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. 1994 Jul;106(1):118-24.
doi: 10.1378/chest.106.1.118.

Intravenously administered atrial natriuretic factor in patients with COPD. Effects on ventilation-perfusion relationships and pulmonary hemodynamics

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Intravenously administered atrial natriuretic factor in patients with COPD. Effects on ventilation-perfusion relationships and pulmonary hemodynamics

P Andrivet et al. Chest. 1994 Jul.

Abstract

The potent pulmonary vasodilating property of atrial natriuretic factor (ANF) may alter gas exchange in patients with COPD. We examined the hemodynamic and gas exchange responses to intravenous infusion of ANF (0.01 and 0.03 ng/min/kg body weight) in eight stable patients with COPD studied during spontaneous breathing, using the inert gas elimination technique. When compared with baseline, ANF infusion was associated with a dose-dependent decrease in pulmonary artery pressure (from 27.3 +/- 2.5 to 23.9 +/- 1.8 and 20.2 +/- 1.7 mm Hg, respectively) and a dose-dependent increase in blood flow perfusing poorly ventilated and unventilated units (VA/Q < 0.1: from 5.80 +/- 2.05 to 7.25 +/- 2.5 and 12.0 +/- 5.4 percent of total blood flow, respectively; p = 0.02). However, PaO2 remained unchanged (70.2 +/- 3.6, 68.1 +/- 3.8 65.4 +/- 3.5 mm Hg, respectively) because of a significant increase in minute ventilation (VE) from 8.6 +/- 0.8 to 9.6 +/- 0.8 and 10.3 +/- 0.7 L/min (p < 0.002). Six additional COPD patients receiving intravenously administered ANF at the same dosages were studied during controlled mechanical ventilation using right heart catheterization. In these patients, pulmonary vasodilation was associated with a significant increase in venous admixture (from 12.7 +/- 2.4 to 14.4 +/- 2.9 and 17.5 +/- 3.5 percent of total blood flow, respectively; p < 0.02), and a dose-dependent reduction in arterial PO2 (from 117 +/- 17 to 110 +/- 15 and 96.4 +/- 8.8 mm Hg, respectively; p < 0.05). The present results show that ANF infusion is associated with alterations in the VA/Q relationship in patients with COPD. However, a decrease in arterial oxygenation may be prevented by an increase in VE.

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