What question did this study set out to answer?

To determine whether expressing the fast-kinetics calcium pump isoform SERCA1a improves postischemic cardiac performance and limits tissue damage following ischemia-reperfusion injury.

July 13, 2007View

Expression of SERCA isoform with faster Ca2+ transport properties improves postischemic cardiac function and Ca2+ handling and decreases myocardial infarction

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Why the study?

Does expression of the SERCA1a isoform improve postischemic cardiac function and decrease myocardial infarction in mice?

Population

SERCA1a transgenic (SERCA1a(+/+)) and nontransgenic (NTG) mice

Comparison

Expression of SERCA1a isoform (transgenic model) vs Nontransgenic (NTG) mice

Design

Preclinical

Follow-up

45 min (in vitro) and 24 h (in vivo) of reperfusion

Authors

MTM.A. Hassan TalukderPennsylvania State University AKAnuradha KalyanasundaramUniversity of North Texas XZXue ZhaoJohns Hopkins University

Discussion

Member takes

Implication

May attenuate ischemia-reperfusion injury via SERCA1a in mice; leaves open translation to human cardioprotection.

Key Points

To determine whether expressing the fast-kinetics calcium pump isoform SERCA1a improves postischemic cardiac performance and limits tissue damage following ischemia-reperfusion injury.
Assessed isolated Langendorff-perfused hearts from SERCA1a transgenic (SERCA1a+/+) and nontransgenic control mice exposed to 30 minutes of global ischemia followed by 45 minutes of reperfusion.
Evaluated in vivo regional myocardial ischemia-reperfusion injury and infarct size after 24 hours of reperfusion.
Measured left ventricular developed pressure, coronary flow, intracellular calcium levels, arrhythmia incidence, and myofibrillar and mitochondrial ultrastructure.
SERCA1a+/+ hearts exhibited significantly higher baseline coronary flow and left ventricular developed pressure than nontransgenic hearts.
SERCA1a+/+ hearts showed markedly improved postischemic contractile recovery, fewer persistent arrhythmias, significantly lower intraischemic calcium levels, and preserved mitochondrial ultrastructure independent of oxidative stress.
In vivo regional ischemia-reperfusion resulted in significantly reduced myocardial infarct size after 24 hours in SERCA1a+/+ mice compared to nontransgenic controls.

Structured PICO

Does expression of the SERCA1a isoform improve postischemic cardiac function and decrease myocardial infarction in mice?

Population

SERCA1a transgenic (SERCA1a(+/+)) and nontransgenic (NTG) mice

Intervention

Expression of SERCA1a isoform (transgenic model)

Comparator

Nontransgenic (NTG) mice

Outcome

Postischemic cardiac function, myocardial salvage, and intraischemic Ca(2+) levelssurrogate

Expression of the SERCA1a isoform protects against ischemia-reperfusion injury by reducing postischemic calcium overload and improving contractile recovery in a mouse model.

Cite This Study

Talukder et al. (2007) studied this question.

synapsesocial.com/papers/6a72c2de5d37378ac1df68ec https://doi.org/10.1152/ajpheart.00663.2007

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Expression of SERCA isoform with faster Ca2+ transport properties improves postischemic cardiac function and Ca2+ handling and decreases myocardial infarction

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Expression of SERCA isoform with faster Ca2+ transport properties improves postischemic cardiac function and Ca2+ handling and decreases myocardial infarction

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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