Abstract

In patients with respiratory failure, almitrine causes an increase in arterial O2 partial pressure (paO2) by stimulating peripheral chemoreceptors. Since such patients often require long-term O2 therapy inhibiting peripheral chemoreceptor activity, the effect on arterial blood gases by almitrine (100 mg orally) and increasing amounts of nasally supplied O2 was studied. In ten patients with severe chronic airways obstruction and pulmonary emphysema, almitrine produced a mean increase of paO2 by 5.2 mm Hg both while breathing normal air and during nasal administration of O2 (0.5-2.0 l/min), whereas paCO2 levels remained constant. In 4 patients with pulmonary fibrosis almitrine did not change the paO2. These results show that patients with chronic airways obstruction and pulmonary emphysema respond to a single dose of 100 mg almitrine by an increase of paO2 equivalent to that achieved by administering 1.0 l/min of O2 via the nose.

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