The "Pulmonary Arterial Hypertension (PAH) Market By Drug Class (
Prostacyclin And
Prostacyclin Analogs, Soluble Guanylate Cyclase (SGC) Stimulators, Endothelin Receptor Antagonists (ERA), Phosphodiesterase 5 (PDE-5)) And Segment Forecasts To 2025" report has been added to ResearchAndMarkets.com's offering.
In pre-eclampsia there is dominance of Thromboxane A2 over
prostacyclin that is strong vasoconstrictor.
Pulmonary edema complicating
prostacyclin therapy in pulmonary hypertension associated with scleroderma: A case of pulmonary capillary hemangiomatosis.
(1981) Spectral evidence for the cytochrome P450 nature of
prostacyclin synthetase.
The global scleroderma diagnostics and therapeutics market segmentation is based on indication (localized, systemic), test type (blood tests, electrocardiogram and echocardiogram, imaging techniques, pulmonary function tests, skin biopsy), drug class (calcium channel blockers, chelating agents, corticosteroids, endothelin receptor agonists, immunosuppressive agents, PDE-5 inhibitors,
prostacyclin analogues, ACE inhibitors, H2 blockers, proton pump inhibitors).
Seki, "An imbalance between
prostacyclin and thromboxane in relation to cerebral blood flow in neonates with maternal preeclampsia," Prostaglandins & Other Lipid Mediators, vol.
Many promising newer therapies like
prostacyclin analogue, endothelin receptor antagonist, phosphodiesterase inhibitors improve clinical function and haemodynamic measures.
James, Roles of cyclooxygenase (COX)-1 and COX-2 in prostanoid production by human endothelial cells: selective up-regulation of
prostacyclin synthesis by COX-2, The Journal of Immunology, 167(5), 2831-2838 (2001).
Prostacyclin's synthesis not affected by the turmeric mechanism of action which acts as a liposomal membranes stabilizer, activity of and leucotrienes and thromboxane inhibited, inhibitor for prostaglandin.
The short-term (eight to 12 weeks) use of IV or injected
prostacyclin has shown some benefits for treating pulmonary hypertension; however, evidence does not support its use on a long-term basis.
NSAIDs inhibit endothelial cyclooxygenase, thus inhibiting the conversion of arachidonic acid to prostaglandin H, and subsequent production of bioactive prostanoids, including thromboxane [A.sub.2] ([TxA.sub.2]) and
prostacyclin (PGI.,).