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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Changes in mitochondrial properties may contribute to enhanced resistance to ischemia–reperfusion injury in the diabetic rat heart
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Changes in mitochondrial properties may contribute to enhanced resistance to ischemia–reperfusion injury in the diabetic rat heart

机译:线粒体性质的变化可能有助于增强糖尿病大鼠心脏中缺血再灌注损伤的抗性

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摘要

Diabetes mellitus, besides having deleterious effects, induces cardiac adaptation that may reduce the heart’s susceptibility to ischemia–reperfusion (IR) injury. This study aimed to investigate whether changes in mitochondrial properties are involved in the mechanisms of increased resistance of the diabetic heart to IR. Adult male Wistar rats were made diabetic by a single dose of streptozotocin (65 mg·kg –1 , i.p.), and on the day 8, Langendorff-perfused hearts were subjected to 30 min global ischemia and 40 min reperfusion. Baseline preischemic parameters in the diabetic hearts did not differ markedly from those in the nondiabetic controls, except for lower left ventricular developed pressure, higher mitochondrial membrane fluidity, and protein levels of manganese superoxide dismutase. On the other hand, diabetic hearts showed significantly better post-IR functional restoration and reduced arrhythmogenesis associated with lower reactive oxygen species production as compared with healthy controls. IR decreased membrane fluidity in both experimental groups; however, it led to a complete recovery of mitochondrial Mg 2+ -ATPase activity in diabetics in contrast to its reduction in nondiabetics. These findings indicate that the heart may become adapted to diabetes-induced alterations that might increase its tolerance to an ischemic insult. Preserved mitochondrial function might play a role in the mechanisms of the heart’s resistance to IR injury in diabetics.
机译:糖尿病除了具有有害影响外,还可诱导心脏适应,从而降低心脏对缺血再灌注(IR)损伤的易感性。本研究旨在探讨线粒体特性的变化是否参与糖尿病心脏对IR抵抗增加的机制。成年雄性Wistar大鼠通过单剂量链脲佐菌素(65 mg·kg-1,i.p.)制造糖尿病,第8天,Langendorff灌流心脏进行30分钟的全缺血和40分钟的再灌注。糖尿病心脏的基线缺血前参数与非糖尿病对照组无显著差异,除了左心室发展压力较低、线粒体膜流动性较高以及锰超氧化物歧化酶的蛋白质水平。另一方面,与健康对照组相比,糖尿病心脏在IR后的功能恢复和与较低活性氧产生相关的心律失常发生率显著改善。IR降低了两个实验组的膜流动性;然而,与非糖尿病患者相比,糖尿病患者线粒体Mg 2+-ATP酶活性完全恢复。这些发现表明,心脏可能会适应糖尿病引起的改变,从而提高其对缺血损伤的耐受性。线粒体功能的保存可能在糖尿病患者心脏抵抗IR损伤的机制中发挥作用。

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