Abstract
BackgroundCardiopulmonary bypass (CPB) results in severe lung injury via inflammation and endothelial injury. The aim of this study was to evaluate the effect of endothelial colony-forming cells (ECFCs) on lung injury in rats subjected to CPB.MethodsThirty-two rats were randomized into the sham, CPB, CPB/ECFC and CPB/ECFC/L-NIO groups. The rats in the sham group received anaesthesia, and the rats in the other groups received CPB. The rats also received PBS, ECFCs and L-NIO-pre-treated ECFCs. After 24 h of CPB, pulmonary capillary permeability, including the PaO2/FiO2 ratio, protein levels in bronchoalveolar lavage fluid (BALF) and lung tissue wet/dry weight were evaluated. The cell numbers and cytokines in BALF and peripheral blood were tested. Endothelial injury, lung histological injury and apoptosis were assessed. The oxidative stress response and apoptosis-related proteins were analysed.ResultsAfter CPB, all the data deteriorated compared with those obtained in the S group (sham vs CPB vs CPB/ECFC vs CPB/ECFC/L-NIO: histological score 1.62 ± 0.51 vs 5.37 ± 0.91 vs 3.37 ± 0.89 vs 4.37 ± 0.74; PaO2/FiO2 389 ± 12 vs 233 ± 36 vs 338 ± 28 vs 287 ± 30; wet/dry weight 3.11 ± 0.32 vs 6.71 ± 0.73 vs 4.66 ± 0.55 vs 5.52 ± 0.57; protein levels in BALF: 134 ± 22 vs 442 ± 99 vs 225 ± 41 vs 337 ± 53, all P < 0.05). Compared to the CPB treatment, ECFCs significantly improved pulmonary capillary permeability and PaO2/FiO2. Similarly, ECFCs also decreased the inflammatory cell number and pro-inflammatory factors in BALF and peripheral blood, as well as the oxidative stress response in the lung tissue. ECFCs reduced the lung histological injury score and apoptosis and regulated apoptosis-related proteins in the lung tissue. Compared with the CPB/ECFC group, all the indicators were partly reversed by the L-NIO.ConclusionsECFCs significantly reduced lung injury induced by inflammation after CPB.
Highlights
Cardiopulmonary bypass (CPB) results in severe lung injury via inflammation and endothelial injury
CPB-induced lung injury is associated with systemic inflammation induced by the introduction of blood elements to artificial circuits [2] and lung ischaemia/reperfusion injury [4], and activated inflammatory cells contribute to alveolar inflammation [5]
We found that L-NIO significantly reduced the expression of eNOS in the endothelial colony-forming cells (ECFCs) (4.3 ± 0.8 vs 1.2 ± 0.3) (P < 0.001) (Fig. 2)
Summary
Cardiopulmonary bypass (CPB) results in severe lung injury via inflammation and endothelial injury. The aim of this study was to evaluate the effect of endothelial colony-forming cells (ECFCs) on lung injury in rats subjected to CPB. Postoperative lung injury after cardiopulmonary bypass (CPB) is a rare but severe complication that prolongs the duration of mechanical ventilation and the hospital stay and even increases mortality [1, 2]. As the outgrowth of endothelial progenitor cells, endothelial colony-forming cells (ECFCs) have high proliferative potency [7] and anti-inflammatory effects [8]. Considering the key role of inflammation in lung injury induced by CPB, we hypothesized that ECFCs can ameliorate lung injury after CPB. In our previous study, we found that eNOS inhibitor (L-NIO) decreases the recruitment of endothelial progenitor cells in transplanted lung [14].
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call