Table 5.

Effects of anesthetic agents on TQ-induced I/R injury in TKA.

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
RCT/venous blood/350 mmHg	Propofol, 2 mg/kg/h, 90 ± 7 min, n = 18, 66 ± 7 yr	Normal saline, 0.2 ml/kg/h, 93 ± 10 min, n = 17, 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, n = 11, 67 ± 5 yr	Midazolam, 5 mg, 69 ± 14 min, n = 11, 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, n = 10, 70 ± 6 yr	Sevoflurane, 1.5–2%, 83 ± 15 min, n = 10, 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, n = 15, 69 ± 6 yr	Halothane, 0.7–1%, 116 ± 25 min, n = 15, 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]

hsCRP: high-sensitivity C-reactive protein; I/R: ischemia and reperfusion; MAP: mean arterial pressure; MDA: malondialdehyde; N/A: not available; PaCO₂: arterial carbon dioxide partial pressure; PaO₂: arterial oxygen tension; RCT: randomized controlled trial; ROS: reactive oxygen species; SBP: systolic blood pressure; SOD: superoxide dismutase; TAC: total antioxidative capacity; TQ: tourniquet.