Hypoxia-induced pulmonary vasoconstriction in man: inhibition due to diethyl ether and halothane anesthesia.

Abstract

Impaired pulmonary gas exchange resulting in arterial hypoxemia is frequently observed in patients during general anesthesia. Recent animal investigations have revealed that pulmonary hypoxia‐induced vasoconstriction (a local mechanism which redistributes pulmonary blood flow from poorly to more amply ventilated regions) is abolished by commonly used inhalation anesthetics. Injectable anesthetics do not have this effect.The present work was undertaken to study whether pulmonary vasoconstriction in response to ventilation hypoxia could be elicted in man during intravenous anesthesia, and to find out whether any response thus obtained is reduced by diethyl ether and halothane. Under intravenous anesthesia, unilateral hypoxia (UH) was induced in two groups of young men by ventilating one lung, the test lung, with N2 and the other with O2. In both groups the time period of UH was subdivided into two sequences, one sequence with and one without inhalation anesthesia. In 10 subjects (group A), inhalation anesthesia was administered during the second sequence, and in 7 subjects (group B), inhalation anesthesia was given during the first sequence. The blood flow distribution (BFD) to the test lung during air breathing and following each of the two sequences of UH was determined by lung scintigraphy. The median test lung BFD in group A decreased from 49% (range 40–45%) of total pulmonary blood flow to 24.5% (range 19–32%) during UH. By superimposing ipsilateral inhalation anesthesia, it increased to 34% (range 27–48%). The increase was significant both for the diethyl ether and halothane subgroups. BFD to the test lung during the first period of UH was significantly higher during diethyl ether or halothane administration (group B) than during administration of intravenous anesthesia only (group A). The damping effect of inhalation anesthetics on the response to hypoxia was demonstrated at blood concentrations comparable to those used in clinical anesthesia. It is therefore likely that inhibition of hypoxia‐induced pulmonary vasoconstriction contributes to the development of arterial hypoxemia during diethyl ether and halothane anesthesia in man.