Send to

Choose Destination
Circ Heart Fail. 2013 Sep 1;6(5):1077-86. doi: 10.1161/CIRCHEARTFAILURE.113.000299. Epub 2013 Jun 28.

Hydrogen sulfide attenuates cardiac dysfunction after heart failure via induction of angiogenesis.

Author information

Department of Surgery, Division of Cardiothoracic Surgery, Emory University School of Medicine, Atlanta, Georgia, 30308 and The Carlyle Fraser Heart Center.
Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan 466-8550.
Departments of Pathology and Medicine, LSU Health Sciences Center-Shreveport, Shreveport, LA 7113.
Contributed equally



Hydrogen sulfide (H2S) has been shown to induce angiogenesis in in vitro models and to promote vessel growth in the setting of hindlimb ischemia. The goal of the present study was to determine the therapeutic potential of a stable, long-acting H2S donor, diallyl trisulfide, in a model of pressure-overload heart failure and to assess the effects of chronic H2S therapy on myocardial vascular density and angiogenesis.


Transverse aortic constriction was performed in mice (C57BL/6J; 8-10 weeks of age). Mice received either vehicle or diallyl trisulfide (200 µg/kg) starting 24 hours after transverse aortic constriction and were followed up for 12 weeks using echocardiography. H2S therapy with diallyl trisulfide improved left ventricular remodeling and preserved left ventricular function in the setting of transverse aortic constriction. H2S therapy increased the expression of the proangiogenic factor, vascular endothelial cell growth factor, and decreased the angiogenesis inhibitor, angiostatin. Further studies revealed that H2S therapy increased the expression of the proliferation marker, Ki67, as well as increased the phosphorylation of endothelial NO synthase and the bioavailability of NO. Importantly, these changes were associated with an increase in vascular density within the H2S-treated hearts.


These results suggest that H2S therapy attenuates left ventricular remodeling and dysfunction in the setting of heart failure by creating a proangiogenic environment for the growth of new vessels.


H2S donor; angiogenesis; diallyl trisulfide; endothelial nitric oxide synthase; nitric oxide

[Indexed for MEDLINE]
Free PMC Article

Publication types, MeSH terms, Substances, Grant support

Publication types

MeSH terms


Grant support

Supplemental Content

Full text links

Icon for Atypon Icon for PubMed Central
Loading ...
Support Center