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To elucidate the cardioprotective mechanisms of therapeutic hypothermia during ischemia-reperfusion injury, focusing on Akt signaling and mitochondrial oxidant generation.

April 10, 2010AJP Heart and Circulatory PhysiologyOpen Access

Therapeutic hypothermia cardioprotection via Akt- and nitric oxide-mediated attenuation of mitochondrial oxidants

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To elucidate the cardioprotective mechanisms of therapeutic hypothermia during ischemia-reperfusion injury, focusing on Akt signaling and mitochondrial oxidant generation.
Isolated cardiomyocytes from 1- to 2-day-old C57BL6/J mice and subjected them to 90 minutes of simulated ischemia followed by 3 hours of reperfusion.
Applied therapeutic hypothermia by cooling cells to 32°C during the final 20 minutes of ischemia and the first hour of reperfusion.
Evaluated cell viability, mitochondrial membrane potential, reactive oxygen species, and Akt/HSP27 phosphorylation using biochemical assays and specific pathway inhibitors.
Therapeutic hypothermia significantly decreased cardiomyocyte death compared to normothermia (19.3 ± 3.3% [n = 11] vs. 44.7 ± 2.7% [n = 10], P < 0.001).
Hypothermia maintained mitochondrial membrane potential, increased nitric oxide, and suppressed reactive oxygen species generation upon reperfusion, which was reversed by Akt and nitric oxide synthase inhibition.
Phosphorylation of Akt and heat shock protein 27 (Ser82) increased during ischemia prior to reperfusion under hypothermic conditions.

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Implication

Experimental study reveals therapeutic hypothermia prevents cell death in ischemic cardiomyocytes via Akt and nitric oxide, indicating a mitochondrial protective mechanism.

Cite This Study

Shao et al. (2010) studied this question.

synapsesocial.com/papers/6a1b31675853c704fce58ab5 https://doi.org/10.1152/ajpheart.00994.2009

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Implication

Experimental study reveals therapeutic hypothermia prevents cell death in ischemic cardiomyocytes via Akt and nitric oxide, indicating a mitochondrial protective mechanism.

Therapeutic hypothermia cardioprotection via Akt- and nitric oxide-mediated attenuation of mitochondrial oxidants

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Discussion

Implication

Cite This Study

Therapeutic hypothermia cardioprotection via Akt- and nitric oxide-mediated attenuation of mitochondrial oxidants

Key Points

Discussion

Implication

Cite This Study

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