[Effect of endogenous and inhaled nitric oxide on pulmonary microcirculation]

The sites of action of endogenous and inhaled nitric oxide (NO) were reassured during hypoxic pulmonary vasoconstriction. Lungs of 21 adult cats were perfused in situ with autologous blood in zone-3 conditions. Capillary pressures were measured by the double-occlusion techniques and pressures in arterioles and venules 70-100 microns in diameter were measured by the servo-null micropuncture technique, both during normoxia (FiO2 = 0.3) and during hypoxia (FiO2 = 0.02). The effects of NG-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg), an inhibitor of NO synthase, and of inhaled NO (5-100 ppm) were also measured. The PO2 of the prefusate decreased from 187.6 +/- 5.3 mmHg during normoxia to 25.7 +/- 1.3 mmHg during hypoxia, and further decreased to 20.8 +/- 2.2 mmHg during hypoxia with 50 ppm NO (p < 0.05, compared with hypoxia only). Increases in pulmonary vascular pressure drop in response to hypoxia were 4.8 +/- 1.0 cmH2O and 9.1 +/- 1.4 cmH2O in non-treated and L-NAME-treated lungs, respectively (p < 0.05). L-NAME significantly increased hypoxic construction in the venous segment. The concentration of exhaled NO increased from 13 +/- 4 ppb during normoxia to 18 +/- 4 ppb during hypoxia (p < 0.1). Inhaled NO lowered not only pulmonary artery pressure but also capillary pressure in a dose-dependent manner, which reduced hypoxic pulmonary vasoconstriction. Pulmonary veins were more sensitive to inhaled NO than were arteries. Inhaled NO (50 ppm) dilated vessels smaller than 70 to 100 microns in diameter, by 39% (p < 0.05), and dilated venules greater than 100 microns in diameter by 26% (p < 0.05), but did not significantly dilate arterioles greater than 100 microns in diameter (11%). Inhaled NO did not significantly change the ratio of wet weight to dry weight. We conclude that both endogenous and inhaled NO attenuate hypoxic pulmonary vasoconstriction, with significant pulmonary venous dilation. The main site of action of inhaled NO is vessels smaller than 100 microns in diameter and venules greater than 100 microns in diameter. Inhaled NO (5-100 ppm) does not cause interstitial edema.