Inhaled nitric oxide lowers pulmonary capillary pressure and changes longitudinal distribution of pulmonary vascular resistance in patients with acute lung injury

In acute lung injury (ALI), where pulmonary microvascular permeability is increased, transvascular fluid filtration depends mainly on the hydrostatic capillary pressure. In the presence of intrapulmonary vasoconstriction pulmonary capillary pressure (PCP) may increase thereby promoting transvascular fluid filtration and lung oedema formation. We studied the effect of 40 ppm inhaled nitric oxide (NO) on PCP and longitudinal distribution of pulmonary vascular resistance (PVR) in 18 patients with ALI. PCP was estimated by visual analysis of the pressure decay profile following pulmonary artery balloon inflation. Contribution of venous pulmonary resistance to total PVR was calculated as the percentage of the pressure gradient in the pulmonary venous system to the total pressure gradient across the lung. Inhalation of 40 ppm NO produced a prompt decrease in mean pulmonary artery pressure (PAP) from 34.1 6.8 to 29.65.7 (s.d.) mmHg; ( P < 0.0001). PCP declined from 24.86.2 to 21.65.2 mmHg; ( P < 0.0001) while pulmonary artery wedge pressure (PAWP) did not change. PVR decreased from 16673 to 12850 dyn sec cm ‐5 ; ( P < 0.0001). Pulmonary venous resistance (PVRven) decreased to a greater extent (from 7641 to 5028 dyn. sec. cm ‐5 ; ( P < 0.001) than pulmonary arterial resistance (PVRart) (from 9036 to 7929 dyn sec cm ‐5 ; ( P < 0.01). The contribution of PVRven to PVR feU from 44.310.8 to 37.811.9%; ( P < 0.01). Cardiac output (CO) remained constant. The findings demonstrate that NO has a predominant vasodilating effect on pulmonary venous vasculature thereby lowering PCP in patients with ALI.