O2 modulation of single-vessel hydraulic conductance

To investigate the response of the microvascular endothelial barrier to O2 lack, hydraulic conductivities (Lp) were compared under control and hypoxic conditions. In 29 decerebrate frogs (Rana pipiens) the mesentery was exposed and continuously superfused with room air-equilibrated frog Ringer (14 degrees C, pH 7.4). Single mesenteric microvessels (15- to 50-microm diam) were cannulated and perfused with frog Ringer containing 5-40 mg/ml bovine serum albumin and 5-10% (vol/vol) human erythrocytes. The modified Landis technique was used to measure transmural water flux per unit area (Jv/S) from marker red cell movement at pressures ranging from 15 to 45 cmH2O. In 21 vessels, a 10-min superfusion with 100% N2-equilibrated Ringer increased Lp 2.4-fold (+/- 0.72 SD) over control (P less than or equal to 0.05). In an additional six vessels, simultaneous exposure to 100% N2-equilibrated perfusate and superfusate resulted in a 10-fold (+/- 3.0) increase in Lp (P less than or equal to 0.05). In 15 of the vessels, a 10- to 75-min reexposure to control conditions decreased Lp, averaging a 77% recovery toward base line. These data support an active role for O2 in the regulation of microvascular membrane permeability, which appears to be sensitive to the severity of O2 lack. The rapid increase in capillary water conductivity following exposure to hypoxic conditions may be the initial process in the events leading to edema formation.