| Prenatal hypoxia induces increased cardiac contractility on a background of decreased capillary density. | |
| | |
MedLine Citation:
|
PMID: 19126206 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
|
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. |
| | |
Authors:
|
David Hauton; Victoria Ousley |
Related Documents
:
|
15115986 - Hypoxia: unique myocardial morphology? 8002526 - Effect of hyperoxia at 1 and 2 ata on hypoxia and hypercapnia in human skin during expe... 1884456 - Repolarization inhomogeneities in ventricular myocardium change dynamically with abrupt... 681206 - Effects of time and vasoconstrictor tone on o2 extraction during hypoxic hypoxia. 16819586 - Comparison of plant cell turgor pressure measurement by pressure probe and micromanipul... 10226246 - Analysis of ambulatory blood pressure monitoring: the problem of 'white-coat' hypertens... |
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: 2009-11-18 |
Medline Journal Info:
|
Nlm Unique ID: 100968539 Medline TA: BMC Cardiovasc Disord Country: England |
Other Details:
|
Languages: eng Pagination: 1 Citation Subset: IM |
Affiliation:
|
Department of Physiology, School of Clinical and Experimental Medicine, University of Birmingham, Birmingham, UK. d.hauton@bham.ac.uk |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
Animals Capillaries / metabolism, pathology Coronary Circulation / physiology Coronary Vessels / pathology Female Fetal Hypoxia / embryology*, enzymology, pathology, physiopathology Male Myocardial Contraction / physiology Myocardial Reperfusion Injury / congenital, physiopathology Myocardium / enzymology*, pathology Nitric Oxide Synthase Type III / metabolism* Pregnancy Prenatal Exposure Delayed Effects Rats Rats, Wistar Sarcoplasmic Reticulum Calcium-Transporting ATPases / metabolism* Ventricular Pressure / physiology |
| Chemical | |
Reg. No./Substance:
|
EC 1.14.13.39/Nitric Oxide Synthase Type III; EC 1.14.13.39/Nos3 protein, rat; EC 3.6.3.8/Sarcoplasmic Reticulum Calcium-Transporting ATPases |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: The first case of isolated facial cutanenous leishmaniasis in a Down syndrome infant: a case report ...
Next Document: Evaluation of recombinant invasive, non-pathogenic Eschericia coli as a vaccine vector against the i...