From the Journal archives: Understanding the mechanism(s) regulating hypoxic pulmonary vasoconstriction: how an early study has led to novel translational approaches

Abstract

Hypoxic pulmonary vasoconstriction (HPV) is a fundamental physiological process whereby ventilation/perfusion matching is optimized through the constriction of the pulmonary circulation supplying poorly ventilated lung units. In their 1981 paper in the Journal, Noble, Kay, and Fisher used a series of animal experiments to show that alveolar carbon dioxide (CO2) plays a critical role in the regulation of hypoxic pulmonary vasoconstriction. At physiological concentrations, CO2 potentiates the HPV response, and the absence of alveolar CO2 blunts HPV. The enhancement of HPV by CO2 resulted in reduced perfusion of specific hypoxic lung regions, thereby improving systemic oxygenation in lung-ventilated dogs. William H. Noble, J. Colin Kay, Joseph A. Fisher Can Anaesth Soc J 1981; 28: 422-30. To determine the dominant effect of variations in alveolar carbon dioxide tension on hypoxic pulmonary vasoconstriction. The group found that 1) increasing alveolar carbon dioxide concentrations enhanced hypoxic pulmonary vasoconstriction; 2) this enhancement improved oxygenation in ventilated dogs with regional alveolar hypoxia; and 3) this enhanced oxygenation was not due to increased cardiac output. Increased alveolar carbon dioxide enhances hypoxic pulmonary vasoconstriction. In clinical scenarios where hypoventilated or hypoxic lung regions exist, e.g., one-lung ventilation or lung consolidation, permissive hypercapnea may improve oxygenation.