What is the clinical evidence from this study?

Study design: Other. Population: Cardiac ischaemia and reperfusion injury. Intervention: Amobarbital vs. Krebs Ringer solution (untreated). Primary outcome: Cardiac function, mitochondrial redox state, mt[Ca2+], superoxide levels, and infarct size.

What does this research mean for the field?

Temporary blockade of mitochondrial complex I activity by amobarbital immediately prior to ischaemia protects hearts against ischaemia-reperfusion injury by attenuating superoxide production, mitochondrial calcium overload, and infarct size. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

August 24, 2007Cardiovascular ResearchOpen Access

Inhibited mitochondrial respiration by amobarbital during cardiac ischaemia improves redox state and reduces matrix Ca2+ overload and ROS release

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Key result

Amobarbital before ischemia protects guinea pig hearts by reducing superoxide, mitochondrial calcium, and infarct size.

Population

Guinea pig Langendorff-perfused hearts

Comparison

Amobarbital in Krebs Ringer solution for 1 min… vs Krebs Ringer solution for 1 min immediately…

Design

Preclinical

Authors

MAMohammed AldakkakMedical College of Wisconsin DSDavid F. StoweCross-Cutting Cardiology QCQun ChenKunming University of Science and Technology

Discussion

Member takes

Implication

Hypothesis-generating for mitochondrial-targeted cardioprotection; clinical trials needed before human translation.

Structured PICO

Population

Guinea pig Langendorff-perfused hearts subjected to global ischaemia and reperfusion.

Intervention

Amobarbital (2.5 mM) in Krebs Ringer solution for 1 min immediately before 30 min of no flow, global ischaemia, followed by reperfusion

Comparator

Krebs Ringer solution (untreated) for 1 min immediately before 30 min of no flow, global ischaemia, followed by reperfusion

Outcome

Cardiac function, mitochondrial NADH, FAD, mt[Ca2+], O2-* levels, and infarct sizesurrogate

Temporary blockade of mitochondrial complex I activity by amobarbital protects hearts from ischaemia-reperfusion injury by reducing superoxide production and mitochondrial calcium loading.

Cite This Study

Aldakkak et al. (2007) studied Cardiac ischaemia and reperfusion injury. Amobarbital vs. Krebs Ringer solution (untreated) was evaluated on Cardiac function, mitochondrial redox state, mt[Ca2+], superoxide levels, and infarct size. Temporary blockade of mitochondrial complex I activity by amobarbital before ischaemia protects guinea pig hearts by reducing superoxide production, mitochondrial calcium loading, and infarct size.

synapsesocial.com/papers/6aa867ea5d9410427ecdf406 https://doi.org/10.1016/j.cardiores.2007.08.008

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Inhibited mitochondrial respiration by amobarbital during cardiac ischaemia improves redox state and reduces matrix Ca2+ overload and ROS release

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Inhibited mitochondrial respiration by amobarbital during cardiac ischaemia improves redox state and reduces matrix Ca2+ overload and ROS release

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

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