Key result
Moderate intra-ischemic therapeutic hypothermia enhanced recovery of cardiac function, decreased fatty acid oxidation, reduced taurine release, and enhanced PTEN, Akt, and ERK1/2 signaling.
Why the study?
Although therapeutic hypothermia protects against ischemia/reperfusion injury, how it regulates metabolic recovery remains unknown.
Does moderate intra-ischemic therapeutic hypothermia improve metabolic and functional recovery in isolated rat hearts subjected to ischemia/reperfusion injury?
Does moderate intra-ischemic therapeutic hypothermia improve metabolic and functional recovery in isolated rat hearts subjected to ischemia/reperfusion injury?
Moderate intra-ischemic therapeutic hypothermia provides cardioprotection in rat hearts by modulating PTEN/Akt/ERK signaling and decreasing fatty acid oxidation.
TH-associated metabolic recovery in rat I/R hearts is hypothesis-generating; leaves open clinical translation.
Therapeutic hypothermia (TH) provides cardioprotection from ischemia/reperfusion (I/R) injury. However, it remains unknown how TH regulates metabolic recovery. We tested the hypothesis that TH modulates PTEN, Akt, and ERK1/2, and improves metabolic recovery through mitigation of fatty acid oxidation and taurine release. Left ventricular function was monitored continuously in isolated rat hearts subjected to 20 min of global, no‐flow ischemia. Moderate cooling (30°C) was applied at the start of ischemia and hearts were rewarmed after 10 min of reperfusion. The effect of TH on protein phosphorylation and expression at 0 and 30 min of reperfusion was investigated by western blot analysis. Post‐ischemic cardiac metabolism was investigated by 13C‐NMR. TH enhanced recovery of cardiac function, reduced taurine release, and enhanced PTEN phosphorylation and expression. Phosphorylation of Akt and ERK1/2 was increased at the end of ischemia but decreased at the end of reperfusion. On NMR analysis, TH‐treated hearts displayed decreased fatty acid oxidation. Direct cardioprotection by moderate intra‐ischemic TH is associated with decreased fatty acid oxidation, reduced taurine release, enhanced PTEN phosphorylation and expression, and enhanced activation of both Akt and ERK1/2 prior to reperfusion.
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Justice et al. (2023) studied Ischemia/reperfusion injury. Therapeutic hypothermia (moderate cooling to 30°C) vs. Control (implied normothermia) was evaluated on Left ventricular function, protein phosphorylation and expression, and cardiac metabolism. Moderate intra-ischemic therapeutic hypothermia enhanced recovery of cardiac function, decreased fatty acid oxidation, reduced taurine release, and enhanced PTEN, Akt, and ERK1/2 signaling.
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