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- W253851187 abstract "When blood flow to the myocardium is interrupted, for example during a coronary occlusion or coronary artery spasm, the resulting ischemia is characterised by certain metabolic and ultrastructural perturbations including a fall in intracellular pH, decreased ATP levels, decreased glucose levels, increased lactate levels, membrane damage, electromechanical uncoupling and uncoupling of mitochondrial oxidative phosphorylation [1]. This hypoxic phase, with its associated oxygen depletion, therefore leads to significant metabolic stress. When blood flow and, therefore, oxygen are returned to the hypoxic tissue during reperfusion, oxidative stress occurs due to oxygen-derived free radical formation which causes further damage to membranes (via lipid peroxidation), nucleic acids and proteins. In addition, reperfusion is associated with intracellular and mitochondrial calcium overload which causes further damage and uncoupling of respiration and contraction. If ischemia is prolonged, inevitably the changes become irreversible and cell death and tissue necrosis occur." @default.
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- W253851187 date "1996-01-01" @default.
- W253851187 modified "2023-09-25" @default.
- W253851187 title "The molecular basis of adaptation to ischemia in the heart: The role of stress proteins and anti-oxidants in the ischemic and reperfused heart" @default.
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- W253851187 doi "https://doi.org/10.1007/978-3-0348-8988-9_23" @default.
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