• Silverio Sbrana, Anna Nunziata, Simona Storti, Dorela Haxhiademi, Annamaria Mazzone, Maria Leone, Marco Solinas, and Paolo Del Sarto.
• Flow Cytometry Laboratory, CNR Institute of Clinical Physiology, Ospedale del Cuore, Massa, Italy.
• Perfusion. 2020 Jan 1; 35 (1): 48-56.

IntroductionThe increase of the anti-inflammatory CD163highHLA-DRlow blood monocyte subset is one of the mechanisms dampening inflammation during cardiac surgery with cardiopulmonary bypass. We evaluated the effect of two different anesthetic protocols, intravenous Propofol infusion or Sevoflurane-gas administration, on the perioperative frequency of this subset.MethodsBlood from patients (Propofol = 11, Sevoflurane = 13) undergoing minimally invasive mitral valve surgery was drawn preoperatively (T1), before declamping (T2), at 6 (T3), 24 (T4), 48 (T5), and 72 hours (T6) after declamping. C-reactive protein, haptoglobin, and lactate dehydrogenase were measured. A hemolytic index, as C-reactive protein/haptoglobin ratio, was introduced. Monocyte expression of HLA-DR, CD163, and the CD163highHLA-DRlow subset fraction was quantified by flow cytometry. Baseline-referred variations of plasmatic and cellular data at T2 were normalized for clamping times. Subsequent time-point variations were normalized for the final cardiopulmonary bypass times.ResultsVariations of hemolytic index and lactate dehydrogenase were higher with Propofol at T3 (p = 0.004 and p = 0.02, respectively) when compared with Sevoflurane. At T2, the down-modulation of CD163 was higher with Propofol (p = 0.005). Starting from T3, the up-regulatory trend of CD163 was basically higher with Propofol, although not significantly. Propofol induced higher increments of HLA-DR low fractions, at T2 (p = 0.04) and, to a lesser extent, at T4 (p = 0.06). Starting from T3, the CD163highHLA-DRlow subset variations were higher with Propofol, especially at T4 and T6.ConclusionPropofol seems to induce a higher postoperative fraction of the CD163highHLA-DRlow monocyte subset. This could represent either a compensatory mechanism dampening the higher inflammatory condition observed with Propofol at T2 or a consequence of a higher postoperative Propofol-induced hemolysis.

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