Abstract
Crush syndrome (CS), a serious medical condition, which is characterized by damage to myocytes due to pressure and is associated with high mortality, even when patients receive fluid therapy. Icing therapy over the affected muscle has been reported to be effective in improving mitochondrial dysfunction and inflammation. These effects are thought to be secondary to improvements in the leakage of potassium and myoglobin from the damaged myocytes in the early stages of disease. However, their effects on the various symptoms of CS are unclear. It was hypothesized that treatment with icing will inhibit the influence of potassium by vasoconstriction, exert anti-inflammatory effects in the affected myocytes and improve mitochondrial function The CS model constructed by subjecting anesthetized rats to bilateral hindlimb compression with a rubber tourniquet for 5 h. The rats were then randomly divided into six groups: i) Sham; ii) CS without treatment (CS); iii) and iv) icing for 30 or 180 min over the entire hindlimb on CS rats (CI-30 and -180), respectively; and v) and vi) local icing for 30 or 180 min over the affected area on CS rats (CLI-30 and -180), respectively. Under continuous monitoring and recording of arterial blood pressures, blood and tissue samples were collected for biochemical analyses at designated time points prior to and following reperfusion. The survival rate, vital signs, and blood gas parameters in the CS group were lethal compared with the sham group. These were also improved in the CI-30 and CLI-30 groups compared with the CS group; however, they worsened in the CI-180 and CLI-180 groups due to hypothermia. The CI-30 and CLI-30 groups demonstrated tendencies of improvements compared with the CS group. Systemic inflammation and mitochondria dysfunction had improved in these groups compared with the CS group. We suggest icing therapy to temporarily prolong the viability after crush injury. Its effectiveness can be improved by combining it with other infusion therapies.