Cellular mechanisms in shock and ischemia and their correction.
Various metabolic, cellular, and subcellular alterations in cell function and morphology occur during shock or low flow conditions. Alterations in mitochondrial function during low flow conditions consist of decreases in the metabolic capability of mitochondria, alterations in mitochondrial cation contents, increased mitochondrial free fatty acids and Ca2+, and decreased adenine nucleotide translocase activity. The cell membrane transport of Na+ and K+, transmembrane potential, cellular ATP and cyclic nucleotide levels, and other phenomena are also significantly altered. The potential mechanisms responsible for altered mitochondrial and cellular functions during shock and the consequences of such alterations are discussed. Based on the cellular alterations that occur during shock, attempts have been made to support cell function during such conditions. These (along with volume replacement) include substrates, membrane-stabilizing solutions, and energy compounds. Although provision of substrates may improve cellular energy levels, they may not necessarily improve microcirculation. The use of ATP-MgCl2 as an adjunct in the treatment of shock and ischemia has been described, and potential mechanisms of the beneficial effects of this compound are discussed.
D000227:Adenine Nucleotides / Q000378:metabolism; D000818:Animals; D002462:Cell Membrane / Q000502:physiology; D002952:Citric Acid Cycle; D000242:Cyclic AMP / Q000378:metabolism; D004579:Electron Transport; D004734:Energy Metabolism; D006019:Glycolysis; D006801:Humans; D007511:Ischemia / Q000503:physiopathology*; D008564:Membrane Potentials; D008928:Mitochondria / Q000378:metabolism; D008930:Mitochondria, Liver / Q000378:metabolism; D010101:Oxygen Consumption; D012769:Shock / Q000503:physiopathology*
D000227:Adenine Nucleotides; D000242:Cyclic AMP