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Review
, 2014, 768607

The Cardioprotective Actions of Hydrogen Sulfide in Acute Myocardial Infarction and Heart Failure

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Review

The Cardioprotective Actions of Hydrogen Sulfide in Acute Myocardial Infarction and Heart Failure

David J Polhemus et al. Scientifica (Cairo).

Abstract

It has now become universally accepted that hydrogen sulfide (H2S), previously considered only as a lethal toxin, has robust cytoprotective actions in multiple organ systems. The diverse signaling profile of H2S impacts multiple pathways to exert cytoprotective actions in a number of pathological states. This paper will review the recently described cardioprotective actions of hydrogen sulfide in both myocardial ischemia/reperfusion injury and congestive heart failure.

Figures

Figure 1
Figure 1
History of the emergence of hydrogen sulfide (H2S) as a physiological regulator of cardiovascular homeostasis. H2S is believed to be responsible for mass extinctions that occurred over 250 million years ago as toxic gases were spewed from deep in the earth. In the 1700s, H2S was linked to injuries sustained by sewer workers. In 1989, H2S was detected in the brain of mammals by several groups. In 1996-1997, H2S was shown to modulate vascular tone and neuronal function. Finally in 2002, H2S was implicated in vascular function and blood pressure regulation in seminal studies. H2S was then shown to posttranslationally modify proteins via s-sulfhydration by Dr. Sol Snyder's group. Adopted from Hideo Kimura, Ph.D. Ward [71], Savage and Gould [72], Goodwin et al. [73], Warenycia et al. [74], and Mustafa et al. [75].
Figure 2
Figure 2
Circulating hydrogen sulfide levels are diminished in heart failure patients. We evaluated H2S levels in heart failure patients (n = 24) compared to age-matched control subjects (n = 20). Serum free H2S (μM) levels were significantly reduced (P < 0.05) in heart failure patients. Serum samples were obtained from patients enrolled in the Atlanta Cardiomyopathy Consortium (TACC). This prospective cohort study enrolls patients from the Emory University-affiliated teaching hospitals, the Emory University Hospital and Emory University Hospital Midtown, and Grady Memorial Hospital in Atlanta. All patients undergo detailed medical history surveys, electrocardiogram, standardized questionnaires, and blood and urine sample collection at baseline. All patients provide written informed consent prior to enrollment. The Emory University Institutional Review Board has approved this study. H2S levels were measured in the blood according to previously described methods [20].
Figure 3
Figure 3
Hydrogen sulfide cardioprotective signaling. H2S is known to modify proteins (s-sulfhydration), to modify the function of various ion channels (i.e., Ca2+, K+, and TRPV), to mitigate apoptosis and oxidative stress, and to be a potent modulator of cellular metabolism.

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