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Chemical preconditioning effect of 3-nitropropionic acid in anesthetized rat heart

机译:3-硝基丙酸在麻醉大鼠心脏中的化学预处理作用

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Short ischemic episodes increase tolerance against subsequent severe ischemia in the heart. Nitropropionate (3-NP), an irreversible inhibitor of succinic dehydrogenase of the mitochondrial complex 11, was shown to induce protective effect against ischemic brain injury. The aim of this study was to investigate the possible protective effect of 3-NP on regional ischemia in preconditioned rat heart in vivo. Hearts were assigned into three groups: first, in order to induce ischemic preconditioning (IP) 5 min ischemia separated by 10 min reperfusion protocol was used; second, non-preconditioned group was used as control; and third, 3-NP (20 mg/kg, i.p.) was injected 3 h before the surgical procedure in order to induce chemical preconditioning. In all these groups, 30 min regional ischemia was followed by 60 min reperfusion. Infarct size, bax expression, number of ventricular ectopic beats (VEB), duration of ventricular tachycardia (VT) and ventricular fibrillation (VF) were significantly decreased in ischemic preconditioning and 3-NP pretreatment groups, whereas bcl-2 values were not markedly changed in these groups during occlusion period. These results showed that in the anesthetized rat heart 3-NP induced chemical preconditioning by decreasing infarct size, number of VEB, duration of VT and VF. Protective effect is associated with via decreased production of bax protein expression. (c) 2008 Elsevier Inc. All rights reserved.
机译:短暂的缺血发作增加了对心脏随后发生的严重缺血的耐受性。线粒体复合物11的琥珀酸脱氢酶的不可逆抑制剂硝基丙酸酯(3-NP)具有诱导抗缺血性脑损伤的保护作用。这项研究的目的是调查3-NP对体内预处理大鼠心脏局部缺血的可能保护作用。将心脏分为三组:首先,为了诱导缺血预处理(IP),使用5分钟缺血再灌注10分钟的方案进行缺血;第二,非预处理组作为对照组。第三,在手术前3小时注射3-NP(20mg / kg,腹膜内)以诱导化学预处理。在所有这些组中,局部缺血30分钟,然后再灌注60分钟。缺血预处理和3-NP预处理组的梗死面积,bax表达,室性异位搏动数(VEB),室性心动过速持续时间(VT)和室颤(VF)均显着降低,而bcl-2值并未明显改变这些组在闭塞期。这些结果表明,在麻醉的大鼠心脏3-NP中,通过减小梗死面积,VEB数量,VT持续时间和VF持续时间来诱导化学预处理。保护作用与减少bax蛋白表达的产生有关。 (c)2008 Elsevier Inc.保留所有权利。

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