Organ Protection with ATP-Magnesium Chloride

Abstract

The heart and other organs are dependent on aerobic metabolism. When the arterial blood flow is reduced to the point that insufficient oxygen is available for oxidative phosphorylation, the production of adenosine triphosphate (ATP) is decreased. This reduction in ATP occurs at a time when more energy is needed to protect the cell against injury. Thus, since ATP plays an essential role in numerous cellular functions, it is not surprising that ischemia and hypovolemic shock produce alterations in cellular and subcellular function in the heart and other organs (1,2). Indeed, the resynthesis of ATP is a major rate-limiting factor following hypovolemic shock and ischemia (3,4). Very low levels of ATP are invariably associated with the irreversible state following myocardial ischemia (5,6). Thus, despite attempts to restore adequate tissue perfusion, including oxygen and substrates, there is a failure to replenish and regenerate ATP during such conditions. This results in persistent and progressive cellular injury that can progress to organ failure. Therefore, replenishing cellular energy following ischemia and hypovolemic shock has been one of a variety of different strategies that have been investigated to prevent or minimize cell injury. Moreover, the most direct approach for raising ATP levels under these conditions appears to be the infusion of ATP rather than the administration of substrates and/or agents that would synthesize it.