Source:http://linkedlifedata.com/resource/pubmed/id/20051450
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
4
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| pubmed:dateCreated |
2010-3-25
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| pubmed:abstractText |
We investigated the impact of hydrogen sulfide (H(2)S) on myocardium in the setting of cold crystalloid cardioplegia and cardiopulmonary bypass (CP/CPB). Eighteen male Yorkshire pigs underwent 1 h CP/CPB followed by 2 h of reperfusion. Pigs received either: placebo (control, n=9), or H(2)S (as NaHS) as a bolus/infusion (bolus/infusion, n=6), or as an infusion (infusion, n=6). The expression pattern of various myocardial effector pathways was investigated. Coronary microvascular relaxation to endothelium-dependent and -independent agonists was assessed. No differences in cardiac function were observed among groups. Endothelium-dependent microvascular relaxation to adenosine diphosphate was improved in the H(2)S bolus/infusion group only (P<0.05). The expression of hemeoxygenase-1, phospho-heat shock proteins27 and phospho-p44/42 MAPK extracellular signal-regulated kinase were higher in H(2)S-treated groups (P<0.05). Phospho-endothelial nitric oxide synthase (P=0.08), phospho-B-cell lymphoma 2 (P=0.09), and phospho-Bad (P=0.06) all displayed a trend to be higher with H(2)S treatment. The expressions of apoptosis inducing factor and Bcl 2/adenovirus E1B 19 kDa-interacting protein were lower in H(2)S treated groups (P<0.05). The microtubule-associated protein 1 light chain 3 ratio was lower in the infusion group vs. control animals (P<0.05). There was a trend for lower phospho-mammalian target of rapamycin expression in the infusion group (P=0.07), whereas phosphorylation of p70S6K1 was higher with H(2)S-treatment (P=0.09). This study demonstrates that H(2)S-treatment may offer biochemical myocardial protection via attenuation of caspase-independent apoptosis and autophagy in the setting of CP/CPB.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Apoptosis Regulatory Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Cardiotonic Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Heat-Shock Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Hydrogen Sulfide,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Compounds,
http://linkedlifedata.com/resource/pubmed/chemical/Troponin I,
http://linkedlifedata.com/resource/pubmed/chemical/potassium cardioplegic solution
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| pubmed:status |
MEDLINE
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| pubmed:month |
Apr
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| pubmed:issn |
1569-9285
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:volume |
10
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
506-12
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| pubmed:meshHeading |
pubmed-meshheading:20051450-Animals,
pubmed-meshheading:20051450-Apoptosis,
pubmed-meshheading:20051450-Apoptosis Regulatory Proteins,
pubmed-meshheading:20051450-Autophagy,
pubmed-meshheading:20051450-Cardiopulmonary Bypass,
pubmed-meshheading:20051450-Cardiotonic Agents,
pubmed-meshheading:20051450-Cell Survival,
pubmed-meshheading:20051450-Coronary Circulation,
pubmed-meshheading:20051450-Heart Arrest, Induced,
pubmed-meshheading:20051450-Heat-Shock Proteins,
pubmed-meshheading:20051450-Hemodynamics,
pubmed-meshheading:20051450-Hydrogen Sulfide,
pubmed-meshheading:20051450-Infusions, Intravenous,
pubmed-meshheading:20051450-Injections, Intravenous,
pubmed-meshheading:20051450-Male,
pubmed-meshheading:20051450-Microcirculation,
pubmed-meshheading:20051450-Myocardium,
pubmed-meshheading:20051450-Potassium Compounds,
pubmed-meshheading:20051450-Reperfusion Injury,
pubmed-meshheading:20051450-Swine,
pubmed-meshheading:20051450-Time Factors,
pubmed-meshheading:20051450-Troponin I,
pubmed-meshheading:20051450-Vasodilation,
pubmed-meshheading:20051450-Ventricular Function, Left
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| pubmed:year |
2010
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| pubmed:articleTitle |
Effect of hydrogen sulfide on myocardial protection in the setting of cardioplegia and cardiopulmonary bypass.
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| pubmed:affiliation |
Department of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Ave, DANA 801, Boston, MA 02215, USA.
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| pubmed:publicationType |
Journal Article
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