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Prostacyclin – PGI2, an arachidonic acid derived lipid mediator (Epoprostenol, Flolan, Treprostenil) – is a vasodilator and, at the same time, the most potent inhibitor of platelet aggregation. [30] More importantly, PGI2 (and not nitrous oxide) is also associated with an improvement in splanchnic perfusion and oxygenation. [31]
Until the 1980s, nitric oxide, a product of fossil fuel combustion, was thought only to play a role the detrimental effects of air pollution on the respiratory tract. [17] In 1987, experiments with coronary arteries showed that nitric oxide was the long sought endothelium-derived relaxing factor.
Inhaled nitric oxide is a gas that is inhaled. [1] It was initially described in 1987 as an "endothelial-derived relaxing factor" and has since been used to treat pulmonary disorders. [3] It works by relaxing smooth muscle to widen (dilate) blood vessels, especially in the lungs. [1] Inhaled nitric oxide selects only pulmonary smooth muscles.
The criteria for vasoreactivity have changed. Only those patients whose mean pulmonary artery pressure falls by more than 10 mm Hg to less than 40 mm Hg with an unchanged or increased cardiac output when challenged with adenosine, epoprostenol, or nitric oxide are considered vasoreactive. [70]
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Nitric oxide is absorbed systemically after inhalation. Most of it moves across the pulmonary capillary bed where it combines with hemoglobin that is 60% to 100% oxygen-saturated. Nitrate has been identified as the predominant nitric oxide metabolite excreted in the urine, accounting for >70% of the nitric oxide dose inhaled.
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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. [12] The drug has been known to cause flushing, headaches and hypotension. [13]
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