Nitric Oxide Modulation of Pulmonary Vascular Resistance Is Red Blood Cell Dependent in Isolated Rat Lungs

摘要: Nitric oxide (NO) or endothelium-derived relaxing factor may play an important role in modulating pulmonary vascular resistance (PVR), although previous studies have produced conflicting results. Endogenous NO inhibition causes increase PVR intact animals but not saline-perfused isolated lungs. We hypothesized that blood is essential for to serve as a modulator of PVR. Therefore, the effects endogenous (Nomega-nitro-L-arginine methyl ester [L-NAME]) were determined rat lungs related presence different components under normoxic conditions and after 1 wk hypoxia (fraction inspired oxygen [FIO2] = 10%). Exogenously administered inhaled was evaluated from hypoxic rats. In rats, L-NAME (10-100 micro M) caused dose-dependent whole (hematocrit [Hct] 40%) diluted (Hct 12%) blood-perfused (10-800 had no effect perfused with modified salt solution equal viscosity either alone, containing plasma (50%) free oxyhemoglobin (10 M). lungs, (100 increased more versus (141% vs 100%). Inhaled decreased rats partially reversed L-NAME, conclusion, modulate this by prolonged hypoxia. The response dependent on red cells independent changes plasma. (Anesth Analg 1996;83:1212-7)