The arterial site of action of nitric oxide in the neonatal pig lung determined by microfocal angiography.

To determine the site of action of inhaled nitric oxide (iNO) in the newborn pig lung, lungs were isolated and perfused at constant flow for microfocal x-ray angiography. Measurements of pulmonary arterial diameters were made on arteries in the 100--2500 microm diameter range under control conditions, during vasoconstriction caused by hypoxia (decreasing PO(2) from approximately 120 to approximately 50 Torr), or N(omega)-nitro-L-arginine methylester (L-NAME 10(-4) M) administration, with or without vasodilation induced by iNO (40 ppm) or by the NO donor S-nitroso-N-acetylpenicillamine (SNAP 5 x 10(-6) M) given intravascularly. Hypoxia caused constriction only in smaller arteries whereas L-NAME constricted arteries throughout the size range studied. iNO dilated the smaller arteries more than the larger arteries under all study conditions. SNAP was used to provide an intravascular source of NO for comparison to iNO. SNAP also dilated smaller arteries more than larger arteries, but it had a significantly greater effect on the large arteries than did iNO. This suggests that differential accessibility of the vascular smooth muscle to NO between sources, air and blood, is a factor in the diameter dependence of the responses.