Related Experiment Video

Updated: Aug 7, 2026

Model of Ischemia and Reperfusion Injury in Rabbits
06:11

Model of Ischemia and Reperfusion Injury in Rabbits

Published on: November 3, 2023

Reversal of mitochondrial defects before ischemia protects the aged heart

Edward J Lesnefsky1, DingChao He, Shadi Moghaddas

  • 1Department of Medicine (Division of Cardiology), Case Western Reserve University and Medical Service, Cleveland, Ohio, USA. EXL9@cwru.edu

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|June 24, 2006
PubMed

Insights

Acetyl-L-carnitine (ALCAR) treatment improved mitochondrial function in aged hearts, reducing injury during ischemia and reperfusion. This intervention enhanced heart recovery and decreased damage in older rats, suggesting a potential therapeutic strategy.

Area of Science:

  • Cardiovascular Science
  • Mitochondrial Biology
  • Aging Research

Background:

  • Aging impairs cardiac mitochondrial oxidative metabolism, increasing susceptibility to ischemia-reperfusion injury.
  • Interfibrillar mitochondria (IFM) show reduced oxidative capacity with age, contributing to myocardial dysfunction.

Purpose of the Study:

  • To investigate if reversing age-related mitochondrial defects in the aged heart before ischemia can reduce injury.
  • To determine the effect of acetyl-L-carnitine (ALCAR) on aged heart function during ischemia and reperfusion.

Main Methods:

  • Aged (24 months) and adult (6 months) Fischer 344 rats were treated with ALCAR (300 mg/kg) or controls.
  • Isolated hearts underwent 25 minutes of global ischemia followed by 30 minutes of reperfusion.
  • Mitochondrial function (oxidative phosphorylation, complex III & IV activity) and cardiac injury (LDH release) were assessed.

Main Results:

  • ALCAR restored oxidative phosphorylation and mitochondrial complex activity in aged hearts to adult levels.
  • ALCAR-treated aged hearts showed improved contractile recovery and reduced LDH release post-ischemia/reperfusion compared to controls.
  • ALCAR did not significantly alter functional recovery or injury in adult hearts.

Conclusions:

  • Restoring mitochondrial function with ALCAR before ischemia mitigates age-related cardiac injury.
  • ALCAR treatment enhances myocardial contractile recovery and reduces tissue damage in the aged heart following ischemia-reperfusion.
  • Targeting mitochondrial defects in aging hearts presents a promising approach to improve cardiac resilience.

More Related Videos

A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation07:14

A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation

Published on: July 13, 2018

Related Concept Videos

Mitochondria01:37

Mitochondria

Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...