The Cardioprotective Effects of Exogenous Hydrogen Sulfide (H2S) against Myocardial Ischemia-Reperfusion Injury
Abstract
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.