This study compared the effects of sevoflurane and propofol on the inflammatory response and pulmonary function of patients with lung cancer during the perioperative period. Forty patients who underwent a selective resection of the inferior lobe of the left lung were randomly divided into two groups, with one group anesthetized with sevoflurane and the other with propofol (groups S and P, respectively). Radial arterial and mixed venous blood were extracted for blood gas analysis, in order to calculate the alveolar-arterial oxygen partial pressure difference (PA-aDO₂), respiratory index (RI) and pulmonary shunt ratio (Qs/Qt) prior to the induction of anesthesia (T₀), prior to one-lung ventilation (OLV) (T₁), 1 h subsequent to the commencement of OLV (T₂), 1 h following restoration of two-lung ventilation (T₃), 2 h following restoration of two-lung ventilation (T₄) and 24 h post-surgery (T₅). In addition, blood was extracted from the radial artery at T₀, T₁, T₂, T₃, T₄ and T₅ in order to detect the presence of tumor necrosis factor-α (TNF-α), IL-6 and IL-10 in the blood serum. Between T₁ and T_4, the tidal volume, airway plateau pressure and end-expiratory positive airway pressure were recorded, in order to calculate the lung dynamic compliance (Cdyn). Heart rate, mean arterial pressure, central venous pressure, cardiac output and the duration of OLV (OLV-T) were recorded at T_0-5. Compared with T0, the levels of TNF-α, IL-6 and IL-10 significantly increased during T₂ to T₄ in both groups (P<0.05). PA-aDO₂ and RI increased during T₁ to T₄, and Qs/Qt increased at T₂ (P<0.05). Compared with T₁, Cdyn decreased during T₂ to T₄ in the S group, whereas Cdyn was reduced at T₂ in the P group (P<0.05). Compared with the P group, TNF-α level increased and IL-10 decreased at T₃ and T₄ in the S group. PA-aDO₂ and RI increased, but Cdyn decreased at T₂ and T₃ in the S group. Qs/Qt increased at T₂ in the S group. The results of the present study demonstrated that, in comparison with propofol, sevoflurane exhibited an enhanced capacity to aggravate injury to pulmonary function during the perioperative stages. This occurred via the release of inflammatory factors, the aggravation of lung edema and the inhibition of hypoxic pulmonary vasoconstriction.

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