The Cardioprotective Effects of Exogenous Hydrogen Sulfide (H2S) against Myocardial Ischemia-Reperfusion Injury
McCarthy, Caitlin J.
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Though necessary for the patient’s ultimate survival, restoring blood flow to a patient’s heart after a coronary insult increases the risk of irreversible damage to the myocardium. This damage is the result of ischemia/reperfusion (I/R) injury, a phenomenon characterized by the death of myocytes due to the restoration of blood flow following an ischemic insult (Sodha et al., 2008). One factor underlying myocardial I/R injury is increased production of oxygen free radicals at the onset of reperfusion. Injury results when the level of these free radicals exceeds endogenous scavenging mechanisms. Hydrogen sulfide is an endogenous gasotransmitter shown to have cardioprotective properties based on its ability to decrease levels of oxygen free radicals (Johansen et al., 2006). The objective of the present study was to evaluate the ability of H2S to reduce the degree of myocardial damage in hearts undergoing ischemia/reperfusion injury. The rabbit myocardial infarction model was utilized to study the effects of exogenous administration of sodium hydrogensulfide (NaHS), a hydrogen sulfide donor. Rabbits underwent 30 minutes of coronary artery occlusion followed by a 4-hour reperfusion period. The NaHS was administered to rabbits intravenously prior to the onset of regional ischemia (n=4), or at the onset of reperfusion (n=3), and infarct sizes were compared to those of the vehicle control group (saline, n=5). Myocardial infarct size, expressed as a percentage of the area at risk, was determined by tetrazolium staining and calculated for all groups. No significant differences in area at risk or area of infarct were found between the treatment and control groups. The data suggest, however, that H2S may have a protective effect during myocardial ischemia/reperfusion injury if administered immediately prior to the restoration of blood flow. Further work is required to elucidate the potential role, mechanism, and critical timing of administration of endogenous H2S as a cytoprotective media against myocardial ischemia-reperfusion injury.