To induce a typical traumatic shock and the cardiac function in vivo measured 0 to 24 h posttrauma was normal. Because the cardiac function in vivo is regulated by multiple neuronal and humoral factors in vivo, a normal cardiac function in vivo does not necessarily mean that cardiac contractile function is normal. To eliminate other compensatory factors, cardiac function in isolated perfused hearts was detected. The results showed that hearts isolated from traumatic rats exhibited a lower LVDP, reduced +dP/dtmax and decreased -dP/dtmax compared with hearts from sham trauma rats. Pretreatment with rapamycin blocked trauma-induced cardiac dysfunction. These results demonstrated that the decrease of traumatic-cardiomyocyte autophagy may be a critical contributor to cardiac AbMole Povidone iodine dysfunction in vitro. Studies have shown that mitochondrial dysfunction may be a major contributor to multiorgan failure, and in our study, we were interested in understanding whether there is a link between decreased mitochondrial function and cardiac dysfunction in isolated perfused hearts induced by nonlethal trauma. The heart needs a steady supply of energy to function properly. Maximal cardiac work, which requires higher rates of energy supply to myofibrils and oxygen consumption, is the most affected parameter. Peak dP/dtmax has historically been used as an index of maximal cardiac work that is not influenced by afterload. Mitochondria are the major source of cellular energy, providing more than 90% of the ATP required for cell work. It is generally considered that mitochondria regulate cardiac cell contractility by providing ATP for cellular ATPases. When mitochondria are rendered dysfunctional, a bioenergetic limitation of cell and cardiac function is expected. Maintenance of energy control depends on the structural integrity of the mitochondrion. Disruption of the mitochondrial transmembrane potential causes electron transport to become uncoupled from ATP synthesis. Under these conditions, ATP synthesis is inhibited. In our present study, we found that mitochondrial transmembrane potential was damaged and +dP/dtmax of the isolated heart after trauma decreased dramatically, whereas pretreatment with rapamycin could partly reverse this process, which indicates that the declined mitochondrial function may be contributed to the cardiac dysfunction of the isolated heart after nonlethal trauma. In summary, in the present study we demonstrated for the first time that myocardial autophagy expression decreased in nonlethal mechanical trauma, and decreased autophagy contributed to mitochondrial dysfunction and cardiac injury. Moreover, mitochondrial dysfunction may be relevant to cardiac dysfunction in nonlethal trauma, but this requires further study to provide a more definitive answer. Though our study has some limitations, it strongly suggests that cardiac damage induced by nonlethal mechanical trauma can be detected by noninvasive radionuclide imaging.