Abstract
One-lung ventilation in thoracic surgery provokes profound systemic inflammatory responses and injury related to lung tidal volume changes. We hypothesized that the highly selective a2-adrenergic agonist dexmedetomidine attenuates these injurious responses. Sixty patients were randomly assigned to receive dexmedetomidine or saline during thoracoscopic surgery. There is a trend of less postoperative medical complication including that no patients in the dexmedetomidine group developed postoperative medical complications, whereas four patients in the saline group did (0% versus 13.3%, p = 0.1124). Plasma inflammatory and injurious biomarkers between the baseline and after resumption of two-lung ventilation were particularly notable. The plasma high-mobility group box 1 level decreased significantly from 51.7 (58.1) to 33.9 (45.0) ng.ml−1 (p < 0.05) in the dexmedetomidine group, which was not observed in the saline group. Plasma monocyte chemoattractant protein 1 [151.8 (115.1) to 235.2 (186.9) pg.ml−1, p < 0.05] and neutrophil elastase [350.8 (154.5) to 421.9 (106.1) ng.ml−1, p < 0.05] increased significantly only in the saline group. In addition, plasma interleukin-6 was higher in the saline group than in the dexmedetomidine group at postoperative day 1 [118.8 (68.8) versus 78.5 (58.8) pg.ml−1, p = 0.0271]. We conclude that dexmedetomidine attenuates one-lung ventilation-associated inflammatory and injurious responses by inhibiting alveolar neutrophil recruitment in thoracoscopic surgery.
Highlights
One-lung ventilation (OLV) is mandatory during thoracic surgery, but it may provoke profound systemic inflammatory responses that participate in the development of lung injury [1,2,3]
We investigated whether intraoperative DEX infusion alleviates the expression of OLV-induced injurious mediators in thoracoscopic surgery
The major finding of this study is that intraoperative DEX infusion attenuates OLV-induced injurious responses in patients undergoing thoracoscopic surgery
Summary
One-lung ventilation (OLV) is mandatory during thoracic surgery, but it may provoke profound systemic inflammatory responses that participate in the development of lung injury [1,2,3]. Atelectasis during OLV and lung redistension after resumption of two-lung ventilation are additional mechanisms to promote neutrophil sequestration in the lung and aggravate inflammatory responses [1, 9]. Proinflammatory mediators, such as plasma neutrophil elastase, and anti-inflammatory mediators, such Clara cell protein (CC16), related to these lung tidal volume changes play potential roles in OLVinduced inflammatory responses [10, 11].
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