Beneficial effects of antioxidant therapy in crush syndrome in a rodent model: enough evidences to be used in humans?

Excerpt

Rhabdomyolysis or skeletal muscle breakdown results in a huge release of myoglobin, sarcoplasmic proteins, and electrolytes into the plasma. The term “crush syndrome (CS)” describes muscle destruction after direct trauma, injury, or compression [1]. CS is the archetype of ischemia–reperfusion injury (IRI) which encompasses tissue and cellular damage due to inadequate blood supply followed by resumption of blood flow. Acute kidney injury (AKI) is the most common systemic complication of rhabdomyolysis. It occurs at an incidence ranging between 10 and 55% and is associated with a poor outcome, particularly in the presence of multiple organ failure [1]. Rhabdomyolysis-induced AKI is likely initiated by lack of oxygen, depletion of high-energy molecules, accumulation of toxic metabolites, and intratubular protein precipitation during the ischemia phase but becomes substantially worsened by myoglobin-induced oxidative stress, inflammation, endothelial dysfunction, vasoconstriction, and apoptosis during reperfusion [2]. Despite increasing insight into the pathophysiologic mechanisms underlying CS, treatment has scarcely evolved over time. Akin to any case of CS are adequate surgical management with timely fasciotomies and debridement, ample intravenous fluid resuscitation, mannitol diuresis, urine alkalinization with bicarbonate, serum potassium control, and organ support [1]. …