Myocardial ischemia selectively depletes cardiolipin in rabbit heart subsarcolemmal mitochondria

1  Division of Cardiology and 2  Division of Clinical Pharmacology, Department of Medicine, and 3  Department of Pharmacology, Case Western Reserve University, and 4  Geriatric Research, Education, and Clinical Center and Medical Service, Louis Stokes VA Medical Center, Cleveland, Ohio 44106 Mitocho...

Full description

Saved in:
Bibliographic Details
Published in:American journal of physiology. Heart and circulatory physiology 2001-06, Vol.280 (6), p.H2770-H2778
Main Authors: Lesnefsky, Edward J, Slabe, Thomas J, Stoll, Maria S. K, Minkler, Paul E, Hoppel, Charles L
Format: Article
Language:English
Subjects:
Animals
Cardiolipins - analysis
Cardiolipins - metabolism
Chromatography, High Pressure Liquid
Cytochrome c Group - analysis
Cytochrome c Group - metabolism
Disease Models, Animal
Mitochondria, Heart - metabolism
Myocardial Ischemia - metabolism
Myocardium - chemistry
Myocardium - metabolism
Myofibrils - metabolism
Oxidative Phosphorylation
Phospholipids - analysis
Phospholipids - metabolism
Rabbits
Sarcolemma - metabolism
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:1  Division of Cardiology and 2  Division of Clinical Pharmacology, Department of Medicine, and 3  Department of Pharmacology, Case Western Reserve University, and 4  Geriatric Research, Education, and Clinical Center and Medical Service, Louis Stokes VA Medical Center, Cleveland, Ohio 44106 Mitochondria contribute to myocyte injury during ischemia. After 30 and 45 min of ischemia in the isolated perfused rabbit heart, subsarcolemmal mitochondria (SSM), located beneath the plasma membrane, sustain a decrease in oxidative phosphorylation through cytochrome oxidase. In contrast, oxidation through cytochrome oxidase in interfibrillar mitochondria (IFM), located between the myofibrils, remains unaffected. Cytochrome oxidase activity in the intact membrane requires an inner mitochondrial membrane lipid environment enriched in cardiolipin. During ischemia, the content of cardiolipin decreased only in SSM, whereas the content of other phospholipids was preserved. Ischemia did not alter the composition of the cardiolipin that remained in SSM. Cardiolipin content was preserved in IFM during ischemia. Thus cardiolipin is a relatively early target of ischemic mitochondrial damage, leading to loss of oxidative phosphorylation through cytochrome oxidase in SSM. cytochrome oxidase; phospholipids; electron transport chain
ISSN:0363-6135
1522-1539
DOI:10.1152/ajpheart.2001.280.6.h2770