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Multiple organ failure remains the major cause of death in critically ill patients. In view of therapeutic strategies, current research activities focus on the cellular response to different kinds of cellular stress (hypoxia, oxidative damage and mechanical distress) in the pathogenic sequelae of organ failure. The cellular stress reactions are characterized by induction of adaptive programs of gene expression (e.g. acute phase proteins, heat shock proteins, hypoxia-associated proteins) to protect the cells from energy depletion and cell death. Generally, the mitochondria are early indicators of cellular stress showing a loss of cytochrome c and a breakdown of the transmembrane potential. Shortage of ATP and decrease of pH can be observed in the cytoplasm which leads to a disintegration of the cytoskeleton. As a consequence, the cell becomes spherical and separates from the surrounding cells. Depending on the acuity of the stressor, the cell dies due to necrosis or apoptosis. Dysregulation of the balance of apoptosis and necrosis in different organs seems to be an important mechanism in the development of organ failure. New insights into the cellular mechanisms during organ dysfunction promote the development of new diagnostic (e.g., optical and spectroscopic) and pharmacological tools leading to a better prevention and therapy of organ failure. |
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