• Takae Kawamura, Mamoru Kadosaki, Noriko Nara, Atsushi Kaise, Hirotaka Suzuki, Shigeatu Endo, Jicheng Wei, and Katsuya Inada.
• Department of Anesthesiology, Sendai Medical Center, Miyagi, Japan. tkawamura@snh.go.jp
• J. Cardiothorac. Vasc. Anesth. 2006 Aug 1;20(4):503-8.

ObjectiveThe effects of sevoflurane on proinflammatory cytokines related to ischemic-reperfusion injury are not clear. The hypothesis was tested that sevoflurane decreases myocardial ischemic-reperfusion injury by suppressing proinflammatory cytokines.DesignProspective, randomized study.SettingA medical university heart center.ParticipantsTwenty-three patients undergoing coronary artery bypass surgery allocated randomly into 2 groups.InterventionsAnesthesia for 23 patients undergoing coronary artery bypass surgery was maintained using either fentanyl (30 microg/kg) with propofol (2-8 mg/kg/h) in the control group (n = 10) or fentanyl (30 microg/kg) with 0.5% to 1.0% sevoflurane in the sevoflurane group (n = 13).Measurements And Main ResultsInterleukin (IL)-6, IL-8, IL-10, and IL-1 receptor antagonist (IL-1ra) were measured by enzyme-linked immunosorbent assay. Troponin-T and creatine kinase-MB isoenzyme (CK-MB) were measured by enzyme immunoassay and ultraviolet absorption spectrophotometry, respectively. Serum IL-6 and IL-8 concentrations in both groups increased significantly over baseline from 60 minutes after declamping the aorta (p < 0.001). The increases were greater in the control group than in the sevoflurane group (p < 0.05). Serum IL-10 and IL-1ra concentrations in both groups increased significantly over baseline from 60 minutes after declamping the aorta (p < 0.001). There were no differences between the two groups. Serum troponin-T and CK-MB concentrations increased significantly in both groups from 60 minutes after declamping the aorta (p < 0.001); the increases were greater in the control group (p < 0.05).ConclusionSevoflurane suppressed the production of IL-6 and IL-8, but not IL-10 and IL-1ra. Changes in the balance between pro- and anti-inflammatory cytokines may be one of the most important mechanisms of myocardial protection caused by sevoflurane.

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