Ventilation prevents pulmonary endothelial dysfunction and improves oxygenation after cardiopulmonary bypass without...

Endothelial dysfunction of the pulmonary arterial tree occurring after cardiopulmonary bypass (CPB) contributes to pulmonary hypertension and respiratory failure in the postoperative period. The goal of the present study was to characterize the alterations of endothelial cell signal transduction pathways in pulmonary arteries following CPB, the effect of ventilation and nitric oxide (NO) inhalation on endothelium-dependent relaxations and the alterations in hemodynamics and oxygenation.

Six groups of Landrace swine were compared: control, sham without CPB, CPB 150min+no reperfusion, CPB 150min+reperfusion 60 min, CPB 150min+ventilation (tidal volume 12 ml/kg)+reperfusion 60 min, and CPB 150min+NO inhalation (with ventilation, NO 40 ppm)+60 min of reperfusion. No cross-clamping was applied, the heart was left beating, empty. Pulmonary artery reactivity was evaluated in organ chambers to assess the endothelium-dependent relaxations.

CPB alone did not alter endothelial function. CPB and pulmonary reperfusion induced a statistically significant decrease in endothelium-dependent relaxations to acetylcholine. Mechanical ventilation during CPB prevented the reduction of relaxations to acetylcholine. Ventilation and NO inhalation during CPB did not differ from ventilation alone in terms of endothelium-dependent relaxations. There were no differences between groups for relaxations to bradykinin. There was a significant increase in arterial oxygen tension in the ventilated group compared to the non-ventilated group.

Pulmonary reperfusion after CPB causes a selective dysfunction of Gi-protein-mediated relaxations. Mechanical ventilation prevents the pulmonary endothelial dysfunction due to reperfusion after CPB. Ventilation also improves oxygenation after CPB. Mechanical ventilation could be used as a preventive approach for patients undergoing cardiac surgery with extracorporeal circulation.