Na/H exchange inhibition-induced cardioprotection in dogs: Effects on neutrophils versus cardiomyocytes
American Journal of Physiology - Heart and Circulatory Physiology, ISSN: 0363-6135, Vol: 279, Issue: 4 48-4, Page: H1563-70
2000
- 49Citations
- 13Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations49
- Citation Indexes49
- 49
- CrossRef30
- Captures13
- Readers13
- 13
Article Description
Numerous studies have examined the effect of Na/H exchanger (NHE) inhibition on the myocardium; however, the effect of NHE-1 inhibition on neutrophil function has not been adequately examined. An in vivo canine model of myocardial ischemiareperfusion injury in which 60 min of left anterior descending coronary artery occlusion followed by 3 h of reperfusion was used to examine the effect of NHE-1 inhibition on infarct size (IS) and neutrophil function. BIIB-513, a selective inhibitor of NHE-1, was infused before ischemia. IS was expressed as a percentage of area at risk (IS/AAR). NHE-1 inhibition significantly reduced IS/AAR and reduced neutrophil accumulation in the ischemic myocardium. NHE-1 inhibition attenuated both phorbol 12-myristate 13-acetate- and platelet-activating factor-induced neutrophil respiratory burst but not CD18 upregulation. Furthermore, NHE-1 inhibition directly protected cardiomyocytes against metabolic inhibition-induced lactate dehydrogenase release and hypercontracture. This study provides evidence that the cardioprotection induced by NHE-1 inhibition is likely due to specific protection of cardiomyocytes and attenuation of neutrophil activity.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0033712090&origin=inward; http://dx.doi.org/10.1152/ajpheart.2000.279.4.h1563; http://www.ncbi.nlm.nih.gov/pubmed/11009442; https://www.physiology.org/doi/10.1152/ajpheart.2000.279.4.H1563; http://www.physiology.org/doi/10.1152/ajpheart.2000.279.4.H1563; http://www.physiology.org/doi/pdf/10.1152/ajpheart.2000.279.4.H1563
American Physiological Society
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