Reducing Ischaemia/Reperfusion-Induced Organ Injury
Reducing Ischaemia/Reperfusion-Induced Organ Injury
Most of the studies on ischaemia and reperfusion injury have been conducted in animal heart and brain models. Energy in cells is made available primarily as ATP; during aerobic metabolism, 38 molecules of ATP are generated for every molecule of glucose metabolized, whereas during anaerobic metabolism, only two molecules of ATP are generated for every glucose molecule. ATPs are essential for the proper functioning of cells, including membrane transport, synthesis of chemical compounds, and mechanical work. Ischaemia of tissues severe enough will stop oxidative phosphorylation in the mitochondria leading to a rapid depletion of stored ATPs, despite the continued anaerobic glycolysis of glucose. Ischaemia of short duration can result in full recovery of the tissue after reperfusion. However, prolonged ischaemia causes irreversible necrotic tissue damage during the ischaemic period and after reperfusion, further injury is sustained by the latter. This condition is referred to as reperfusion injury, and it is associated with the generation of huge amounts of free radicals.
Ischaemia/Reperfusion Injury
Most of the studies on ischaemia and reperfusion injury have been conducted in animal heart and brain models. Energy in cells is made available primarily as ATP; during aerobic metabolism, 38 molecules of ATP are generated for every molecule of glucose metabolized, whereas during anaerobic metabolism, only two molecules of ATP are generated for every glucose molecule. ATPs are essential for the proper functioning of cells, including membrane transport, synthesis of chemical compounds, and mechanical work. Ischaemia of tissues severe enough will stop oxidative phosphorylation in the mitochondria leading to a rapid depletion of stored ATPs, despite the continued anaerobic glycolysis of glucose. Ischaemia of short duration can result in full recovery of the tissue after reperfusion. However, prolonged ischaemia causes irreversible necrotic tissue damage during the ischaemic period and after reperfusion, further injury is sustained by the latter. This condition is referred to as reperfusion injury, and it is associated with the generation of huge amounts of free radicals.
