1983
DOI: 10.1016/s0022-5223(19)39185-8
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Inhibition of surgically induced ischemia/reperfusion injury by oxygen free radical scavengers

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Cited by 181 publications
(12 citation statements)
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“…Evolving evidence has shown that oxidative stress is vital in the pathophysiologic mechanism of cerebral I/R injury. The buildup of excessive free radicals leads to oxidative damage on proteins, lipids, and nucleic acids, which subsequently leads to the progression of ischemic injury after stroke ( 52 , 97 99 ). Of interest, we have showed that Nrf2, a transcription factor that regulates the expression of antioxidant proteins, attenuated tissue injury in the cerebral ischemia model in mice ( 100 , 101 ).…”
Section: Mechanisms Of Limb Remote Ischemic Pre- Per- and Postcondimentioning
confidence: 99%
“…Evolving evidence has shown that oxidative stress is vital in the pathophysiologic mechanism of cerebral I/R injury. The buildup of excessive free radicals leads to oxidative damage on proteins, lipids, and nucleic acids, which subsequently leads to the progression of ischemic injury after stroke ( 52 , 97 99 ). Of interest, we have showed that Nrf2, a transcription factor that regulates the expression of antioxidant proteins, attenuated tissue injury in the cerebral ischemia model in mice ( 100 , 101 ).…”
Section: Mechanisms Of Limb Remote Ischemic Pre- Per- and Postcondimentioning
confidence: 99%
“…It has been shown that during this sequence, known as ischemia‐reperfusion injury (IRI), the re‐introduction of oxygen‐rich blood to tissues that were previously ischemic leads to the generation of oxygen free radicals, the release of pro‐inflammatory cytokines, and the opening of mitochondrial permeability transition pores 2–4 . First described in myocardial tissue 30 years ago, 5–7 these events result in tissue injury with clinical manifestations ranging from dysmotility and malabsorption to anastomotic failure and even complete bowel necrosis 8,9 …”
Section: Introductionmentioning
confidence: 99%
“…T HE HYPOTHESIS that oxygen‐derived free radicals contribute to myocardial reperfusion dysfunction has gained much attention (1–3). It has been suggested that the reactive products of oxygen can induce structural alterations in both vascular endothelial cells and cardiac myocytes (4), leading to a decrease in myocardial contractility and a marked increase in coronary vascular resistance (5–7).…”
mentioning
confidence: 99%