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^-1. Its gas channel was ventilated with 5 ppm NO, 0.02% CO and 22% O2 at 5 L min^-1. DNO and DCO were calculated from inlet and outlet gas concentrations and flow rates. DNO = 13.45 (SD = 5.84) ml.min^-1 torr ^-1 and DCO = 1.22(SD = 0.3) ml.min^-1 torr ^-1. DNO and DCO increased (P =.002) with blood volume/surface area. 1/ DNO (P <.001) and 1/ DCO (P <.001) increased with 1/Hb. DNO (P=.01)and DCO (P =.004)fell with increasing gas flow. DNO but not DCO increased with haemolysis (P =.001) indicating DNO dependence on red cell diffusive resistance. The post haemolysis value for Dm = 41 ml.min^-1 torr ^-1 is the true membrane diffusing capacity of the system.No change in DNO or DCO occurred with changing blood flow rate. 1/DCO increased (P = .009) with increasing pO2. DNO and DCO appear 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 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 haematocrit (over a larger range than encountered clinically) while keeping other variables constant . Though structurally very different, it offers a functional model of lung NO and CO transfer.