UNLABELLED: Cardiac surgery with cardiopulmonary bypass (CPB) induces postoperative immunosuppression and impaired pulmonary function. Maintaining mechanical ventilation (MV) during CPB improves pulmonary function and diminishes postoperative systemic inflammation. However, there are no data about the influence of maintaining MV during CPB on postoperative immune dysfunction. METHODS: Fifty patients were prospectively divided into two groups: without MV during bypass (n = 25) and dead space MV with positive end-expiratory pressure (n = 25). PaO2 (arterial oxygen tension)/FIO2 (inspired oxygen fraction) ratio, CXCL10 (C-X-C motif chemokine 10), CCL2 (chemokine ligand 2), tumor necrosis factor α (TNF-α), interleukin 10 (IL-10), human leukocyte antigen-DR antigen (HLA-DR), monocytic myeloid-derived suppressor cells (Mo-MDSCs, CD14HLA-DR monocytes), and blood cell count were collected before and after surgery. RESULTS: Cardiopulmonary bypass induced a marked immunosuppression with a significant increase in plasmatic levels of TNF-α and IL-10 and a significant decrease in HLA-DR monocytic expression. The postoperative proportion of Mo-MDSCs was subsequently significantly increased. Maintaining MV during CPB significantly improved PaO2/FIO2 ratio and decreased postoperative plasmatic levels of TNF-α and IL-10 compared with patients without MV during CPB. Furthermore, nonventilated patients had a lower lymphocyte count after surgery compared with patients with MV during CPB. CONCLUSION: Our study suggests that maintaining MV during CPB for cardiac surgery decreases postoperative immune dysfunction and could be an interesting strategy to diminish the occurrence of postoperative nosocomial infection without hampering the surgical procedure. However, these findings have to be confirmed in a clinical trial using the incidence of nosocomial infection as an endpoint.
UNLABELLED: Cardiac surgery with cardiopulmonary bypass (CPB) induces postoperative immunosuppression and impaired pulmonary function. Maintaining mechanical ventilation (MV) during CPB improves pulmonary function and diminishes postoperative systemic inflammation. However, there are no data about the influence of maintaining MV during CPB on postoperative immune dysfunction. METHODS: Fifty patients were prospectively divided into two groups: without MV during bypass (n = 25) and dead space MV with positive end-expiratory pressure (n = 25). PaO2 (arterial oxygen tension)/FIO2 (inspired oxygen fraction) ratio, CXCL10 (C-X-C motif chemokine 10), CCL2 (chemokine ligand 2), tumor necrosis factor α (TNF-α), interleukin 10 (IL-10), human leukocyte antigen-DR antigen (HLA-DR), monocytic myeloid-derived suppressor cells (Mo-MDSCs, CD14HLA-DR monocytes), and blood cell count were collected before and after surgery. RESULTS: Cardiopulmonary bypass induced a marked immunosuppression with a significant increase in plasmatic levels of TNF-α and IL-10 and a significant decrease in HLA-DR monocytic expression. The postoperative proportion of Mo-MDSCs was subsequently significantly increased. Maintaining MV during CPB significantly improved PaO2/FIO2 ratio and decreased postoperative plasmatic levels of TNF-α and IL-10 compared with patients without MV during CPB. Furthermore, nonventilated patients had a lower lymphocyte count after surgery compared with patients with MV during CPB. CONCLUSION: Our study suggests that maintaining MV during CPB for cardiac surgery decreases postoperative immune dysfunction and could be an interesting strategy to diminish the occurrence of postoperative nosocomial infection without hampering the surgical procedure. However, these findings have to be confirmed in a clinical trial using the incidence of nosocomial infection as an endpoint.
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