What is the primary effect of inhaled nitric oxide (iNO) on pulmonary vasculature?

The primary effect of inhaled nitric oxide (iNO) on pulmonary vasculature is to cause selective pulmonary vasodilation. Nitric oxide (NO) is a potent vasodilator, meaning it causes blood vessels to relax and widen. When inhaled, NO selectively dilates the pulmonary blood vessels in the ventilated regions of the lung. This localized vasodilation improves ventilation-perfusion (V/Q) matching. V/Q matching refers to the relationship between the amount of air reaching the alveoli (ventilation) and the amount of blood flow through the pulmonary capillaries (perfusion). In certain conditions, such as acute respiratory distress syndrome (ARDS) or persistent pulmonary hypertension of the newborn (PPHN), pulmonary vasoconstriction can lead to increased pulmonary artery pressure and impaired gas exchange. By selectively dilating pulmonary blood vessels in ventilated areas, iNO redirects blood flow away from poorly ventilated or non-ventilated areas of the lung and towards well-ventilated areas, where gas exchange can occur more effectively. This reduces intrapulmonary shunting (blood passing through the lungs without picking up oxygen) and improves arterial oxygenation. The effect of iNO is localized to the pulmonary vasculature because NO is rapidly inactivated by hemoglobin in the blood. This prevents systemic vasodilation and limits the effects of iNO to the lungs. While iNO can improve oxygenation and reduce pulmonary artery pressure, it does not treat the underlying cause of the pulmonary hypertension or V/Q mismatch.