Hypoxia-induced vasoconstriction in human lung exposed to enflurane anaesthesia.

The degree of hypoxic pulmonary vasoconstriction was studied in eight subjects during enflurane anaesthesia and was compared with that during intravenous pentobarbital anaesthesia in the same subjects. The lungs were ventilated separately with the aid of a double-lumen endobronchial catheter. After preoxygenation of both lungs for 30 min, during intravenous anaesthesia, the right lung (test lung) was rendered hypoxic by ventilation with 6% O2 in nitrogen. The left lung (control lung) was ventilated continuously with 100% oxygen. Cardiac output (QT) was determined by thermodilution, and the distribution of blood flow between the lungs was assessed from the elimination of a continuously infused, poorly soluble inert gas (SF6). The hypoxic challenge resulted in a reduction of the distribution of perfusion to the test lung from 57% to 36% of QT. Mean pulmonary arterial pressure increased by 37% and pulmonary vascular resistance of the test lung doubled. Arterial oxygen tension decreased from 45.9 to 9.5 kPa. Administration of enflurane to an end-tidal concentration of 2% to both lungs caused no significant change in the distribution of the pulmonary blood flow, PVR, or any other circulatory variable. The arterial blood gases remained unaltered. When the hypoxic challenge was discontinued, all variables returned towards control values. The findings suggest that the inhalational anaesthetic enflurane does not reduce the hypoxic vasoconstrictor response in the human lung.