Detection of mitochondrial membrane damages in myocardial ischemia with ESR spin labeling technique

Shin, Genko; Sugiyama, Masayasu; Shoji, Takachika; Kagiyama, Akihiro; Sato, Hidemi; Ogura, Ryohei

doi:10.1016/0022-2828(89)90801-8

Cited by 32 publications

(16 citation statements)

References 11 publications

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“…Canines subjected to 60 min of ischemia via occlusion of the circumflex coronary artery displayed significant structural alterations to the SSM, accompanied by a decrease in membrane fluidity. These data support the contention that cardiac mitochondrial subpopulations are affected differently during ischemia while providing evidence for damage to mitochondrial membranes during the ischemic period (119). Rabbits subjected to 30 and 45 min of global ischemia displayed decreased oxidative phosphorylation through cytochrome oxidase dysfunction, as well as decreased mitochondrial cytochrome c and cardiolipin contents in the inner mitochondrial membrane (IMM) of SSM.…”

Section: Pathological Influencesupporting

confidence: 79%

“…Among these insights has been the recognition that in cardiac muscle, mitochondria exist in a number of different subcellular locales. This phenomenon has been corroborated in numerous mammalian species including mouse, rat, muskrat, guinea pig, hamster, rabbit, dog, pig, monkey, cow, and human (22,37,46,77,84,87,118,119,124,134). This phenomenon is consistent with the evaluation of other noncardiac cells such as neurons where functional heterogeneity between dendritic, somatic, axonal, and presynaptic segments due to variations in energy demands and calcium (Ca 2ϩ ) signaling dynamics are associated with structural and biochemical differences in mitochondria situated in a particular neuronal region.…”

Section: Structural and Functional Differencesmentioning

confidence: 74%

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Physiological and structural differences in spatially distinct subpopulations of cardiac mitochondria: influence of cardiac pathologies

Hollander

Thapa

Shepherd

2014

American Journal of Physiology-Heart and Circulatory Physiology

137

118

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Section: Pathological Influencesupporting

confidence: 79%

Section: Structural and Functional Differencesmentioning

confidence: 74%

Physiological and structural differences in spatially distinct subpopulations of cardiac mitochondria: influence of cardiac pathologies

Hollander

Thapa

Shepherd

2014

American Journal of Physiology-Heart and Circulatory Physiology

137

118

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show abstract

“…Mitochondria sustain progressive damage during myocardial ischemia (45,47,69,79,90,113,120,126,140), including to the electron transport chain (10,45,47,83,90,113,120,143). Ten to twenty minutes of ischemia decreases complex I activity (47,120).…”

Section: Mitochondria As Targets Of Damage During Ischemiamentioning

confidence: 99%

“…Thus SSM are more susceptible to calcium overload-mediated cytochrome c release and mitochondrial damage compared with IFM (108). Progression of ischemic damage is more rapid in SSM than in IFM (45, 69,90,126,140).…”

Section: Mitochondria As Targets Of Damage During Ischemiamentioning

confidence: 99%

Modulation of electron transport protects cardiac mitochondria and decreases myocardial injury during ischemia and reperfusion

Chen

Camara

Stowe

et al. 2007

American Journal of Physiology-Cell Physiology

239

240

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Chen Q, Camara AK, Stowe DF, Hoppel CL, Lesnefsky EJ. Modulation of electron transport protects cardiac mitochondria and decreases myocardial injury during ischemia and reperfusion. Am J Physiol Cell Physiol 292: C137-C147, 2007. First published September 13, 2006; doi:10.1152/ajpcell.00270.2006.-Mitochondria are increasingly recognized as lynchpins in the evolution of cardiac injury during ischemia and reperfusion. This review addresses the emerging concept that modulation of mitochondrial respiration during and immediately following an episode of ischemia can attenuate the extent of myocardial injury. The blockade of electron transport and the partial uncoupling of respiration are two mechanisms whereby manipulation of mitochondrial metabolism during ischemia decreases cardiac injury. Although protection by inhibition of electron transport or uncoupling of respiration initially appears to be counterintuitive, the continuation of mitochondrial oxidative phosphorylation in the pathological milieu of ischemia generates reactive oxygen species, mitochondrial calcium overload, and the release of cytochrome c. The initial target of these deleterious mitochondrial-driven processes is the mitochondria themselves. Consequences to the cardiomyocyte, in turn, include oxidative damage, the onset of mitochondrial permeability transition, and activation of apoptotic cascades, all favoring cardiomyocyte death. Ischemia-induced mitochondrial damage carried forward into reperfusion further amplifies these mechanisms of mitochondrial-driven myocyte injury. Interruption of mitochondrial respiration during early reperfusion by pharmacologic blockade of electron transport or even recurrent hypoxia or brief ischemia paradoxically decreases cardiac injury. It increasingly appears that the cardioprotective paradigms of ischemic preconditioning and postconditioning utilize modulation of mitochondrial oxidative metabolism as a key effector mechanism. The initially counterintuitive approach to inhibit mitochondrial respiration provides a new cardioprotective paradigm to decrease cellular injury during both ischemia and reperfusion.cardiolipin; cytochrome c; complex I; cytochrome oxidase MITOCHONDRIA are both targets and sources of injury during cardiac ischemia and reperfusion. This review addresses the emerging concept that modulation of mitochondrial oxidative metabolism during ischemia or early reperfusion protects mitochondrial function and decreases myocardial cell death. Mitochondria contribute to their own damage during ischemia, since blockade of electron transport immediately before ischemia dramatically attenuates damage to mitochondrial electron transport, with preserved oxidative phosphorylation, retention of cytochrome c, and decreased release of reactive oxygen species (ROS). Ischemic preconditioning (IPC) leads to a partial uncoupling of mitochondrial respiration, resulting in decreased mitochondrial injury following subsequent sustained ischemia. A substantial portion of damage to mitochondrial electron transport and oxi...

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“…Mitochondrial dysfunction and ultrastructural subcellular damage have been previously identified as one of the first signs of cardiac ischemic injury, and this in turn affects infarcted cardiac wall motion [8,9]. Ischemic damage results in changes to mitochondrial respiration [9].…”

Section: Introductionmentioning

confidence: 99%

Reduced cardiac output is associated with decreased mitochondrial efficiency in the non-ischemic ventricular wall of the acute myocardial-infarcted dog

et al. 2006

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Cardiogenic shock is the leading cause of death among patients hospitalized with acute myocardial infarction (MI). Understanding the mechanisms for acute pump failure is therefore important. The aim of this study is to examine in an acute MI dog model whether mitochondrial bio-energetic function within non-ischemic wall regions are associated with pump failure. Anterior MI was produced in dogs via ligation of left anterior descending (LAD) coronary artery, that resulted in an infract size of about 30% of the left ventricular wall. Measurements of hemodynamic status, mitochondrial function, free radical production and mitochondrial uncoupling protein 3 (UCP3) expression were determined over 24 h period. Hemodynamic measurements revealed a > 50% reduction in cardiac output at 24 h post infarction when compared to baseline. Biopsy samples were obtained from the posterior non-ischemic wall during acute infarction. ADP/O ratios for isolated mitochondria from non-ischemic myocardium at 6 h and 24 h were decreased when compared to the ADP/O ratios within the same samples with and without palmitic acid (PA). GTP inhibition of (PA)-stimulated state 4 respiration in isolated mitochondria from the non-ischemic wall increased by 7% and 33% at 6 h and 24 h post-infarction respectively when compared to sham and pre-infarction samples. This would suggest that the mitochondria are uncoupled and this is supported by an associated increase in UCP3 expression observed on western blots from these same biopsy samples. Blood samples from the coronary sinus measured by electron paramagnetic resonance (EPR) methods showed an increase in reactive oxygen species (ROS) over baseline at 6 h and 24 h post-infarction. In conclusion, mitochondrial bio-energetic ADP/O ratios as a result of acute infarction are abnormal within the non-ischemic wall. Mitochondria appear to be energetically uncoupled and this is associated with declining pump function. Free radical production may be associated with the induction of uncoupling proteins in the mitochondria.

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Detection of mitochondrial membrane damages in myocardial ischemia with ESR spin labeling technique

Cited by 32 publications

References 11 publications

Physiological and structural differences in spatially distinct subpopulations of cardiac mitochondria: influence of cardiac pathologies

Physiological and structural differences in spatially distinct subpopulations of cardiac mitochondria: influence of cardiac pathologies

Modulation of electron transport protects cardiac mitochondria and decreases myocardial injury during ischemia and reperfusion

Reduced cardiac output is associated with decreased mitochondrial efficiency in the non-ischemic ventricular wall of the acute myocardial-infarcted dog

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