Nitric oxide increases dramatically in air exhaled from lung regions with occluded vessels

We observed dramatic changes in exhaled nitric oxide concentration (DeltaNOE) during wedge measurements, and hypothesised that occlusion and redistribution of pulmonary blood flow affects NOE.

We inflated the balloon of the pulmonary artery catheter and measured NOE and central hemodynamics in closed chest anesthetised pigs (n = 11) ventilated with hyperoxic gas (fraction of inspired oxygen [FIO2] = 0.5), before and during lung injury, and in open chest anesthetised pigs (n = 17) before and during left lower lobar (LLL) hypoxia (FIO2 0.05), and during hyperoxic (FIO2 0.8) ventilation of the other lung regions (HL).

In the closed chest pigs NOE increased from 2.0 (0.9) to 3.4 (2.0) p.p.b. (P < 0.001) during wedge, and returned to 2.0 (1.0) p.p.b. when the balloon was deflated. The increase in mean pulmonary artery pressure (MPaP) during wedge was small and insignificant (P > 0.07). When the balloon was inflated in the right pulmonary artery in the open chest pigs, the perfusion of the HL decreased from 2.57 (0.58) to 2.34 (0.55) l min(-1) (P < 0.001), and NOEHL increased from 2.5 (0.9) to 6.2 (3.2) p.p.b. (P < 0.001). The perfusion of the LLL increased from 0.33 (0.26) to 0.54 (0.34) l min(-1) (P < 0.001), and NOELLL decreased from 1.7 (0.6) to 1.5 (0.5) p.p.b. (P < 0.001). Neither lung injury nor LLL hypoxia had any influence on DeltaNOE (P > 0.07) during wedge. The correlation coefficient (R2) was 0.66 between changes in regional blood flow and DeltaNOE, and 0.37 between changes in MPaP and DeltaNOE.

Nitric oxide concentration increases dramatically from lung regions with occluded vessels, whereas changes in MPaP have minor effects on NOE. This is an important fact to consider when comparing NOE within or between studies, and indicates a possible marker of diseases with occluded lung vessels.