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We define the concept of reperfusion injury, and we present a background chronology of experimental work supporting and questioning this concept. We identify several new influences, such as current clinical interest in thrombolytic therapy for acute ischemia of heart and brain and the growing recognition of endothelium as a regulator of homeostasis. We propose that these influences will encourage a reexamination of reperfusion injury as a factor in the ultimate outcome of tissue exposed to reversible ischemia. We briefly discuss the major mechanisms presently implicated in reperfusion injury--loss of calcium homeostasis, free radical generation, leukocyte-mediated injury, and acute hypercholesterolemia.
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Hallenbeck et al. (Thu,) studied this question.
synapsesocial.com/papers/69dff6f9bdd89ea5318607fa — DOI: https://doi.org/10.1001/archneur.1990.00530110107027
John M. Hallenbeck
National Institutes of Health
A J Dutka
Seattle Children's Hospital
Archives of Neurology
Naval Medical Research Command
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