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  • Title: [Pulmonary hemodynamic effects of intravenous almitrine in patients with chronic bronchitis and respiratory insufficiency].
    Author: Weitzenblum E, Ehrhart M, Schneider JC, Hirth C, Roegel E.
    Journal: Bull Eur Physiopathol Respir; 1982; 18(5):765-73. PubMed ID: 6152773.
    Abstract:
    The effects on ventilation, gas exchange and pulmonary haemodynamics of 1 h infusion of 0.5 mg X kg-1 almitrine (Vectarion) were studied in 14 patients with chronic bronchitis, with clear hypoxemia (PaO2 less than 65 mmHg) and hypercapnia (PaCO2 greater than or equal to 45 mmHg). The separate effects of the almitrine solvent and/or the solution were studied in six similar chronic bronchitics. In this latter group, blood gases and haemodynamic values were not significantly altered. In subjects treated with almitrine, PaO2 raised from 51.9 +/- 6.6 (control: T0) to 61.9 +/- 9.9 mmHg at the 60th min (t60) of infusion (p less than 0.001); PaCO2 decreased from 52.8 +/- 6.3 (t0) to 45.7 +/- 5.2 mmHg at t60 (p less than 0.001). The effects on blood gases were still marked 10 min after infusion (t70). The significant increase in PaO2 was faster (10th min) than that of PaCO2 (20th min). The mean pulmonary artery pressure (Ppa) rose appreciably, from 27.8 +/- 11.3 at t0 to 35.5 +/- 12.5 mmHg at t60 (p less than 0.001). This rise was significant from the 10th min (p less than 0.005) and was related to that of pulmonary vascular resistance since on average cardiac output and pulmonary wedge pressure did not change. Ppa came back to its initial value at t70. Thus pulmonary vasoactive effects were at the same time early and transitory. They seemed due to an arterial vasoconstriction (role of chemoreceptors?), which could also explain the perfusion redistribution to the best ventilated areas and the improvement of VA/Q inequalities.
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