Endogenous cell-signaling molecule produced from l-arginine by NO synthases. Causes vasodilation of smooth muscle cells and inhibition of platelet aggregation and adhesion. Selectively dilates the pulmonary vasculature.
persistent pulmonary hypertension of the newbornevaluation of pulmonary vasodilating capacity (during cardiac catheterization)determination of diffusion capacity (DL) across the alveolar-capillary unitpersistent PH of the newbornacute hypoxemic respiratory failureacute vasodilator testing in adult patients with PAH
Metabolism
Rapid inactivation by hemoglobin binding and oxidation to nitrite, which interacts with oxyhemoglobin to form nitrate and met-hemoglobin.
Excretion
Nitrate (predominant metabolite, >70% of dose) excreted in urine.
Common
platelet inhibitionnoisy breathinghematuriaatelectasis
Serious
- pulmonary toxicity (with levels >50–100 ppm)
- methemoglobinemia
- potential to further impair left ventricular performance (in patients with impaired left ventricle function)
- lethal at high doses (500–1000 ppm)
- elevations in methemoglobin
- pulmonary toxicities associated with inspired NO2 (including acute respiratory distress syndrome)
- reduced O2 delivery capacity of circulation (due to methemoglobinemia)
Nitrous AcidSevere
Database
Clinical effect not specified
Source: DDInter
Clinical effect not specified
Source: DDInter
8 additional low-confidence interactions hidden — those rows lack a documented mechanism or management plan in our sources.