Drugs such as alprostadil, a PGE-1 analog, can be used to keep a PDA open until the primary defect is corrected surgically. Prognosis
If left untreated, the disease may progress from left-to-right shunt (acyanotic heart) to right-to-left shunt (cyanotic heart), called Eisenmengers syndrome. Pulmonary hypertension is a potential long-term outcome, which may require a heart and/or lung transplant. Another complication of PDA is intraventricular hemorrhage. History
Robert Edward Gross, MD performed the first successful ligation of a patent ductus arteriosus on a seven-year-old girl at Childrens Hospital Boston in 1938. Adult
Since PDA is usually identified in infants, it is less common in adults, but it can have serious consequences, and is usually corrected surgically upon diagnosis. See also
George Alexander Gibson

References
External links
Patent Ductus Arteriosus Causes from US Department of Health and Human Services
Patent Ductus Arteriosus from Merck
Patent ductus arteriosus information for parents.
It was developed by Trophos company and currently is in Phase I clinical trial. Stem cell therapy
Recent investigations suggest a possible beneficial effect of mesenchymal stem cells on heart and kidney reperfusion injury. Superoxide dismutase
Superoxide dismutase is an effective anti-oxidant enzyme which converts superoxide anions to water and hydrogen peroxide. Recent researches have shown significant therapeutic effects on pre-clinical models of reperfusion injury after ischemic stroke. Metformin
A series of 2009 studies published in the Journal of Cardiovascular Pharmacology suggest that Metformin may prevent cardiac reperfusion injury by inhibition of Mitochondrial Complex I and the opening of MPT pore and  in rats. Riboflavin
In neonatal in vivo model of brain ischemia/reperfusion, tissue  injury can be alleviated by the administration of FMN precursor, riboflavin that prevents inactivation of mitochondrial complex I.

Cannabinoids
A study published in 2012 show that the synthetic analogue of the phytocannabinoid Tetrahydrocannabivarin (THCV), Δ8-Tetrahydrocannabivarin (Δ8-THCV) and its metabolite 11-OH-Δ8-THCV, prevent hepatic ischaemia/reperfusion injury by decreasing oxidative stress and inflammatory responses through cannabinoid CB2 receptors and thereby decrease tissue injury and inflammation with a protective effect against liver damage. Pretreatment with a CB2 receptor antagonist attenuated the protective effects of Δ8-THCV, while a CB1 antagonist tended to enhance it.An earlier study published in 2011 found, that Cannabidiol (CBD) also protects against hepatic ischemia/reperfusion injury by attenuating inflammatory signaling and response of oxidative and nitrative stress, and thereby cell death and tissue injury, but independent from classical CB1 and CB2 receptors.