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Mitochondrial Integrity in a Neonatal Bovine Model of Right Ventricular Dysfunction.
MedLine Citation:
PMID:  25416385     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Right ventricular (RV) function is a key determinant of survival in patients with both right and left ventricular failure, yet the mechanisms of RV failure are poorly understood. Recent studies suggest cardiac metabolism is altered in RV failure in pulmonary hypertension (PH). Accordingly, we assessed mitochondrial content, dynamics and function in hearts from neonatal calves exposed to hypobaric hypoxia (HH). This model develops severe PH with concomitant RV hypertrophy, dilation, and dysfunction. After 2 weeks of HH, pieces of RV and LV were obtained along with samples from age-matched controls. Comparison with control assesses the effect of hypoxia, whereas comparison between the LV and RV in HH assesses the additional impact of RV overload. Mitochondrial DNA was unchanged in HH, as was mitochondrial content as assessed by electron microscopy. Immunoblotting for electron transport chain subunits revealed a small increase in mitochondrial content in HH in both ventricles. Mitochondrial dynamics were largely unchanged. Activity of individual respiratory chain complexes was reduced (complex I) or unchanged (complex V) in HH. Key enzymes in the glycolysis pathway were upregulated in both HH ventricles, alongside upregulation of hypoxia inducible factor 1-α protein. Importantly, none of the changes in expression or activity were different between ventricles, suggesting the changes are in response to HH and not RV overload. Upregulation of glycolytic modulators without chamber specific mitochondrial dysfunction suggests that mitochondrial capacity and activity are maintained at the onset of PH and the early RV dysfunction in this model results from mechanisms independent of the mitochondria.
Authors:
Danielle R Bruns; R Dale Brown; Kurt R Stenmark; Peter M Buttrick; Lori A Walker
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2014-11-21
Journal Detail:
Title:  American journal of physiology. Lung cellular and molecular physiology     Volume:  -     ISSN:  1522-1504     ISO Abbreviation:  Am. J. Physiol. Lung Cell Mol. Physiol.     Publication Date:  2014 Nov 
Date Detail:
Created Date:  2014-11-22     Completed Date:  -     Revised Date:  2014-11-25    
Medline Journal Info:
Nlm Unique ID:  100901229     Medline TA:  Am J Physiol Lung Cell Mol Physiol     Country:  -    
Other Details:
Languages:  ENG     Pagination:  ajplung.00270.2014     Citation Subset:  -    
Copyright Information:
Copyright © 2014, American Journal of Physiology - Lung Cellular and Molecular Physiology.
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