Inhaled nitric oxide reduces pulmonary transvascular albumin flux in patients with acute lung injury

Abstract

Background: In acute lung injury, when pulmonary microvascular permeability is enhanced, transvascular fluid filtration mainly depends on pulmonary capillary pressure. Inhaled nitric oxide has been shown to decrease pulmonary capillary pressure. Therefore, the effect of inhaled nitric oxide at a concentration of 40 ppm on pulmonary transvascular albumin flux was studied in nine patients with acute lung injury. Methods: Transvascular albumin flux was measured by a double radioisotope method using 99mTc- labeled albumin and 51Cr-labeled autologous red blood cells. Radioactivity of both isotopes was externally measured over the right lung by a gamma scanner and simultaneously in arterial blood. The normalized ratio of 99mTc/51Cr lung to 99mTc/51Cr blood (normalized index) was calculated. The normalized slope index which is the slope of the regression line of the normalized index versus time represents the accumulation rate of albumin in the interstitial space of the lungs. Normalized slope index and pulmonary capillary pressure were determined before, during, and after inhalation of 40 ppm nitric oxide. Pulmonary capillary pressure was estimated using the visual analysis of the pressure decay curve after pulmonary artery occlusion. Results: Normalized slope index decreased from 0.0077 ± 0.0054 min-1 (SD) off nitric oxide to -0.0055 ± 0.0049 min-1 (P < 0.01) during nitric oxide and increased to 0.0041 ± 0.0135 min-2 after nitric oxide. Pulmonary capillary pressure declined from 24 ± 4 mmHg off nitric oxide to 21 ± 4 mmHg during nitric oxide (P < 0.01), whereas pulmonary artery wedge pressure and cardiac output did not change. Conclusions: It is concluded that 40 ppm inhaled nitric oxide decreases pulmonary transvascular albumin flux in patients with acute lung injury. This effect may be the result of the decrease in pulmonary capillary pressure.