Abstract
Clinical and experimental evidence has demonstrated the development of cardiac dysfunction and heart failure in patients with advanced viral or bacterial infection, severe trauma, burns and allograft rejection involving multiple organ dysfunction syndrome (MODS) or systemic inflammatory response syndrome (SIRS). Although a number of scenarios, including elevated levels of inflammatory cytokines such as tumor necrosis factor-α have been speculated to contribute to the pathogenesis of MODS- or SIRS-associated cardiac dysfunction, the precise link between MODS or SIRS and cardiac contractile dysfunction is still proving to be elusive, limiting the optimization of therapeutic strategies against this devastating health problem. Recent investigations support the contributions of nitric oxide/nitrosative damage, Toll-like receptor, endothelin-1, insulin insensitivity, ceramide, adhesion molecules and oxidative stress in the pathogenesis of MODS- or SIRS-associated cardiac dysfunction. Identification of these cell signaling mechanisms should lead to a better understand of the cellular mechanisms responsible for MODS- or SIRS-associated cardiac dysfunction so that new and effective therapeutic strategies may be developed to combat the devastating heart problems caused by these conditions.