Molecular oxygen: Friend and foe*The role of the oxygen free radical system in the calcium paradox, the oxygen paradox and ischemia/reperfusion injury

1984 ◽  
Vol 16 (11) ◽  
pp. 969-985 ◽  
Author(s):  
M HESS ◽  
N MANSON
Keyword(s):  
Free Radical ◽  
Reperfusion Injury ◽  
Molecular Oxygen ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Oxygen Free Radical ◽  
Calcium Paradox ◽  
Oxygen Paradox

Inflammation and oxygen free radical formation during pulmonary ischemia-reperfusion injury

1992 ◽  
Vol 72 (2) ◽  
pp. 621-628 ◽  
Author(s):  
A. Hamvas ◽  
R. Palazzo ◽  
L. Kaiser ◽  
J. Cooper ◽  
T. Shuman ◽  
...  
Keyword(s):  
Free Radical ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Tissue Injury ◽  
Ischemia Reperfusion ◽  
Quantitative Imaging ◽  
Neutrophil Infiltration ◽  
Oxygen Free Radical ◽  
Severity Of Injury ◽  
Pulmonary Ischemia

In a companion study, we showed that 2 h of warm unilateral lung ischemia followed by reperfusion resulted in bilateral tissue injury, indicated by increases in extravascular density (EVD) and permeability, measured as the pulmonary transcapillary escape rate (PTCER) for radiolabeled transferrin. EVD and PTCER measurements were obtained with the quantitative imaging technique of positron emission tomography (PET). In the current study, we evaluated this increase in EVD histologically and correlated EVD and PTCER with measurements of oxidant-reactive sulfhydryls (RSH) in plasma as a marker of oxygen free radical (OFR) formation. Histologically edema, leukocyte infiltration, and hemorrhage were all present on the ischemic side, but only after reperfusion, whereas only neutrophil infiltration was observed on the nonischemic side. Histology scores correlated with EVD (r = 0.81) and PTCER (r = 0.75), but permeability was abnormal at times even in the absence of neutrophil infiltration. Plasma RSH concentration from the ischemic lung decreased significantly (P less than 0.05) during pulmonary ischemia (i.e., before reperfusion) and returned to baseline on reperfusion. The degree of RSH oxidation did not correlate with the severity of injury as measured by PET or histology. Thus pulmonary ischemia-reperfusion injury is characterized by inflammation, hemorrhage, edema, and OFR formation. Injury occurred after reperfusion, not after ischemia alone. In addition, injury to the contralateral nonischemic lung suggests a neutrophil-independent circulating mediator of injury.

scholarly journals Inhibition of surgically induced ischemia/reperfusion injury by oxygen free radical scavengers

1983 ◽  
Vol 86 (2) ◽  
pp. 262-272 ◽  
Author(s):  
James R. Stewart ◽  
William H. Blackwell ◽  
Stephen L. Crute ◽  
Victor Loughlin ◽  
Lazar J. Greenfield ◽  
...  
Keyword(s):  
Free Radical ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Oxygen Free Radical ◽  
Free Radical Scavengers ◽  
Radical Scavengers ◽  
Surgically Induced

Potential role of mitochondrial calcium metabolism during reperfusion injury

1989 ◽  
Vol 256 (6) ◽  
pp. C1196-C1206 ◽  
Author(s):  
A. A. Vlessis ◽  
L. Mela-Riker
Keyword(s):  
Reperfusion Injury ◽  
Superoxide Radical ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Oxygen Free Radical ◽  
Ruthenium Red ◽  
Free Radical Theory ◽  
Radical Theory ◽  
Dose Dependent Fashion

Ischemia-reperfusion injury has been associated with intracellular H2O2 and superoxide radical production from accumulated hypoxanthine (HX) and xanthine oxidase (XO). The effect of H2O2 and superoxide radical on mitochondrial Ca2+ efflux was characterized in isolated renal mitochondria using a HX-XO system. Mitochondria were suspended in buffered medium containing 200 microM HX. Extramitochondrial Ca2+ was monitored kinetically at 660-685 nm using the Ca2+ indicator arsenazo III. After preloading mitochondria with 18-25 nmol Ca2+/mg protein, addition of XO to the medium caused a rapid oxidation of mitochondrial NAD(P)H followed by Ca2+ release. Ca2+ efflux was attributed to mitochondrial metabolism of H2O2 because efflux could be prevented with catalase but not superoxide dismutase. The Ca2+ efflux rate (r = 0.995) and lag time to Ca2+ efflux (r = 0.987) both correlate well with the NAD(P)H oxidation rate. Exogenous ATP prevents Ca2+ efflux in a dose-dependent fashion (Km = 35 microM ATP) without affecting NAD(P)H oxidation; ATP plus oligomycin, however, had no effect. The protective effect of ATP on Ca2+ efflux was diminished by ruthenium red (RR). XO-induced Ca2+ efflux increased state 4 respiration 148% via a futile Ca2+ cycle involving the Ca2+ uniport. The increase in state 4 respiration could be reversed with RR (alpha less than 0.001) or ATP (alpha less than 0.01); ATP plus oligomycin, however, had no effect. The results are discussed in relation to the oxygen free radical theory of reperfusion injury.

1843: Role of Cxcr2 in Renal Ischemia/Reperfusion Injury

2004 ◽  
Vol 171 (4S) ◽  
pp. 487-487
Author(s):  
Motoo Araki ◽  
Masayoshi Miura ◽  
Hiromi Kumon ◽  
John Belperio ◽  
Robert Strieter ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Renal Ischemia Reperfusion Injury

Role of JNK phosphorylation in intestinal ischemia/reperfusion injury in mice

2010 ◽  
Vol 30 (2) ◽  
pp. 140-143
Author(s):  
De-yi ZHENG ◽  
Jian-ming WNAG ◽  
Yi-tao JIA ◽  
Jin-feng FU ◽  
Kai-yang LU ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Intestinal Ischemia Reperfusion
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