Why the study?
Reperfusion to treat myocardial ischemia can cause myocardial ischemia-reperfusion injury, and previous studies have indicated a protective role for hydrogen sulfide in this setting.
This review summarizes preclinical evidence that hydrogen sulfide acts as a cardioprotective gasotransmitter against myocardial ischemia-reperfusion injury.
Preclinical evidence supports H2S cardioprotection in ischemia-reperfusion models; leaves open clinical translation.
Ischemic heart disease is one of the major causes of cardiovascular‑related mortality worldwide. Myocardial ischemia can be attenuated by reperfusion that restores the blood supply. However, injuries occur during blood flow restoration that induce cardiac dysfunction, which is known as myocardial ischemia‑reperfusion injury (MIRI). Hydrogen sulfide (H₂S), the third discovered endogenous gasotransmitter in mammals (after NO and CO), participates in various pathophysiological processes. Previous in vitro and in vivo research have revealed the protective role of H₂S in the cardiovascular system that render it useful in the protection of the myocardium against MIRI. The cardioprotective effects of H₂S in attenuating MIRI are summarized in the present review.
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Wu et al. (2021) studied this question.
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