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Titolo:
"Chemical preconditioning" by 3-nitropropionate reduces ischemia-reperfusion injury in cardiac-arrested rat lungs
Autore:
Hirata, T; Fukuse, T; Ishikawa, S; Hanaoka, S; Chen, Q; Shoji, T; Wada, H;
Indirizzi:
Kyoto Univ, Fac Med, Dept Thorac Surg, Sakyo Ku, Kyoto 6068397, Japan Kyoto Univ Kyoto Japan 6068397 orac Surg, Sakyo Ku, Kyoto 6068397, Japan
Titolo Testata:
TRANSPLANTATION
fascicolo: 3, volume: 71, anno: 2001,
pagine: 352 - 359
SICI:
0041-1337(20010215)71:3<352:"PB3RI>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
HEART-BEATING DONORS; OXIDATIVE-PHOSPHORYLATION; SUPEROXIDE GENERATION; TRANSPLANTATION; ATP; MITOCHONDRIA; MECHANISMS; INHIBITION; ACID; RESPIRATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
44
Recensione:
Indirizzi per estratti:
Indirizzo: Hirata, T Kyoto Univ, Fac Med, Dept Thorac Surg, Sakyo Ku, 54 Kawahara Cho, Kyoto 6068397, Japan Kyoto Univ 54 Kawahara Cho Kyoto Japan 6068397 o 6068397, Japan
Citazione:
T. Hirata et al., ""Chemical preconditioning" by 3-nitropropionate reduces ischemia-reperfusion injury in cardiac-arrested rat lungs", TRANSPLANT, 71(3), 2001, pp. 352-359

Abstract

Background. Chemical preconditioning was defined as the induction of resistance to massive disruption of energy metabolism through prior chemical suppression of oxidative phosphorylation, by which phenomena similar to those resulting from increased ischemic tolerance as a result of ischemic preconditioning can be induced, It could be induced by the inhibitor of either mitochondrial complex I or II, We investigated whether or not chemical preconditioning by 3-nitropropionate (an inhibitor of the mitochondrial complex II) can suppress ischemia-reperfusion injury in cardiac-arrested lungs, whichwill be the major problem in lung transplants donated from non-heart-beating cadavers. Methods and Results, In an isolated rat lung perfusion model with fresh rat blood as perfusate, administration of 3-nitropropionate (20 mg/kg) immediately before the induction of cardiac arrest attenuated pulmonary dysfunction during reperfusion after 1 hr postmortem warm ischemia and 1 hr cold preservation, 3-Nitropropionate administration reduced the mitochondrial respiratory functions (state 3 and state 4 respiration, and the respiratory control ratio) before cardiac arrest and kept them at a lower level of activitythan when decreased by ischemia alone, 3-Nitropropionate administration also reduced the ATP levels immediately after drug administration. However, 3-nitropropionate did not significantly reduce lipid peroxidation in the lung tissue and mitochondria. Conclusions. These results demonstrated that chemical. preconditioning by 3-nitropropionate administration immediately before cardiac arrest suppressed succinate-related oxidation during postmortem warm ischemia and reduced ischemia-reperfusion injury in cardiac arrested rat lungs.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/04/20 alle ore 00:06:09