What question did this study set out to answer?

To evaluate the origin and functional consequences of mitochondrial enzyme alterations in right ventricular cardiac hypertrophy and heart failure.

July 11, 2016Cardiovascular ResearchOpen Access

Mitochondrial complex I dysfunction and altered NAD(P)H kinetics in rat myocardium in cardiac right ventricular hypertrophy and failure

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Why the study?

Does monocrotaline-induced right ventricular hypertrophy and failure alter mitochondrial complex I and II function in rats?

Population

Rats with right ventricular cardiac hypertrophy (CH) or heart failure (HF) induced by monocrotaline injection

Comparison

Monocrotaline injection to induce pulmonary… vs Saline injection (CON)

Design

Preclinical

Authors

RWRob C. I. WüstHeart Failure / Cardiomyopathy HVHeder de VriesAmsterdam Neuroscience LWLiesbeth T. WintjesRadboud University Nijmegen

Discussion

Member takes

Implication

Complex I dysfunction may underlie energetic failure in hypertrophy and HF; leaves open therapeutic targeting in patients.

Key Points

To evaluate the origin and functional consequences of mitochondrial enzyme alterations in right ventricular cardiac hypertrophy and heart failure.
Induced right ventricular cardiac hypertrophy (CH) and heart failure (HF) in rats via monocrotaline-induced pulmonary artery hypertension, comparing them to saline controls.
Measured NAD(P)H and FAD autofluorescence kinetics in intact cardiac trabeculae during stimulation frequency transitions to monitor complex I and II dynamics.
Assessed complex-coupled oxygen consumption, mitochondrial ultrastructure, protein content, and enzymatic activities.
Complex I-coupled respiration decreased ~3.5-fold in both CH and HF, whereas complex II-coupled respiration was reduced 2-fold only in HF.
Rapid NAD(P)H autofluorescence responses to pacing transitions were severely depressed in CH and HF, alongside modest reductions in complex I protein content and supercomplex activity.
Mitochondrial volume density remained unchanged, but significant ultrastructural remodeling and altered fusion/fission indices occurred in CH and HF.

Structured PICO

Does monocrotaline-induced right ventricular hypertrophy and failure alter mitochondrial complex I and II function in rats?

Population

Rats with right ventricular cardiac hypertrophy (CH) or heart failure (HF) induced by monocrotaline injection

Intervention

Monocrotaline injection to induce pulmonary artery hypertension

Comparator

Saline injection (CON)

Outcome

Mitochondrial complex I and complex II function assessed by NAD(P)H and FAD autofluorescence, oxygen consumption, mitochondrial morphology, protein content, and enzymatic activitysurrogate

In a rat model of right ventricular hypertrophy and failure, mitochondrial dysfunction is primarily attributed to complex I dysfunction.

Cite This Study

Wüst et al. (2016) studied this question.

synapsesocial.com/papers/6a71f15aabc331a85807b2db https://doi.org/10.1093/cvr/cvw176

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Mitochondrial complex I dysfunction and altered NAD(P)H kinetics in rat myocardium in cardiac right ventricular hypertrophy and failure

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Mitochondrial complex I dysfunction and altered NAD(P)H kinetics in rat myocardium in cardiac right ventricular hypertrophy and failure

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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