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Related to PGI2: prostaglandin, PGF2, PGD2


A prostaglandin produced in the walls of blood vessels that acts as a vasodilator and inhibits platelet aggregation.


(Biochemistry) biochem any of several prostaglandins produced in the blood vessels, causing vasodilation and inhibiting platelet aggregation


(ˌprɒs təˈsaɪ klɪn)

a prostaglandin, C20H32O5, that specifically inhibits the formation of blood clots.
[1975–80; prosta (te) + cycl (ic) + -in1, on the model of prostaglandin]
References in periodicals archive ?
Other promising treatment modalities include PGI2, magnesium sulphate, bosentan, adenosine, steroids and apocynin, but there is insufficient evidence to recommend any for routine or combination use (Table 7).
Abbreviations NO --nitric oxide EDRF --endothelium-derived relaxing factor NOS --nitric oxide synthase eNOS --endothelial nitric oxide synthase iNOS --inducible nitric oxide synthase nNOS --neuronal nitric oxide synthase MVE --microvascular endothelial TGF --transforming growth factor TNF-[alpha] --tumor necrosis factor cGMP --cyclic guanosine monophosphate ANG --angiotensin EE --endocardial endothelium ET-1 --endothelin-1 PGI2 --prostaglandin I2
By contrast, the effects of ET-1 on the ETB receptor result in the release of NO and PGI2 from the endothelium.
Tais efeitos devem-se a inibicao da COX-1, impedindo assim a sintese de prostaglandinas gastricas, especialmente PGI2 e PGE2 que agem como agentes citoprotetores da mucosa gastrica e tambem diminuem o adesivamento plaquetario aumentando o risco de sangramentos (MONTEIRO et.
Unlike ACE inhibitors, ARBs have no effects on bradykinin accumulation and do not induce NO and PGI2 via the B2 receptor.
Supernatant was collected and analyzed by using ELISA-kits for the vasodilatory prostaglandin(PG)E1, PGE2, and PGI2.
6) Unesterified arachidonate is converted via cyclooxygenase (COX)-1 and -2 to PGH2, which is converted to specific prostanoid end products, such as PGE2, PGF2[alpha], PGI2, PGD2, and thromboxane A2.
Effects of PGI2 and TxA2 analogs and inhibitors in orthodontic tooth movement.
TXA2 increases renal salt and fluid retention, increases blood pressure, and enhances myocardial and vascular remodeling, whereas PGI2 facilitates renal salt and fluid excretion and lowers systemic blood pressure.
The edema is potentiated by PGE2 and prostaglandin F2-alpha (PGF2-alpha), where PGI2 and PGE2 promote local blood flow, causing the localized warmth in the area of inflammation, but also allow for entry of inflammatory cells into the wound, which is due to increased vascular permeability (2).
Ademas se aumenta la formacion de prostaglandinas y la proporcion del prostanoide vasodilator PGI2 con relacion al vasoconstrictor Tromboxano A2 (TXA2) lo que conlleva a una vasodilatacion sistemica generalizada.