Molecular mechanism of carvedilol in attenuating the reversion to fetal energy metabolism during cardiac hypertrophy development

胡琴; 李隆贵

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Molecular mechanism of carvedilol in attenuating the reversion to fetal energy metabolism during cardiac hypertrophy development

Updated：2026-03-12

- Molecular mechanism of carvedilol in attenuating the reversion to fetal energy metabolism during cardiac hypertrophy development
- Molecular mechanism of carvedilol in attenuating the reversion to fetal energy metabolism during cardiac hypertrophy development
- 解放军医学杂志（英文版） 2003年第5期页码：290-294
- Affiliations：
  
  1. Cardiology Center of Chinese PLA
  2. Xinqiao Hospital
  3. Third Military Medical University
  4. ,China
- Author bio：
- Funds：
- DOI：
  中图分类号： R541
- 纸质出版：2003
- Accepted：
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Molecular mechanism of carvedilol in attenuating the reversion to fetal energy metabolism during cardiac hypertrophy development[J]. 解放军医学杂志（英文版）, 2003,(5):290-294.

[1]胡琴,李隆贵.Molecular mechanism of carvedilol in attenuating the reversion to fetal energy metabolism during cardiac hypertrophy development[J].Journal of Medical Colleges of PLA,2003(05):290-294.
Molecular mechanism of carvedilol in attenuating the reversion to fetal energy metabolism during cardiac hypertrophy development[J]. 解放军医学杂志（英文版）, 2003,(5):290-294. DOI：

[1]胡琴,李隆贵.Molecular mechanism of carvedilol in attenuating the reversion to fetal energy metabolism during cardiac hypertrophy development[J].Journal of Medical Colleges of PLA,2003(05):290-294. DOI：

摘要

Abstract

<正> Objective: To explore the molecular regulation mechanism of carvedilol in attenuating the reversion back towards fetal energy metabolism during the development of cardiac hypertrophy induced by coarctation of abdominal aorta （ CAA） in male Wistar rats. Methods: Hemodynamic and ventricular remodeling parameters

free fatty acid content in the serum were measured in the experimental animals at 16 weeks after the surgical CAA

the rats receiving carvedilol intervention （CAR） after CAA

and those with sham operation （SH）. The expressions of muscle carnitine palmi-toyltransferase Ⅰ （M-CPT Ⅰ ） and medium chain acyl-CoA dehydrogenase （MCAD） mRNA in the cardiac myocytes from every group were studied with RT-PCR. Results: Significant left ventricular hypertrophy were observed in the rats 16 weeks after coarctation operation （P <0. 05）

together with significant free fatty acids accumulation and downregu-lation of M-CPT Ⅰ and MCAD mRNA （P <0. 05） in CAA group. Carvedilol at a dose of 30 mg/kg/d for 12 weeks i

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