Since PGI2 is primarily produced in a nucleated endothelial cell, the COX inhibition by NSAID can be overcome with time by increased COX gene activation and subsequent production of more COX enzymes to catalyze the formation of PGI2. In contrast, TXA2 is released primarily by anucleated platelets, which are unable to respond to NSAID COX inhibition with additional transcription of the COX gene because they lack DNA material necessary to perform such a task. This allows NSAIDs to result in PGI2 dominance that promotes circulation and retards thrombosis. In patients with pulmonary hypertension, inhaled epoprostenol reduces pulmonary pressure, and improves right ventricular stroke volume in patients undergoing cardiac surgery. A dose of 60 μg is hemodynamically safe, and its effect is completely reversed after 25 minutes. No evidence of platelet dysfunction or an increase in surgical bleeding after administration of inhaled epoprostenol has been found. The drug has been known to cause flushing, headaches and hypotension. Synthesis
Biosynthesis
Prostacyclin is produced in endothelial cells, which line the walls of arteries and veins, from prostaglandin H2 (PGH2) by the action of the enzyme prostacyclin synthase. Although prostacyclin is considered an independent mediator, it is called PGI2 (prostaglandin I2) in eicosanoid nomenclature, and is a member of the prostanoids (together with the prostaglandins and thromboxane). PGI2, derived primarily from COX-2 in humans, is the major arachidonate metabolite released from the vascular endothelium.
MRI findings associated with placenta accreta include dark T2 bands, bulging of the uterus, and loss of the dark T2 interface.Although there are isolated case reports of placenta accreta being diagnosed in the first trimester or at the time of abortion <20 weeks gestational age, the predictive value of first-trimester ultrasound for this diagnosis remains unknown. Women with a placenta previa or "low-lying placenta" overlying a uterine scar early in pregnancy should undergo follow-up imaging in the third trimester with attention to the potential presence of placenta accreta. Complications
Damage to local organs (e.g., bowel, bladder, uterus and neurovascular structures in the retroperitoneum and lateral pelvic sidewalls from placental implantation and its removal;
Postoperative bleeding requiring repeated surgery;
Amniotic fluid embolism;
Complications (such as dilutional coagulopathy, consumptive coagulopathy, acute transfusion reactions, transfusion-associated lung injury, acute respiratory distress syndrome, and electrolyte abnormalities) caused by transfusion of large volumes of blood products, crystalloids, and other volume expanders;
Postoperative thromboembolism, infection, multisystem organ failure, and maternal death.The exact incidence of maternal mortality related to placenta accreta and its complications is unknown, but it is significant, especially if the urinary bladder is involved

Treatment
Treatment may be delivery by caesarean section and abdominal hysterectomy if placenta accreta is diagnosed before birth. Oxytocin and antibiotics are used for post-surgical management. When there is partially separated placenta with focal accreta, best option is removal of placenta. If it is important to save the womans uterus (for future pregnancies) then resection around the placenta may be successful.