British Journal of Anaesthesia 2007 99(3):368-375.
T. Schilling1,*, A. Kozian1, M. Kretzschmar1, C. Huth2, T. Welte3, F. Bühling4, G. Hedenstierna5 and T. Hachenberg1
1 Department of Anaesthesiology and Intensive Care Medicine
2 Department of Cardiovascular and Thoracic Surgery, Otto-von-Guericke-University Magdeburg, Germany
3 Department of Pneumology, Hannover Medical School, Germany
4 Institute of Clinical Chemistry, Carl-Thiem-Hospital Cottbus, Germany
5 Department of Clinical Physiology, Uppsala University, Sweden
* Corresponding author: Department of Anaesthesiology and Intensive Care Medicine, Otto-von-Guericke-University, Leipziger Str. 44, D-39120 Magdeburg, Germany. E-mail: thomas.schilling@medizin.uni-magdeburg.de
Background: One-lung ventilation (OLV) induces a pro-inflammatory response including cytokine release and leucocyte recruitment in the ventilated lung. Whether volatile or i.v. anaesthetics differentially modulate the alveolar inflammatory response to OLV is unclear.
Methods: Thirty patients, ASA II or III, undergoing open thoracic surgery were randomized to receive either propofol 4 mg kg–1 h–1 (n = 15) or 1 MAC desflurane in air (n = 15) during thoracic surgery. Analgesia was provided by i.v. infusion of remifentanil (0.25 µg kg–1 min–1) in both groups. The patients were mechanically ventilated according to a standard protocol during two-lung ventilation and OLV. Fibre optic bronchoalveolar lavage (BAL) of the ventilated lung was performed before and after OLV and 2 h postoperatively. Alveolar cells, protein, tumour necrosis factor (TNF), interleukin (IL)-8, soluble intercellular adhesion molecule-1 (sICAM), IL10, and polymorphonuclear (PMN) elastase were determined in the BAL fluid. Data were analysed by parametric or non-parametric tests, as indicated.
Results: In both groups, an increase in pro-inflammatory markers was found after OLV and 2 h postoperatively; however, the fraction of alveolar granulocytes (median 63.7 vs 31.1%, P < 0.05) was significantly higher in the propofol group compared with the desflurane group. The time courses of alveolar elastase, IL-8, and IL-10 differed between groups, and alveolar TNF (7.4 vs 3.1 pg ml–1, P < 0.05) and sICAM-1 (52.3 vs 26.3 ng ml–1, P < 0.05) were significantly higher in the propofol group. Conclusions: These data indicate that pro-inflammatory reactions during OLV were influenced by the type of general anaesthesia. Different patterns of alveolar cytokines may be a result of increased granulocyte recruitment during propofol anaesthesia.