The immune response to one-lung-ventilation is not affected by repeated alveolar recruitment manoeuvres in pigs

Acute lung injury after thoracic surgery relates to alveolar inflammation induced by one-lung ventilation (OLV) and surgical manipulation. However, alveolar recruitment manoeuvres (ARM), conventional ventilation, and airway manipulation may increase alveolar trauma. This study evaluates pulmonary immune effects of these co-factors in a porcine model.

Twenty-two piglets (27.3 kg) were randomised to spontaneous breathing (N.=4), two-lung ventilation (TLV, N.=6), OLV with propofol (6 mg/kg/h, N.=6) or desflurane anesthesia (1MAC, N.=6). Mechanical ventilation settings were constant throughout the experiment: VT=10 mL/kg, FIO2=0.4, PEEP=5 cmH2O. OLV was performed by left-sided bronchial blockade. Thoracic surgery was simulated for 60 min. ARM (airway pressure of 40 mbar for 10 s) was applied before and after each airway manipulation. Cytokines and mRNA-expression were assessed by immunoassays and semi-quantitative RT-PCR in alveolar lavage fluids, serum and tissue samples prior to and after OLV (TLV in controls).

Repetitive ARM and TLV induced no significant proinflammatory effects. OLV enhanced cytokine release but less with desflurane inhalation than propofol infusion (median (IQR) [pg/mL], dependent lung): Interleukin-8: TLV 44 (17) to 68 (35), propofol 82 (17) to 494 (231), desflurane 89 (30) to 282 (44). Likewise, serum cytokines were different: tumour necrosis factor-a: TLV 37 (13) to 62 (7), propofol 55 (39) to 94 (60), desflurane 43 (33) to 41 (25). Expression of interleukin-8-mRNA increased after OLV, but mRNA expression was not modulated by anesthetics.

ARM, standard TLV and repetitive BAL do not additionally contribute to lung injury resulting from OLV for thoracic surgery in healthy porcine lungs. OLV induces expression of interleukin-8-mRNA in alveolar cells, which is not modulated by different anesthetic drugs.