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Study model/specimen/TQ pressure | Anesthetic agent/dose/TQ ischemia time/sample size/age | Main findings (compared between groups) | Interpretation | References |
Intervention | Control | Clinical outcome | Mechanism |
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RCT/venous blood/350 mmHg | Propofol, 2 mg/kg/h, 90 ± 7 min, , 66 ± 7 yr | Normal saline, 0.2 ml/kg/h, 93 ± 10 min, , 69 ± 10 yr | Sedation effect Propofol > control | Plasma SOD, TCA Propofol > control Serum MDA, hsCRP, and blood neutrophil count Propofol < control | Sedation dose of propofol has antioxidative and anti-inflammatory properties | [48] |
RCT/arterial blood/double SBP mmHg | Propofol, 0.2 mg/kg then 2 mg/kg/h, 72 ± 18 min, , 67 ± 5 yr | Midazolam, 5 mg, 69 ± 14 min, , 63 ± 7 yr | N/A | Whole blood ROS production Propofol < midazolam | Sedation dose of propofol attenuates ROS production compared to midazolam | [49] |
RCT/venous blood | Propofol, 2–2.5 mg/kg then 6–10 mg/kg/h, 79 ± 13 min, , 70 ± 6 yr | Sevoflurane, 1.5–2%, 83 ± 15 min, , 69 ± 5 yr | N/A | Serum MDA Propofol < sevoflurane | Propofol reduces oxidative injury in the TQ-induced I/R model | [51] |
RCT/arterial blood, venous blood/350–400 mmHg | Propofol, 2 mg/kg then 4–8 mg/kg/h, 114 ± 19 min, , 69 ± 6 yr | Halothane, 0.7–1%, 116 ± 25 min, , 66 ± 5 yr | MAP, pH, PaO2, PaCO2 Propofol ↔ halothane | Serum MDA Propofol < halothane | Propofol reduces oxidative injury in the TQ-induced I/R model | [52] |
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