Document Detail


Hydrogen sulfide triggers late-phase preconditioning in postischemic small intestine by an NO- and p38 MAPK-dependent mechanism.
MedLine Citation:
PMID:  19168723     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Hydrogen sulfide (H(2)S) is one of three endogenous gases, along with carbon monoxide (CO) and nitric oxide (NO), that exert a variety of important vascular actions in vivo. Although it has been demonstrated that CO or NO can trigger the development of a preconditioned phenotype in postischemic tissues, it is unclear whether H(2)S may also induce protection in organs subsequently exposed to ischemia-reperfusion (I/R). In light of these observations, we postulated that preconditioning with the exogenous H(2)S donor sodium hydrosulfide (NaHS-PC) would inhibit leukocyte rolling (LR) and adhesion (LA) induced by I/R. We used intravital microscopic techniques to demonstrate that NaHS-PC 24 h, but not 1 h, before I/R causes postcapillary venules to shift to an anti-inflammatory phenotype in wild-type (WT) mice such that these vessels fail to support LR and LA during reperfusion. The protective effect of NaHS-PC on LR was largely abolished by coincident pharmacological inhibition of NO synthase (NOS) in WT animals and was absent in endothelial NOS-deficient (eNOS(-/-)) mice. A similar pattern of response was noted in WT mice treated concomitantly with NaHS plus p38 mitogen-activated protein kinase (MAPK) inhibitors (SB 203580 or SK-86002). Whereas the reduction in LA induced by antecedent NaHS was attenuated by pharmacological inhibition of NOS or p38 MAPK in WT mice, the antiadhesive effect of NaHS was still evident in eNOS(-/-) mice. Thus NaHS-PC prevents LR and LA by triggering the activation of an eNOS- and p38 MAPK-dependent mechanism. However, the role of eNOS in the antiadhesive effect of NaHS-PC was less prominent than its effect to reduce LR.
Authors:
Mozow Yusof; Kazuhiro Kamada; Theodore Kalogeris; F Spencer Gaskin; Ronald J Korthuis
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2009-01-23
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  296     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2009 Mar 
Date Detail:
Created Date:  2009-03-03     Completed Date:  2009-04-09     Revised Date:  2010-09-22    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H868-76     Citation Subset:  IM    
Affiliation:
Dept. of Medical Pharmacology and Physiology, Univ. of Missouri School of Medicine, One Hospital Drive, Columbia, MO 65212, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Anti-Inflammatory Agents / pharmacology*
Cell Adhesion / drug effects
Disease Models, Animal
Enzyme Inhibitors / pharmacology
Hydrogen Sulfide / metabolism*
Intestines / blood supply*
Leukocyte Rolling / drug effects
Leukocytes / drug effects*,  immunology
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Microscopy, Video
Nitric Oxide / metabolism*
Nitric Oxide Synthase Type III / antagonists & inhibitors,  deficiency,  genetics
Reperfusion Injury / enzymology,  immunology,  prevention & control*
Signal Transduction / drug effects
Sulfides / pharmacology*
Time Factors
p38 Mitogen-Activated Protein Kinases / antagonists & inhibitors,  metabolism*
Grant Support
ID/Acronym/Agency:
AA-14945/AA/NIAAA NIH HHS; HL-82816/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Anti-Inflammatory Agents; 0/Enzyme Inhibitors; 0/Sulfides; 10102-43-9/Nitric Oxide; 16721-80-5/sodium bisulfide; 7783-06-4/Hydrogen Sulfide; EC 1.14.13.39/Nitric Oxide Synthase Type III; EC 1.14.13.39/Nos3 protein, mouse; EC 2.7.11.24/p38 Mitogen-Activated Protein Kinases
Comments/Corrections

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