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

¹Department of Medicine, Hinchingbrooke Hospital, Huntingdon; and ²Cambridge Perfusion Services and ³Department of Anaesthetic Research, Papworth Hospital, Cambridge, United Kingdom

Submitted 3 August 2005 ; accepted in final form 19 December 2005

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% O₂ at 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^–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 = 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.

nitric oxide; carbon monoxide; diffusing capacity; membrane diffusing capacity

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