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Ischemia-reperfusion injury (IRI) is a major cause of cardiac damage following various pathological processes. Gaseous hydrogen sulfide (H₂S) is protective during IRI by inducing a hypometabolic state in mice which is associated with anti-apoptotic, anti-inflammatory and antioxidant properties. We investigated whether gaseous H₂S administration is protective in cardiac IRI and whether non-hypometabolic concentrations of H₂S have similar protective properties.

Male C57BL/6 mice received a 0, 10, or 100 ppm H₂S-N₂ mixture starting 30 minutes prior to ischemia until 5 minutes pre-reperfusion. IRI was inflicted by temporary ligation of the left coronary artery for 30 minutes. High-resolution respirometry equipment was used to assess CO₂-production and blood pressure was measured using internal transmitters. The effects of H₂S were assessed by histological and molecular analysis.

Treatment with 100 ppm H₂S decreased CO₂-production by 72%, blood pressure by 14% and heart rate by 25%, while treatment with 10 ppm H₂S had no effects. At day 1 of reperfusion 10 ppm H₂S showed no effect on necrosis, while treatment with 100 ppm H₂S reduced necrosis by 62% (p<0.05). Seven days post-reperfusion, both 10 ppm (p<0.01) and 100 ppm (p<0.05) H₂S showed a reduction in fibrosis compared to IRI animals. Both 10 ppm and 100 ppm H₂S reduced granulocyte-influx by 43% (p<0.05) and 60% (p<0.001), respectively. At 7 days post-reperfusion both 10 and 100 ppm H₂S reduced expression of fibronectin by 63% (p<0.05) and 67% (p<0.01) and ANP by 84% and 63% (p<0.05), respectively.