature in the body express COX-2, whose selective inhibition results in levels of prostaglandin I2 ( PGI2, prostacyclin ) down-regulated relative to thromboxane ( since COX-1 in platelets is unaffected ).
• By mechanisms yet to be clearly identified, the two LX's also : a ) stimulate the bacteria-killing capacity of leukocytes and airway epithelial cells; b ) block production of the pro-inflammatory cytokine, TNF?, while increasing production of the anti-inflammatory cytokine, CCR5 by T lymphocytes; c )'enhance the ability of monocytes and macrophages to phagocytos ( i . e . ingest ) and thereby remove potentially injurious apoptotic neutrophils and eosinophils from inflammatory sites ( see Efferocytosis ) either by direct effecting these cells or by stimulating NK cells to do so; d ) cause various cell types to reduce production of pro-inflammatory reactive oxygen species and expression of Cell adhesion molecules and increase production of the platelet inhibitor, PGI2 and the vasodilator, nitric oxide; e ) inhibit production of pro-inflammatory cytokines by mesangial cells, fibroblasts, and other pro-inflammatory cell types; and f ) reduce perception of pain due to inflammation.