Document Detail


eNOS is required for acute in vivo ischemic preconditioning of the heart: effects of ischemic duration and sex.
MedLine Citation:
PMID:  20525875     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Ischemic preconditioning (IPC) is a powerful phenomenon that provides potent cardioprotection in mammalian hearts; however, the role of endothelial nitric oxide (NO) synthase (eNOS)-mediated NO in this process remains highly controversial. Questions also remain regarding this pathway as a function of sex and ischemic duration. Therefore, we performed extensive experiments in wild-type (WT) and eNOS knockout (eNOS(-/-)) mice to evaluate whether the infarct-limiting effect of IPC depends on eNOS, ischemic periods, and sex. Classical IPC was induced by three cycles of 5 min of regional coronary ischemia separated by 5 min of reperfusion and was followed by 30 or 60 min of sustained ischemia and 24 h of reperfusion. The control ischemia-reperfusion protocol had 30 or 60 min of ischemia followed by 24 h of reperfusion. Protection was evaluated by measuring the myocardial infarct size as a percentage of the area at risk. The major findings were that regardless of sex, WT mice exhibited robust IPC with significantly smaller myocardial infarction, whereas eNOS(-/-) mice did not. IPC-induced cardiac protection was absent in eNOS(-/-) mice of both Jackson and Harvard origin. In general, female WT mice had smaller infarctions compared with male WT mice. Although prolonged ischemia caused significantly larger infarctions in WT mice of both sexes, they were consistently protected by IPC. Importantly, prolonged myocardial ischemia was associated with increased mortality in eNOS(-/-) mice, and the survival rate was higher in female eNOS(-/-) mice compared with male eNOS(-/-) mice. In conclusion, IPC protects WT mice against in vivo myocardial ischemia-reperfusion injury regardless of sex and ischemic duration, but the deletion of eNOS abolishes the cardioprotective effect of classical IPC.
Authors:
M A Hassan Talukder; Fuchun Yang; Hiroaki Shimokawa; Jay L Zweier
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural     Date:  2010-06-04
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  299     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2010 Aug 
Date Detail:
Created Date:  2010-07-30     Completed Date:  2010-08-30     Revised Date:  2013-05-29    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H437-45     Citation Subset:  IM    
Affiliation:
Davis Heart and Lung Research Institute, The Ohio State Univ., 473 W. 12th Ave., Columbus, OH 43210, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Disease Models, Animal
Female
Ischemic Preconditioning, Myocardial / methods*
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Myocardial Infarction / enzymology,  pathology,  prevention & control*
Myocardial Reperfusion Injury / enzymology,  pathology,  prevention & control*
Myocardium / enzymology*,  pathology
Nitric Oxide Synthase Type III / deficiency,  genetics,  metabolism*
Sex Factors
Time Factors
Grant Support
ID/Acronym/Agency:
HL-38324/HL/NHLBI NIH HHS; HL-63744/HL/NHLBI NIH HHS; HL-65608/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
EC 1.14.13.39/Nitric Oxide Synthase Type III; EC 1.14.13.39/Nos3 protein, mouse
Comments/Corrections

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