The microcirculation is sensitive to small changes in pO2 and pCO2 as well as to gasotransmitter such as nitric oxide (NO) and carbon monoxide generated by the vascular endothelium [1, 2]. Resistance arteries, located upstream the microvasculature control local blood flow in part through their myogenic reactivity [3], Hydrogen sulfide (H2S), is a potent environmental toxic gas, which has recently been described as a gasotransmitter, similar to nitric oxide or carbon monoxide. Endogenous synthesis of H2S has been documented in both physiological and pathological conditions. In the vasculature, H2S is synthesized from cysteine by cystathionine-γ-lyase in smooth muscle cells and 3-mercaptopyruvate sulfuresterase and cystathionine-γ-lyase in the endothelial cells [4]. Depending on the pathophysiological condtions, H2S has been reported to exhibit pro- and anti-inflammatory properties. H2S has been shown to induce contraction at low doses through the inhibition of the conversion of citrulline into arginine by eNOS and relaxation at high doses through by activation of K+ATP channels in the rat and mouse aorta. More recent investigations have shown that H2S induces a “suspended animation-like” state leading to a better protection of animals against lethal hypoxia. Similarly, the pre-treatment of rats with H2S (intravenous injection or inhalation) prevents death after controlled but unresuscitated hemorrhage. Recent studies have shown that NaHS is protective against the effects of ischemia reperfusion induced by controlled hemorrhage in rats. NaHS was also able to improve cardiovascular homeostasis in the early resuscitation phase after hemorrhagic shock, most probably through a reduction of oxidative stress [5]. Consequently, the use of NaHS represents a promising therapeutic perspective in limiting the consequences of ischemia reperfusion. The role of H2S in the balance between pro- and antioxidant mechanisms in the vasculature will be detailed.