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Dunningham_Thesis_2011.pdf (11.42 MB)

Modelling lung and tissue gas transfer using a membrane oxygenator circuit; determining the effects of a volatile anaesthetic agent and a haemoglobin substitute on oxygen, carbon dioxide and nitric oxide diffusion

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posted on 2023-08-30, 13:37 authored by Helen Dunningham
A novel in vitro membrane oxygenator circuit was developed to test gas exchange where particular elements could be examined whilst keeping other variables constant. The circuit comprises two membrane oxygenators connected to form a continuous blood circuit resembling venous and arterial blood conditions. The effects of Isoflurane, a volatile anaesthetic, on oxygen transfer were investigated. RBC resistance to nitric oxide diffusion (DNO) was tested in this circuit by haemolysis and addition of the haemoglobin-based-oxygen-carrier (HBOC) Oxyglobin. The circuit was primed with equine blood flowing at 2.5 l/min. The oxygenator was ventilated with 5 l/min air/oxygen/N2 mix providing a range of FiO2. The deoxygenator received 5 l/min 5% CO2 in N2 with 0.2-0.3 l/min CO2. Isoflurane 1%, NO 4000-16000 ppb and CO 0.03% were added to the oxygenator gas. Uptake of O2, CO2, CO and NO were calculated by gas inlet and outlet concentrations and flow rates. Arterial and venous oxygen dissociation curve (aODC and vODC) comparisons were made. Isoflurane uptake by the circuit blood was evident and 1% Isoflurane did not affect oxygen uptake (p=0.981), aODC or vODC (p=0.311 and p=0.751). Haemolysis did not affect O2 or CO2 transfer but increased DNO (p<0.001). 250ml free Hb solution addition to the circuit increased DNO by 91% (p<0.0001). Addition of 250ml Oxyglobin increased DNO by 143% from 7.41±2.77 to 17.97±1.83 ml/min/mmHg. Oxyglobin caused a right shift of aODC and vODC (p<0.0001) but NO-bound Oxyglobin caused a left vODC shift (p<0.0001). Conclusion: Isoflurane administered via a membrane oxygenator does not affect O2 uptake or carriage in the blood. RBC surroundings provide significant resistance to DNO in circuit tests. Significant uptake of NO by Oxyglobin supports the potential of HBOCs to scavenge endothelial NO in vivo, causing vasoconstriction.



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