Abstract
Gross metabolic aspects of injury have been under intensive study for years and thus a lot of useful information about the metabolic effects of injury is available (l,2). On the other hand, until a couple of years ago, there were hardly any reports about specific cellular metabolic changes occurring during clinical or experimental shock reactions, such as the hypovolemic hemorrhagic shock or the normovolemic, primarily septic shock reaction, endotoxemia. Recently a few reports have appeared in the literature, indicating a block at the mitochondrial level of the cellular metabolic pathway (3–12).
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