Can a membrane oxygenator be a model for lung NO and CO transfer?

Abstract

To model lung nitric oxide (NO) and carbon monoxide (CO) uptake, a membrane oxygenator circuit was primed with horse blood flowing at 2.5 l/min. Its gas channel was ventilated with 5 parts/million NO, 0.02% CO, and 22% O2at 5 l/min. NO diffusing capacity (Dno) and CO diffusing capacity (Dco) were calculated from inlet and outlet gas concentrations and flow rates: Dno = 13.45 ml·min−1·Torr−1(SD 5.84) and Dco = 1.22 ml·min−1·Torr−1(SD 0.3). Dno and Dco increased ( P = 0.002) with blood volume/surface area. 1/Dno ( P < 0.001) and 1/Dco ( P < 0.001) increased with 1/Hb. Dno ( P = 0.01) and Dco ( P = 0.004) fell with increasing gas flow. Dno but not Dco increased with hemolysis ( P = 0.001), indicating Dno dependence on red cell diffusive resistance. The posthemolysis value for membrane diffusing capacity = 41 ml·min−1·Torr−1is the true membrane diffusing capacity of the system. No change in Dno or Dco occurred with changing blood flow rate. 1/Dco increased ( P = 0.009) with increasing Po2. Dno and Dco appear to be diffusion limited, and Dco reaction limited. In this apparatus, the red cell and plasma offer a significant barrier to NO but not CO diffusion. Applying the Roughton-Forster model yields similar specific transfer conductance of blood per milliliter for NO and CO to previous estimates. This approach allows alteration of membrane area/blood volume, blood flow, gas flow, oxygen tension, red cell integrity, and hematocrit (over a larger range than encountered clinically), while keeping other variables constant. Although structurally very different, it offers a functional model of lung NO and CO transfer.