Hypoxia-induced Pulmonary Vasoconstriction in the Human Lung

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Abstract
The influence of isoflurane on hypoxic pulmonary vasoconstriction (HPV) was studied in eight subjects prior to elective surgery. The lungs were ventilated separately with a double-lumen endobronchial catheter. After oxygen ventilation of both lungs for 30 min during intravenous barbiturate anesthesia, the test lung was rendered hypoxic by ventilation with 8% O2 in nitrogen. The control lung was ventilated continuously with 100% O2. Isoflurane was added to the inspired gas, so that end-tidal concentrations of 1% and 1.5% were obtained. Cardiac output .ovrhdot.QT was determined by thermodilution, and the distribution of blood flow between the lungs was assessed from the excretion of a continuously infused, poorly soluble gas (SF6). The hypoxic challenge during intravenous anesthesia resulted in a reduction in the fractional perfusion of the test lung from 54% to 41% of .ovrhdot.QT. Mean pulmonary arterial pressure increased by 46%, and pulmonary vascular resistance (PVR) of the test lung more than doubled. Arterial oxygen tension fell from 375 mmHg (50 kPa) to 101 mmHg (13.5 kPa). Adding isoflurane to the inhalation gas, first at a concentration of 1%, then 1.5%, caused no further significant change in the distribution of pulmonary blood flow, although six of the eight subjects showed a small increase in test lung blood flow at isoflurane 1.5%. There was no change in PVR or in any other circulatory variable. Arterial blood gases remained essentially unaltered. When the hypoxic challenge was discontinued, all variables returned to control values. It is possible that higher isoflurane concentrations would have caused a clear change in the blood flow distributions, but, at clinical concentrations, the effect of HPV in the human is all but immeasurable.