Key result
Warm no-flow ischemia drives a ~26-fold increase in myocardial low molecular weight iron.
Why the study?
Little was known about changes in the amount of iron in the intracellular low molecular weight pool, which catalyzes Fenton reactions during reperfusion after ischemia.
Does warm no-flow ischemia or anoxic perfusion and subsequent reoxygenation increase the intracellular catalytic low molecular weight iron pool in normal and iron-loaded isolated rat hearts?
Does warm no-flow ischemia or anoxic perfusion and subsequent reoxygenation increase the intracellular catalytic low molecular weight iron pool in normal and iron-loaded isolated rat hearts?
Answers are grounded in this paper and cite their sources.
Ischemic acidification drives a massive 30-fold reductive release of catalytic ferrous iron from ferritin into the low molecular weight pool, priming the myocardium for free radical-mediated reperfusion injury.
Little is known about changes in the amount of iron in the intracellular low molecular weight pool, which catalyzes the Fenton reactions during reperfusion after ischemia. In this study a new approach is presented to measure low molecular weight iron and it is applied to normal hearts during ischemia and to iron-loaded hearts during anoxia and reoxygenation. The results of this study show that (a) during ischemia in normal hearts a progressive 30-fold increase occurs in low molecular weight iron after 45 min of ischemia, whereas (b) during 45 min of anoxic perfusion the low molecular weight iron does not increase. This means that the reductive release from the storage protein ferritin is greatly enhanced by the acidification that occurs during ischemia. (c) Anoxic perfusion of iron-loaded hearts does increase low molecular weight iron and there is a further increase upon reoxygenation, which is prevented by (+)-cyanidanol-3. Based on these findings it is concluded that oxygen deprivation enhances the susceptibility of rat hearts to oxygen radicals by increasing the amount of catalytic, ferrous iron in the low molecular weight pool.
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Voogd et al. (1992) studied Myocardial ischemia, anoxia, and reperfusion/reoxygenation injury. Warm no-flow ischemia or anoxic perfusion (with or without superoxide dismutase, deferoxamine, or (+)-cyanidanol-3) vs. Normoxic Tyrode buffer perfusion for 60 minutes was evaluated on Intracellular low molecular weight iron pool content (nmol/g wet weight) after 45 minutes of warm no-flow ischemia (p=<0.01). Warm no-flow ischemia for 45 minutes increased intracellular low molecular weight iron from 2.1 to 54.2 nmol/g wet weight (p<0.01) in isolated normal rat hearts, whereas anoxic perfusion did not.
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