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alterations in mitochondrial cation contents, increasedmitochondrial free fatty acidsand Ca2+, and decreased adeninenucleotide translocaseactivity. The cell membranetransport of Naâ and Kâ, transmembranepotential, cellular ATP and cyclic nucleotide levels, and other phenomenaare also significantly altered. The potential mechanismsresponsible 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 ofâ substrates may improve cellular energy levels, they may not necessarily improve microcirculation. The use of ATP-MgC12 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. ATP-MgCl,; cellular functions; insulin; reticuloendothelial system becomes a critical series of the organ and the individual. As a result of prolonged reduction in tissue E. D. Churchill (1972) perfusion, various alterations in tissue metabolism, structure, and function occur at the systemic, cellular, Shrlc~k is the state follswing injury which is characterized by a fall in and subcellular levels. Although much has been learned ~nwg~~ produtmtion. about the function and structure
AJP - Regulatory, Integrative and Comparative Physiology – The American Physiological Society
Published: Aug 1, 1983
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