Why the study?
Does sevoflurane postconditioning reduce infarct size and apoptosis in young and old rats subjected to myocardial ischemia/reperfusion injury?
Does sevoflurane postconditioning reduce infarct size and apoptosis in young and old rats subjected to myocardial ischemia/reperfusion injury?
Sevoflurane postconditioning protects young, but not old, rat hearts against ischemia/reperfusion injury, likely due to an age-related inability to activate Akt and ERK1/2 pathways.
May not confer cardioprotection in aged hearts; leaves open whether age limits anesthetic postconditioning in humans.
BACKGROUND: Experimental evidence suggests that anesthetic preconditioning and postconditioning could effectively attenuate myocardial ischemia/reperfusion (I/R) injury. In this study, we aimed at investigating whether there are age-associated differences in response to sevoflurane postconditioning during myocardial I/R injury in young and old rats, and explore the underlying molecular mechanisms. METHODS: Young and old rats were subjected to 30 min myocardial ischemia, followed by 2 h of reperfusion, with or without sevoflurane postconditioning. RESULTS: Both 1 and 2 minimal aveolar concentration (MAC) sevoflurane postconditioning reduced infarct size (IS) (34 ± 3% and 32 ± 2% vs. 58 ± 5%, p < 0.05) and apoptotic index (8 ± 1% and 7 ± 1% vs. 15 ± 2%, p < 0.05) in young rats, compared to young control group. In contrast, they could not reduce IS (45 ± 3% and 43 ± 3% vs. 47 ± 3%, p > 0.05) and apoptotic index (28 ± 3% and 25 ± 2%, vs. 26 ± 2%, p > 0.05) in old rats, compared to old control group. Mechanistically, we found that the phosphorylation of both Akt and ERK1/2 but not STAT3 was substantially enhanced after sevoflurane postconditioning in young rats, compared to young control group, but not in old rats, relative to old control group. CONCLUSION: There are age-related differences after exposure to sevoflurane postconditioning that protects young, but not old rat hearts against I/R injury, which may be at least associated with the inability to activate Akt and ERK1/2.
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Li et al. (2015) studied this question.
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