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Nitric oxide syntha.e media.es the a.elin-induced improvement of myoca.dia. postischemic meta.olic a.d functiona. recovery

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Open Journa. of Molecula. a.d Integra.ive Physiology 2012年第1期2卷 1-7页

作者： Oleg I. Pisa.enko yulia a. pelogeykina Va.entin S. Shulzhenko Irina.M. Studneva La.ora.ory for Myoca.dia. Meta.olism Russian Cardiology Research-and-Production Complex Moscow Russia

The a.ipocytokine a.elin is ca.a.le to reduce myoca.dia. ischemia.reperfusion injury in rodents. Ca.dioprotective a.tivity of a.elin ma. be a.tributed to upregula.ion of endothelia. nitric oxide syntha.e (eNOS). This study wa. designed to exa.ine meta.olic a.d functiona. effects of a.synthesized 12 C-termina. residue of a.elin (a.12) a.d NG-nitro-L-a.ginine methyl ester (L-Na.E), a.non-selective eNOS inhibitor, in isola.ed working ra. hea.ts subjected to globa. ischemia. Preischemic infusion of a.12 increa.ed recovery of ca.dia. function during reperfusion compa.ed with control a.d resulted in enha.ced restora.ion of myoca.dia. a.P, a.enine nucleotide pool, phosphocrea.ine a.d reduction of myoca.dia. la.ta.e a.d la.ta.e/pyruva.e ra.io. Coa.ministra.ion of a.12 a.d L-Na.E a.gra.a.ed recovery of corona.y flow a.d ca.dia. function compa.ed with these indices a.ter a.12 trea.ment. Ca.dia. dysfunction wa. a.socia.ed with increa.e in la.ta.e dehydrogena.e relea.e in myoca.dia. effluent, reduction of glucose oxida.ion a.d a.olishment of a.gmented restora.ion of high energy phospha.es. The results clea.ly demonstra.e involvement of NOS-dependent mecha.isms in ca.dioprotection a.forded by a.elin.

关键词： a.elin Hea.t Ischemia.Reperfusion Injury L-Na.E Energy Meta.olism

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a.elin-12 improves meta.olic a.d functiona. recovery of ra. hea.t a.ter globa. ischemia

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Hea.th 2010年第8期2卷 927-934页

作者： Oleg I. Pisa.enko Va.entin S. Shulzhenko yulia a. pelogeykina Irina.M. Studneva.Denis N. Kha.ri 不详

This work wa. designed to explore effica.y of a.elin-12 (a.12) a. a.ca.dioprotective a.ent when given before ischemia.or a. reperfusion using the isola.ed working hea.t model. Hea.ts of ma.e Wista. ra.s were subjected to 30-min sta.iliza.ion period followed by 35-min globa. ischemia.a.d 30-min reperfusion. a.short-term infusion of Krebs-Henseleit buffer (KHB) con-ta.ning a.12 (35, 70, 140, 280 or 560 ?M) wa. a.-plied prior to ischemia.(a.12-I) or a. onset of reperfusion (a.12-R). KHB infusion wa. used a. control. a.12 infusions induced a.dose-dependent increa.e in recovery of corona.y flow, contra.tile a.d pump function during reperfu-sion, with the la.gest a.gmenta.ion of these indices in the a.12-I group. Both a.12 groups exhibited a.significa.t reduction of LV dia.tolic pressure rise during reperfusion compa.ed with control. Enha.ced functiona. recovery in the a.12-I group wa. combined with a.decrea.e in LDH lea.a.e in perfusa.e on ea.ly reperfusion (by 36% vs. control, p a.12 ma.kedly increa.ed myoca.dia. a.P content, enha.ced preserva.ion of the tota. a.enine nucleotide pool a.d improved recovery of the energy cha.ge in reperfused hea.ts. There wa. a.trend towa.ds increa.e in myoca.dia. phosphocrea.ine by the end of re- perfusion in the a.12-I group;however this benefit did not rea.h sta.istica. significa.ce. a. the end of reperfusion, myoca.dia. la.ta.e a.d la.ta.e/pyruva.e ra.io were on a.era.e 5-fold lower in a.12-I trea.ed hea.ts compa.ed with control ones a.d did not differ significa.tly from the initia. va.ues. Therefore, improved ca.dia. dysfunction a.ter I/R injury a.d less cell mem-bra.e da.a.e induced by a.12 a.e a.socia.ed with ma.nta.ning high energy phospha.es, pa.ticula.ly a.P, in reperfused myoca.dium. Cha.ges in energy meta.olism ma. pla. a.role in mecha.isms of ca.dioprotection a.forded by a.12 during I/R stress.

关键词： a.elin-12 Ra. Hea.t Ischemia. Reperfusion Injury Energy Meta.olism Cell Membra.e Da.a.e

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