Mitochondrial function in shock.
Studies utilizing animal models of circulatory shock have revealed mitochondrial structural and functional damage in the liver, kidney, and brain. Adenosine triphosphate (ATP) synthesis and calcium transport rates of these mitochondria decline significantly during circulatory shock. The specific enzyme functions affected deleteriously by low flow states are the ATP synthetase, adenine nucleotide translocase, and carrier-mediated calcium transport. Other cellular alterations that possibly are responsible for, or are related to, the shock-induced mitochondrial deterioration are discussed. Differences in the mitochondrial responses to endotoxemia and hyperdynamic sepsis are described. Data are presented on the beneficial effects of early glucocorticoid treatment in prevention of mitochondrial functional deterioration during endotoxemia.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000378:metabolism; D005938:Glucocorticoids / Q000627:therapeutic use; D007003:Hypoglycemia / Q000209:etiology; D007668:Kidney / Q000378:metabolism; D008928:Mitochondria / Q000378:metabolism*; D008930:Mitochondria, Liver / Q000378:metabolism; D008931:Mitochondria, Muscle / Q000378:metabolism; D010085:Oxidative Phosphorylation; D018805:Sepsis / Q000378:metabolism; D012769:Shock / Q000150:complications / Q000188:drug therapy / Q000378:metabolism*
D005938:Glucocorticoids; D000255:Adenosine Triphosphate