Mechanism of myocardial mitochondria injury and protection of spironolactone after traumatic amputation

AIM To investigate the effects of aldosterone on the respiration of myocardial mitochondria and of spironolactone on the protection after traumatic amputation. METHODS The model of traumatic amputation was established by surgery. Twenty-four male SD rats were randomly divided into 3 groups (n=8): control group (only anesthesia), trauma group (anesthesia and amputation) and spironolactone group (6-day 20 mg/kg spironolactone intragastric administration and then amputation). The respiratory control ratio (RCR), oxidative phosphorylation ratio (P/O), total ATP enzyme and mitochondrial transmembrane potential（ΔΨm） in myocardial mitochondria were determined 6 hours after amputation. RESULTS The RCR, P/O, total ATP enzyme and ΔΨm in the trauma group were significantly lower than those in the control group (P<0.01). Compared with those in trauma group, the RCR, total ATP enzyme and ΔΨm in the spironolactone group were higher (P<0.05) and no significant changes were found in P/O. CONCLUSION The function of myocardial mitochondria is impaired after trauma and spironolactone can attenuate the impairment. Adlosterone may participate in the myocardial mitochondria aggravation after trauma.