Hemorrhage following accidental injuries is a common cause of death in the industrialized world. Moreover, the impact of elective surgery and solid organ transplantation sometimes results in low flow conditions similar to those seen following hemorrhagic shock. A shortage in O2 availability, or hypoxia, leads to sequential changes in cell metabolism and morphology, including inflammatory responses and the expression of hypoxia-inducible transcription factor-1, which controls the cellular adaptation to hypoxia. These endogenous adaptive responses show that O2 deprivation is not an unforeseen event for cells. The purpose of this review article is to discuss the pathophysiologic principles of shock and the metabolic alterations that cells undergo during low flow conditions. Moreover, the rationale for therapeutic intervention by administering ATP-MgCl2 and sex steroids following shock and trauma will also be discussed. Copyright © 2004 S. Karger AG, Basel.