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Effects of Inhaled Nitric Oxide on Gas Exchange in Lungs with Shunt or Poorly Ventilated Areas

1997; American Thoracic Society; Volume: 156; Issue: 2 Linguagem: Inglês

10.1164/ajrccm.156.2.9607114

1535-4970

Susan R. Hopkins, Elaine C. Johnson, R. S. Richardson, Harrieth Wagner, Mario De Rosa, Peter D. Wagner,

Pulmonary Hypertension Research and Treatments

Inhaled nitric oxide (NO) is a selective pulmonary vasodilator with beneficial effects on some lung diseases, yet conflicting results, particularly in chronic obstructive pulmonary disease, have been reported. We hypothesized that although inhaled NO would improve gas exchange in the presence of shunt (by increasing blood flow to normal areas), it could worsen gas exchange when areas of low ventilation-perfusion (V˙ a/Q˙) ratio were present since these areas could be preferentially vasodilated by NO. We examined how ∼ 80 ppm inhaled NO altered pulmonary gas exchange in anesthetized ventilated dogs with the following: (1) normal lungs (n = 8), (2) shunt (n = 9, 24.7% shunt) produced by complete obstruction of one lobar bronchus, and (3) V˙ a/Q˙ inequality (n = 8) created by partial obstruction of one lobar bronchus resulting in a bimodal V˙ a/Q˙ distribution with 13% perfusion of low V˙ a/Q˙ areas (0.005 < V˙ a/Q˙ < 0.1) without shunt. Inhaled No significantly reduced pulmonary arterial (p < 0.001) and wedge pressures (p < 0.01) and pulmonary vascular resistance (p < 0.01) without changing cardiac output in each group. In normal lungs, NO did not alter PaO2 or V˙ a/Q˙ inequality. However, with complete obstruction, shunt fell slightly (p < 0.001) with NO. In lungs with V˙ a/Q˙ inequality, NO variably affected V˙ a/Q˙ matching, which was improved in some dogs and worsened in others. In these lungs, changes in pulmonary vascular resistance of the abnormal area of the lung were negatively correlated with changes in V˙ a/Q˙ dispersion (logSDQ˙) (R = − 0.85, p < 0.01) and positively correlated with PaO2 (R = 0.79, p < 0.05). We conclude that NO has net effects on pulmonary gas exchange, depending on the underlying lung pathology consistent with competing vasodilatory effects on the normal and abnormal areas that receive the gas.