Mechanism Of Myocardial Damage In Burn And Blast Combined Injury

Heart failure due to burn-blast combined injury results in low-emission high-impedance type of systemic hemodynamic disorder, namely significant decreased cardiac output after injury. This study focused on myocardial apoptosis that caused the reduced number of cardiomyocytes, which may lead to decreased heart function. Rat model of sham, burn-blast combined injury (BB) and BB treated by Ac-DEVD-Cho was established, HE staining and transmission electron microscope was used to detected heart injury. And TUNEL staining was employed to measure myocardial apoptosis. Caspase activity assay kits were also used to analyze Caspase-3 and Caspase-12 activation. Left ventricular ejection fraction (LVEF) was measured using color Doppler ultrasound. Cultured myocardial cell H9C2 was treated with serum from sham or BB group with or without Ac-DEVD-Cho administration. Cell apoptosis was analyzed by flow cytometry, and endoplasmic and apoptotic related proteins were detected using Western blot assay. Compared with that in sham group, myocardial injury was obviously observed. Myocardial apoptosis was significantly increased and LVEF was remarkably suppressed. Activity of Caspase-3 and Caspase-12 was also activated. Ac-DVED-Cho administration could inhibit myocardial apoptosis and recover myocardial function. And protect myocardial cell H9C2 from BB serum induced apoptosis. Ac-DEVD-Cho administration serves a critical role in suppressing myocardial apoptosis and maintains myocardial function of rats with BB injury.