Therapeutic delivery of hydrogen sulfide for salvage of ischemic skeletal muscle after the onset of critical ischemia Peter W. Henderson, MD, Natalia.

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Presentation transcript:

Therapeutic delivery of hydrogen sulfide for salvage of ischemic skeletal muscle after the onset of critical ischemia Peter W. Henderson, MD, Natalia Jimenez, BA, John Ruffino, BA, Allie M. Sohn, BS, Andrew L. Weinstein, BS, David D. Krijgh, BA, Alyssa J. Reiffel, MD, Jason A. Spector, MD Journal of Vascular Surgery Volume 53, Issue 3, Pages 785-791 (March 2011) DOI: 10.1016/j.jvs.2010.10.094 Copyright © 2011 Terms and Conditions

Fig 1 Summary of time of NaHS delivery (arrow) for the preischemic, preischemic (long-term), postischemic (1 minutes before reperfusion), and postischemic (20 minutes before reperfusion) experimental groups. Journal of Vascular Surgery 2011 53, 785-791DOI: (10.1016/j.jvs.2010.10.094) Copyright © 2011 Terms and Conditions

Fig 2 Myotube apoptotic index measured after 1, 3, and 5 hours of hypoxia, all followed by 3 hours of normoxia. The star denotes statistical significance compared with non-NaHS-treated control for each respective time. All cultures were repeated in triplicate. The stars indicate P < .05 relative to non-NaHS-treated cells at each time. Journal of Vascular Surgery 2011 53, 785-791DOI: (10.1016/j.jvs.2010.10.094) Copyright © 2011 Terms and Conditions

Fig 3 Photomicrographs show muscle after postischemic delivery of NaHS (n = 6 for each study group; original magnification, ×100). A, Injury score nonischemic control muscle, (B) ischemic-reperfused muscle that had not been treated with NaHS, (C) ischemic-reperfused tissue that had been treated with 10 μM NaHS 1 minute before reperfusion, and (D) ischemic-reperfused tissue that had been treated with 10 μM NaHS 20 minutes before reperfusion. Note the preservation of normal muscle architecture after treatment with NaHS 20 minutes before reperfusion but minimal preservation when delivered only 1 minute before reperfusion. Journal of Vascular Surgery 2011 53, 785-791DOI: (10.1016/j.jvs.2010.10.094) Copyright © 2011 Terms and Conditions

Fig 4 Muscle after postischemic delivery of NaHS (n = 6 for each study group). Apoptotic index for nonischemic control muscle, ischemic-reperfused muscle that had not been treated with NaHS, ischemic-reperfused tissue that had been treated with 10 μM NaHS 1 minute before reperfusion, and ischemic-reperfused tissue that had been treated with 10 μM NaHS 20 minutes before reperfusion. The error bars show the standard deviation. Journal of Vascular Surgery 2011 53, 785-791DOI: (10.1016/j.jvs.2010.10.094) Copyright © 2011 Terms and Conditions

Fig 5 Proposed multifactorial mechanism by which HS is cytoprotective against ischemia-reperfusion injury when delivered after the onset of ischemia. HS present in the cell can be exogenous or endogenous (produced by cystathionine-β-synthase [CBS] and cystathionine-β-lyase [CSE]) in nature and is thought to act as a free radical scavenger, an activator of the reperfusion injury salvage kinase pathway (RISK) pathway, and an opener of KATP channels, all of which promote cell survival via mitochondrial protection. ERK, Extracellular-regulated kinase; MPTP, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. Journal of Vascular Surgery 2011 53, 785-791DOI: (10.1016/j.jvs.2010.10.094) Copyright © 2011 Terms and Conditions