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Titolo:
PO2-DEPENDENT HYDROXYL RADICAL PRODUCTION DURING ISCHEMIA-REPERFUSIONLUNG INJURY
Autore:
FISHER PW; HUANG YCT; KENNEDY TP; PIANTADOSI CA;
Indirizzi:
DUKE UNIV,MED CTR,DEPT MED,POB 3315 DURHAM NC 27710 DUKE UNIV,MED CTR,DEPT CELL BIOL DURHAM NC 27710
Titolo Testata:
The American journal of physiology
fascicolo: 3, volume: 265, anno: 1993,
parte:, 1
pagine: 120000279 - 120000285
SICI:
0002-9513(1993)265:3<120000279:PHRPDI>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
SUPEROXIDE ANION RELEASE; HUMAN-ENDOTHELIAL-CELLS; HYDROGEN-PEROXIDE; NITRIC-OXIDE; VASCULAR-PERMEABILITY; OXYGEN METABOLITES; PULMONARY-EDEMA; MEDIATED DAMAGE; RABBIT LUNGS; RAT HEARTS;
Keywords:
OXYGEN FREE RADICALS; PULMONARY EDEMA; SUPEROXIDE DISMUTASE; CATALASE; DIMETHYLTHIOUREA; NITROGEN VENTILATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
41
Recensione:
Indirizzi per estratti:
Citazione:
P.W. Fisher et al., "PO2-DEPENDENT HYDROXYL RADICAL PRODUCTION DURING ISCHEMIA-REPERFUSIONLUNG INJURY", The American journal of physiology, 265(3), 1993, pp. 120000279-120000285

Abstract

Pulmonary ischemia-reperfusion results in transient hypertension and edema formation. Implicated in this injury are partially reduced oxygen species including the highly reactive hydroxyl radical. We measured ischemia-reperfusion injury and hydroxyl radical production following 90 min of either air-ventilated, N2-ventilated, or nonventilated ischemia in an isolated rabbit lung preparation. We found that edema formation was independent of alveolar oxygen tension (PO2); all ischemic groups had similar edema formation, regardless of the type of ventilation. Weight gain was 37-50 g of fluid during 40 min of reperfusion. Production of hydroxyl radical, measured by nonenzymatic hydroxylation of salicylate, was influenced by PO2 with a significant increase after air-ventilated ischemia (P < 0.05) but not after N2-ventilated ischemia. Treatment with dimethylthiourea or superoxide dismutase reduced edema formation 60-80% after air (P < 0.05)- and N2 (P < 0.05)-ventilated ischemia, whereas treatment with catalase protected only N2-ventilated ischemia (P < 0.05). Our results implicate two distinct mechanisms by which partially reduced oxygen species may contribute to pulmonary ischemia-reperfusion injury. One is by a mechanism capable of generating hydroxyl radical at normal PO2; the second is from reactions active at low PO2, the products of which are metabolized readily by extracellular enzymatic scavengers. The precise mechanisms of oxidant generation are not clear, but the findings suggest that a complex oxidative injuryoccurs during ischemia-reperfusion.

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Documento generato il 11/07/20 alle ore 16:39:39