Hypoxic Pulmonary Vasoconstriction in the Human Lung

Open Access
Publisher Website
Google Scholar
Abstract
Six patients, age 29-58 yr, were investigated during barbiturate and fentanyl anesthesia. After intubation with a double-lumen bronchial catheter, one lung was ventilated continuously with 100% O2, and the other was rendered hypoxic during three 15-min periods by ventilation with 95% N2 + 5% O2, with intervening 15-min periods of oxygen ventilation. Cardiac output 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 1st hypoxic challenge resulted in a 10% increase in cardiac output (QT) and a reduction in the fractional perfusion of the test lung from 57% to 31% of QT. The pulmonary artery mean pressure increased by 54%, and the vascular resistance of the test lung increased 3-fold. The venous admixture increased from 19% to 40% of QT, whereas the inert gas shunt remained unaltered at 15% (inert gases also being eliminated by N-ventilated areas). The arterial oxygen tension decreased from 353 mm Hg to 79 mm Hg. On resumption of the control state, central hemodynamics and gas exchange returned to the initial values. The 2nd and 3rd hypoxic challenges resulted in reductions in the fractional perfusion of the test lung to 35% and 37% of QT. All other variables were altered to the same degree as during the first challenge. Hypoxic challenge of 1 lung in an i.v. anesthetized human subject elicits a maximum vasoconstrictor response within the first 15 min, and this response cannot be potentiated by repeated challenges.