Cardioprotective signaling cascade of A₂adenosine receptor agonist 5'-N-ethylcarboxaminidoadenosine against myocardial reperfusion injury

Yong Cheol Lee; Young Ho Jang; Chan Jin Kim; Jin Mo Kim

doi:10.4097/kjae.2008.55.6.716

January 1, 2008Korean Journal of AnesthesiologyOpen Access

Cardioprotective signaling cascade of A₂adenosine receptor agonist 5'-N-ethylcarboxaminidoadenosine against myocardial reperfusion injury

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Why the study?

Does NECA reduce myocardial reperfusion injury in isolated rat hearts?

Key Points

Determine the intracellular signaling mechanisms through which the A2 adenosine receptor agonist 5'-N-ethylcarboxaminidoadenosine (NECA) protects the myocardium against reperfusion injury.
Evaluated the cardioprotective profile of the adenosine receptor agonist 5'-N-ethylcarboxaminidoadenosine (NECA) in an experimental model of myocardial ischemia and reperfusion.
Investigated the downstream signaling cascade mediating tissue preservation and infarct reduction.
Demonstrated that A2 adenosine receptor activation by NECA conveys significant anti-infarct cardioprotection.
Identified critical intracellular signaling pathways responsible for mitigating tissue death following reperfusion.

Structured PICO

Does NECA reduce myocardial reperfusion injury in isolated rat hearts?

P

Population

Langendorff perfused isolated rat hearts (male Wistar rats, 280-330g, n=88 analyzed) subjected to 30 minutes of regional ischemia and 120 minutes of reperfusion.

I

Intervention

5'-N-Ethylcarboxaminidoadenosine (NECA) 100 nM perfused for 5 minutes before and 60 minutes after reperfusion.

C

Comparator

Control hearts (no NECA) and various antagonist/inhibitor groups (CSC, MRS1706, KT5823, ODQ, SB216763, atractyloside).

O

Outcome

Area at necrosis (AN) as a percentage of area at risk (AAR) measured by triphenyltetrazolium chloride staining at 120 minutes of reperfusion.surrogate

NECA administered at reperfusion reduces myocardial infarct size through the activation of A2A and A2B adenosine receptors, cGMP/PKG pathway, GSK-3β inactivation, and mPTP opening inhibition.

Limitations

The role of A1AR and A3AR was excluded from this study and needs to be clarified in the future.

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Implication

NECA cardioprotection in rats does not support clinical use; leaves open translation of A2AR agonism to human reperfusion injury.

Abstract

This experiments investigated the signaling cascade responsible for anti-infarct effect by an A2 adenosine receptor (AR) agonist 5'-N-Ethylcarboxaminidoadenosine (NECA).

Discussion

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Cite This Study

Lee et al. (2008) studied this question.

synapsesocial.com/papers/6a197aa1c05413006f586452 https://doi.org/10.4097/kjae.2008.55.6.716

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Cardioprotective signaling cascade of A₂adenosine receptor agonist 5'-N-ethylcarboxaminidoadenosine against myocardial reperfusion injury

Key Points

Structured PICO

Limitations

Ask about this paper

Implication

Abstract

Discussion

Cite This Study

Cardioprotective signaling cascade of A₂adenosine receptor agonist 5'-N-ethylcarboxaminidoadenosine against myocardial reperfusion injury

Key Points

Structured PICO

Limitations

Ask about this paper

Implication

Abstract

Discussion

Cite This Study

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