HEMODYNAMIC AND GAS-EXCHANGE RESPONSES TO INFUSION OF ACETYLCHOLINE AND INHALATION OF NITRIC-OXIDE IN PATIENTS WITH CHRONIC OBSTRUCTIVE LUNG-DISEASE AND PULMONARY-HYPERTENSION

To investigate endothelium-dependent and endothelium-independent nitri c oxide (NO) mediated pulmonary vasodilation in patients with chronic obstructive lung disease (COLD), we examined the responses to incremen tal infusion rates of acetylcholine (ACh) or inhaled NO on hemodynamic and gas exchange. In 13 patients, ACh (15 mg/min) decreased pulmonary artery pressure (Ppa) from 31 +/- 1 to 28 +/- 1 mm Hg (p < 0.01) and systemic arterial pressure while increasing cardiac index from 3.7 +/- 0.4 to 4.7 +/- 0.4 L/min/m2 (p < 0.01). Inhaling 40 parts per million (ppm) NO decreased Ppa from 32 +/- 1 to 26 +/- 1 mm Hg (p < 0.001) wi th no associated hemodynamic change. ACh reduced Pa(O2) from 57 +/- 3 to 48 +/- 2 mm Hg (p < 0.01) and increased venous admixture (QvA/QT) f rom 35 +/- 3 to 45 +/- 3% (p < 0.01). Inhaling 40 ppm NO increased Pa( O2) from 57 +/- 3 to 60 +/- 3 mm Hg (p < 0.01) and decreased QvA/OT fr om 36 +/- 3 to 32 +/- 3% (p < 0.01). Pulmonary vascular resistance cha nges were similar in response to 40 ppm NO or 15 mg/min ACh. In COLD p atients, ACh produces both pulmonary and systemic vasodilation but imp airs arterial oxygenation whereas inhaled NO induces selective pulmona ry vasodilation while improving gas exchange. The resistance to ACh in some patients could be related to pulmonary endothelial dysfunction.