Anoxemia as the cause of death in shock.
The case is presented that both hemorrhagic and septic shock are due to an inadequate oxygen supply to mitochondria of vascular muscle cells in peripheral circulatory beds. Mitochondria disintegrate in the presence of severe hypoxia; this is a normal response which does not, per se, indicate generalized cell damage. Irreversible shock follows when appreciable numbers of the muscle mitochondria become non-functional. The ATP available from glycolysis is inadequate to resynthesize the mitochondrial apparatus and oxygen cannot be used by the damaged mitochondria to produce the needed ATP through oxidative phosphorylation. In the absence of adequate ATP, the tone of these peripheral vessels must fall, leading to irreversible systemic hypotension and death. In hemorrhagic shock, mitochondrial hypoxia of smooth muscle cells is produced by decreased perfusion of the vasa vasorum in the constricted peripheral vessels; in septic shock there is direct competition for oxygen between bacterial cytochromes and muscle mitochondria.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001808:Blood Vessels; D006019:Glycolysis; D006801:Humans; D000860:Hypoxia / Q000150:complications*; D008931:Mitochondria, Muscle / Q000378:metabolism; D009130:Muscle, Smooth / Q000378:metabolism; D009369:Neoplasms / Q000150:complications; D012771:Shock, Hemorrhagic / Q000150:complications*; D012772:Shock, Septic / Q000150:complications*
D000255:Adenosine Triphosphate