Document Detail

Prenatal hypoxia induces increased cardiac contractility on a background of decreased capillary density.
MedLine Citation:
PMID:  19126206     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: Chronic hypoxia in utero (CHU) is one of the most common insults to fetal development and may be associated with poor cardiac recovery from ischaemia-reperfusion injury, yet the effects on normal cardiac mechanical performance are poorly understood.
METHODS: Pregnant female wistar rats were exposed to hypoxia (12% oxygen, balance nitrogen) for days 10-20 of pregnancy. Pups were born into normal room air and weaned normally. At 10 weeks of age, hearts were excised under anaesthesia and underwent retrograde 'Langendorff' perfusion. Mechanical performance was measured at constant filling pressure (100 cm H2O) with intraventricular balloon. Left ventricular free wall was dissected away and capillary density estimated following alkaline phosphatase staining. Expression of SERCA2a and Nitric Oxide Synthases (NOS) proteins were estimated by immunoblotting.
RESULTS: CHU significantly increased body mass (P < 0.001) compared with age-matched control rats but was without effect on relative cardiac mass. For incremental increases in left ventricular balloon volume, diastolic pressure was preserved. However, systolic pressure was significantly greater following CHU for balloon volume = 50 microl (P < 0.01) and up to 200 microl (P < 0.05). For higher balloon volumes systolic pressure was not significantly different from control. Developed pressures were correspondingly increased relative to controls for balloon volumes up to 250 microl (P < 0.05). Left ventricular free wall capillary density was significantly decreased in both epicardium (18%; P < 0.05) and endocardium (11%; P < 0.05) despite preserved coronary flow. Western blot analysis revealed no change to the expression of SERCA2a or nNOS but immuno-detectable eNOS protein was significantly decreased (P < 0.001) in cardiac tissue following chronic hypoxia in utero.
CONCLUSION: These data offer potential mechanisms for poor recovery following ischaemia, including decreased coronary flow reserve and impaired angiogenesis with subsequent detrimental effects of post-natal cardiac performance.
David Hauton; Victoria Ousley
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-01-06
Journal Detail:
Title:  BMC cardiovascular disorders     Volume:  9     ISSN:  1471-2261     ISO Abbreviation:  BMC Cardiovasc Disord     Publication Date:  2009  
Date Detail:
Created Date:  2009-01-16     Completed Date:  2009-03-05     Revised Date:  2013-06-02    
Medline Journal Info:
Nlm Unique ID:  100968539     Medline TA:  BMC Cardiovasc Disord     Country:  England    
Other Details:
Languages:  eng     Pagination:  1     Citation Subset:  IM    
Department of Physiology, School of Clinical and Experimental Medicine, University of Birmingham, Birmingham, UK.
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MeSH Terms
Capillaries / metabolism,  pathology
Coronary Circulation / physiology
Coronary Vessels / pathology
Fetal Hypoxia / embryology*,  enzymology,  pathology,  physiopathology
Myocardial Contraction / physiology
Myocardial Reperfusion Injury / congenital,  physiopathology
Myocardium / enzymology*,  pathology
Nitric Oxide Synthase Type III / metabolism*
Prenatal Exposure Delayed Effects
Rats, Wistar
Sarcoplasmic Reticulum Calcium-Transporting ATPases / metabolism*
Ventricular Pressure / physiology
Reg. No./Substance:
EC Oxide Synthase Type III; EC protein, rat; EC Reticulum Calcium-Transporting ATPases

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