Nitric oxide diminishes pulmonary hypertension without affecting capillary surface area

We hypothesized that pulmonary capillary recruitment does not depend solely on extracapillary factors. We investigated the effects of inhaled nitric oxide (NO) on segmental pulmonary resistances and dynamically perfused capillary surface area (DPCSA) in rabbits (n=9) placed on cardiac bypass Pulmonary and sytemic arterial and left atrial pressures were continuously monitored. Vascular occlusion techniques were used to determine pulmonary segmental pressures. DPCSA was determined from the transpulmonary metabolism of [3H]-Benzoyl-Phe-Ala-Pro. The pulmonary circulation was constricted by serotonin, then relaxed using increasing concentrations of NO (N01, NO2). Fold-increases from baseline, ±s e.ni Resistance Constricted NO1 NO2 Total 1.55 ±0.10 .27 ±0.08 1.00 ±0.040 Artery 1.53 ±0.10 .35 ±0.19 0 96 ±0.10-Mf Arteriole 2.49 ±0.50 .96 ±0.40 1.06 ±0.301 Venule 1.34 ±0.40 .13 ±0.29 1.23 ±0.21 Vein 1.51 ±0.28 .36 ±0.44 1.23 ±0.20 DPCSA 0.99 ±0.10 0.79 ±0.11 0.88 ±0.08 from Baseline,+ from Constricted, # from N01, by ANOVA p<0.05 NO reduced pulmonary arterial and pulmonary arteriolar resistances without affecting capillary surface area. This supports our hypothesis and suggests that tllf⁺. r.anillarv hf»H mau ftrtivplv mnHnlatp itc own iwmitmdnt.