Lung vasculature differs from all other vessels in that it responds to hypoxia not by vasodilation, but rather by vasoconstriction. Hypoxic pulmonary vasoconstriction is an important mechanism because it reduces blood flow through poorly ventilated regions of the lungs. As a result, blood flow is redistributed towards better ventilated areas of the lung and blood oxygenation is optimalized. However, with prolonged hypoxia of most of the lung, such as that occurring in many chronic lung diseases, hypoxic pulmonary vasoconstriction leads to pulmonary hypertension. Despite its clinical significance and intensive research, the mechanism of hypoxic pulmonary vasoconstriction is still not clear.

Falus F., Herget J., Hampl V.:
Almitrine in low dose potentiates vasoconstrictor responses of isolated rat lungs to moderate hypoxia.
European Respiratory Journal 4: 688-693; 1991.
(Click here for abstract)

Almitrine is a respiratory stimulant whose effect of increasing arterial PO₂ appeared to be independent of its effects on lung ventilation. We (and others) hypothesized that almitrine could increase blood oxygenation by potentiating the hypoxic pulmonary vasoconstriction. In this study we found that almitrine in a low dose (0.25 µg/ml ) selectively potentiates hypoxic pulmonary vasoconstriction without changing the baseline perfusion pressure, while higher doses increase baseline pressure which then does not rise further with hypoxia (Figure).

Low dose almitrine potentiates pulmonary vasoconstrictor response to moderate acute hypoxia, while higher doses cause pulmonary vasoconstriction even in normoxia. Isolated rat lungs were perfused with blood at constant flow rate (0.04 ml/min/g body weight), so that increases in perfusion pressure reflect vasoconstriction. *P<0.05 the pressor response at 0.25 µg/ml almitrine differs from that with no almitrine. **P<0.05 the value differs from that with no almitrine.