The Possible Pathophysiological Outcomes and Mechanisms of Tourniquet-Induced Ischemia-Reperfusion Injury during Total Knee Arthroplasty.

摘要: Ischemia and reperfusion (I/R) injury induced by tourniquet (TQ) application leads to the release of both oxygen free radicals inflammatory cytokines. The skeletal muscle I/R may contribute local remote organ damage affecting outcomes after total knee arthroplasty (TKA). aim study is summarize current findings associated with following TKA using a thigh TQ, which include cellular alterations protective therapeutic interventions. PubMed database was searched keywords “ischemia injury,” “oxidative stress,” “tourniquet,” “knee arthroplasty.” search limited research articles published in English language. Twenty-eight clinical studies were included this qualitative review. Skeletal reduces protein synthesis, increases degradation, upregulates genes cell stress pathways. lower extremity elevates systemic oxidative as well reactions impairs renal function. Propofol model. Ischemic preconditioning (IPC) vitamin C prevent radical production. However, high dose N-acetylcysteine possibly induces kidney injury. In summary, TQ-related during metabolism alteration, endothelial dysfunction, stress, response, function disturbance. Propofol, IPC, show effects on markers. relationship between biochemical parameters postoperative has not been validated.