• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

[曲美他嗪治疗实验性缺血性心脏病在年龄方面的疗效]

[Efficiency of trimetazidine treatment of experimental ischemic heart disease in age aspect].

作者信息

Kukes V G, Zhernakova N I, Gorbach T V, Romashchenko O V, Rumbesht V V

出版信息

Eksp Klin Farmakol. 2013;76(2):9-12.

PMID:23631276
Abstract

Introduction of trimetazidine to 10-month-aged rats with experimental ischemic heart disease leads to an increase in carbohydrate utilization with energy purposes in myocardium, which is manifested by increasing activity of glycolysis enzymes with decreasing lactate level in myocardium, increasing activity of pyruvate dehydrogenase and citrate synthase in mitochondrial cardiomyocytes, and increasing ATP content in myocardium. This is accompanied by signs of stabilization of cardiomyocyte membranes and reduction in the degree of tissue hypoxia. The efficiency of trimetazidine decreases with increasing age: in 24-month-aged rats, the direction of changes is retained, but they are less pronounced.

摘要

将曲美他嗪应用于10月龄实验性缺血性心脏病大鼠,可导致心肌中用于能量目的的碳水化合物利用率增加,表现为糖酵解酶活性增加,心肌中乳酸水平降低,线粒体心肌细胞中丙酮酸脱氢酶和柠檬酸合酶活性增加,以及心肌中ATP含量增加。这伴随着心肌细胞膜稳定的迹象以及组织缺氧程度的降低。曲美他嗪的疗效随年龄增长而降低:在24月龄大鼠中,变化方向保持不变,但不那么明显。

相似文献

1
[Efficiency of trimetazidine treatment of experimental ischemic heart disease in age aspect].[曲美他嗪治疗实验性缺血性心脏病在年龄方面的疗效]
Eksp Klin Farmakol. 2013;76(2):9-12.
2
Protective effect of trimetazidine on myocardial mitochondrial function in an ex-vivo model of global myocardial ischemia.曲美他嗪对整体心肌缺血离体模型中心肌线粒体功能的保护作用。
Eur J Pharmacol. 2004 Oct 25;503(1-3):123-8. doi: 10.1016/j.ejphar.2004.09.003.
3
The antianginal drug trimetazidine shifts cardiac energy metabolism from fatty acid oxidation to glucose oxidation by inhibiting mitochondrial long-chain 3-ketoacyl coenzyme A thiolase.抗心绞痛药物曲美他嗪通过抑制线粒体长链3-酮酰基辅酶A硫解酶,将心脏能量代谢从脂肪酸氧化转变为葡萄糖氧化。
Circ Res. 2000 Mar 17;86(5):580-8. doi: 10.1161/01.res.86.5.580.
4
Trimetazidine normalizes postischemic function of hypertrophied rat hearts.曲美他嗪可使肥大大鼠心脏缺血后的功能恢复正常。
J Pharmacol Exp Ther. 2005 Jul;314(1):446-54. doi: 10.1124/jpet.104.082636. Epub 2005 Apr 19.
5
Trimetazidine in the myocardial cell mechanisms of cytoprotection.曲美他嗪在心肌细胞中的细胞保护机制
Rom J Intern Med. 1998 Jul-Dec;36(3-4):137-44.
6
The antianginal agent trimetazidine does not exert its functional benefit via inhibition of mitochondrial long-chain 3-ketoacyl coenzyme A thiolase.抗心绞痛药物曲美他嗪并非通过抑制线粒体长链3-酮酰基辅酶A硫解酶发挥其功能益处。
Circ Res. 2003 Aug 8;93(3):e26-32. doi: 10.1161/01.RES.0000086943.72932.71. Epub 2003 Jul 17.
7
Demand-induced ischemia in volume expanded isolated rat heart; the effect of dichloroacetate and trimetazidine.容量扩张的离体大鼠心脏中的需求诱导性缺血;双氯乙酸和曲美他嗪的作用。
J Physiol Pharmacol. 2010 Apr;61(2):153-62.
8
Trimetazidine-induced enhancement of myocardial glucose utilization in normal and ischemic myocardial tissue: an evaluation by positron emission tomography.曲美他嗪对正常及缺血心肌组织心肌葡萄糖利用的增强作用:正电子发射断层扫描评估
Am J Cardiol. 1998 Sep 3;82(5A):42K-49K. doi: 10.1016/s0002-9149(98)00536-0.
9
Metabolic therapy in the treatment of ischaemic heart disease: the pharmacology of trimetazidine.代谢疗法在缺血性心脏病治疗中的应用:曲美他嗪的药理学
Fundam Clin Pharmacol. 2003 Apr;17(2):133-45. doi: 10.1046/j.1472-8206.2003.00154.x.
10
[Efficiency of mildronate in rats of different age with experimental-induced myocardial ischemia].[米屈肼对不同年龄实验性心肌缺血大鼠的疗效]
Vestn Ross Akad Med Nauk. 2013(1):42-6. doi: 10.15690/vramn.v68i1.536.

引用本文的文献

1
Cell cycle arrest of cardiomyocytes in the context of cardiac regeneration.心脏再生背景下心肌细胞的细胞周期停滞
Front Cardiovasc Med. 2025 Apr 28;12:1538546. doi: 10.3389/fcvm.2025.1538546. eCollection 2025.
2
Trimetazidine in Heart Failure.曲美他嗪用于心力衰竭
Front Pharmacol. 2021 Jan 12;11:569132. doi: 10.3389/fphar.2020.569132. eCollection 2020.