NOS1 and cardiac arrest: Conflicting reports have shown that H2S can (1) directly inhibit NO synthase (NOS) enzyme activity, (2) confer protection against experimental cardiac arrest in an endothelial NOS (eNOS)–dependent manner, (3) interact with NO to form unique reactive species involved in cardiovascular function, and (4) inhibit phosphodiesterase‐5 activity potentiating NOS activity.14–18 Unfortunately, no mechanistic information exists about how H2S affects NO metabolism and bioavailability during ischemic tissue vascular remodeling.