Hypoxia-induced vasoconstriction in isolated perfused lungs exposed to injectable or inhalation anesthetics.

Investigations during the last two decades have revealed a tendency to inpaired pulmonary gas exchange in patients during general anesthesia. In the awake state, arterial hypoxemia is counteracted by a mechanism which tends to normalize the ventilation/perfusion ratio of the lungs by way of a hypoxia-induced vasoconstriction in poorly ventilated areas. This results in a redistribution of perfusion to more adequately ventilated lung regions. Recent observations suggest, however, that this beneficial mechanism is blunted by some commonly used inhalation anesthetics. In the present study the effect of inhalation anesthetics and injectable anesthetics on the vasoconstrictor response to acute alveolar hypoxia have been compared in isolated blood-perfused rat lungs. The experiments showed that the response was unaffected by N2O and injectable anesthetics, while a reversible, dose-dependent damping effect was demonstrated for the volatile inhalation anesthetics, ether, halothane and methoxyflurance. The effect could be demonstrated at blood concentrations comparable to those used in clinical anesthesia, and it was not due to a general paralysis of the vascular smooth muscle. The findings might, at least in part, explain the occurrence of arterial hypoxemia during general inhalation anesthesia.