dc.contributor.author |
Vandsburger, MH |
en |
dc.contributor.author |
French, BA |
en |
dc.contributor.author |
Helm, PA |
en |
dc.contributor.author |
Roy, RJ |
en |
dc.contributor.author |
Kramer, CM |
en |
dc.contributor.author |
Young, Alistair |
en |
dc.contributor.author |
Epstein, FH |
en |
dc.date.accessioned |
2011-09-06T02:14:32Z |
en |
dc.date.issued |
2007-11 |
en |
dc.identifier.citation |
EUR HEART J 28(22):2792-2798 Nov 2007 |
en |
dc.identifier.issn |
0195-668X |
en |
dc.identifier.uri |
http://hdl.handle.net/2292/7712 |
en |
dc.description.abstract |
Aims The role of neuronal nitric oxide synthase (nNOS) in regulating contractile function remains controversial, and in regulating myocardial perfusion is uninvestigated. We used magnetic resonance imaging (MRI) to phenotype nNOS−/− and wild-type (WT) mice regarding left ventricular (LV) structure, baseline function, β-adrenergic responsiveness, and perfusion reserve. Methods and results Cine MRI showed higher LV mass to end-diastolic volume ratio (2.3 ± 0.2 mg/µL nNOS−/− vs. 1.7 ± 0.1 mg/µL WT; P=0.032) and LV ejection fraction (64.9 ± 2.1% nNOS−/− vs. 55.8 ± 1.1% WT; P = 0.003) in nNOS−/−. Myocardial tagging demonstrated similar baseline systolic circumferential strain (Ecc) in nNOS−/− and WT. With dobutamine, the normal change in Ecc was nearly absent in nNOS−/− (−0.5 ± 0.3% nNOS−/− vs. −2.2 ± 0.3% WT; P = 0.001), and the systolic strain rate (dEcc/dt) response to dobutamine seen in WT was reduced in nNOS−/− (−29 ± 13%/s nNOS−/− vs. −106±16%/s WT; P = 0.001). Diastolic strain rate increased significantly with dobutamine only in WT. Arterial spin labelling showed that baseline perfusion and perfusion reserve with either dobutamine or an adenosine receptor agonist are normal in nNOS−/−. Conclusion MRI provides non-invasive in vivo evidence that nNOS does not play a role in basal contractile function or myocardial perfusion, but is required for increasing cardiac inotropy and lusitropy upon β-adrenergic stimulation. |
en |
dc.language |
EN |
en |
dc.publisher |
OXFORD UNIV PRESS |
en |
dc.relation.ispartofseries |
EUR HEART J |
en |
dc.rights |
Items in ResearchSpace are protected by copyright, with all rights reserved, unless otherwise indicated. Previously published items are made available in accordance with the copyright policy of the publisher. Details obtained from http://www.sherpa.ac.uk/romeo/issn/0195-668X/ |
en |
dc.rights.uri |
https://researchspace.auckland.ac.nz/docs/uoa-docs/rights.htm |
en |
dc.subject |
neuronal nitric oxide synthase |
en |
dc.subject |
cardiac function |
en |
dc.subject |
heart |
en |
dc.subject |
MRI |
en |
dc.subject |
adrenergic stimulation |
en |
dc.subject |
myocardial tagging |
en |
dc.subject |
LEFT-VENTRICULAR CHAMBER |
en |
dc.subject |
TAGGED MR-IMAGES |
en |
dc.subject |
MYOCARDIAL-INFARCTION |
en |
dc.subject |
SPATIAL CONFINEMENT |
en |
dc.subject |
MOUSE MODELS |
en |
dc.subject |
HEART |
en |
dc.subject |
NNOS |
en |
dc.subject |
CONTRACTILITY |
en |
dc.subject |
ISOFORMS |
en |
dc.title |
Multi-parameter in vivo cardiac magnetic resonance imaging demonstrates normal perfusion reserve despite severely attenuated beta-adrenergic functional response in neuronal nitric oxide synthase knockout mice |
en |
dc.type |
Journal Article |
en |
dc.identifier.doi |
10.1093/eurheartj/ehm241 |
en |
pubs.issue |
22 |
en |
pubs.begin-page |
2792 |
en |
pubs.volume |
28 |
en |
dc.rights.holder |
Copyright: 2007 The European Society of Cardiology |
en |
dc.identifier.pmid |
17602202 |
en |
pubs.end-page |
2798 |
en |
dc.rights.accessrights |
http://purl.org/eprint/accessRights/RestrictedAccess |
en |
pubs.subtype |
Article |
en |
pubs.elements-id |
114402 |
en |
pubs.org-id |
Bioengineering Institute |
en |
pubs.org-id |
ABI Associates |
en |
pubs.org-id |
Medical and Health Sciences |
en |
pubs.org-id |
Medical Sciences |
en |
pubs.org-id |
Anatomy and Medical Imaging |
en |
pubs.record-created-at-source-date |
2011-10-25 |
en |
pubs.dimensions-id |
17602202 |
en |