OBJECTIVE: The 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. DESIGN: Prospective, randomized study. SETTING:A medical university heart center. PARTICIPANTS: Twenty-three patients undergoing coronary artery bypass surgery allocated randomly into 2 groups. INTERVENTIONS: Anesthesia 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 RESULTS:Interleukin (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 andIL-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). CONCLUSION:Sevoflurane 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.
RCT Entities:
OBJECTIVE: The effects of sevoflurane on proinflammatory cytokines related to ischemic-reperfusion injury are not clear. The hypothesis was tested that sevofluranedecreases myocardial ischemic-reperfusion injury by suppressing proinflammatory cytokines. DESIGN: Prospective, randomized study. SETTING: A medical university heart center. PARTICIPANTS: Twenty-three patients undergoing coronary artery bypass surgery allocated randomly into 2 groups. INTERVENTIONS: Anesthesia 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 RESULTS:Interleukin (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). CONCLUSION:Sevoflurane 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.
Authors: José Eduardo B Orosz; Mariana G Braz; Márjorie A Golim; Márcio Antônio A Barreira; Denise Fecchio; Leandro G Braz; José Reinaldo C Braz Journal: Inflammation Date: 2012-12 Impact factor: 4.092
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