Abstract | BACKGROUND: METHODS: RESULTS: The control infarct-to-risk ratio was 45.1+/-1.72% (means+/-SE). BNP infused 5 min after ischemia limited infarct size in a dosage-dependent manner, with maximal protection observed at 0.01 ug/(kg min) ( infarct-to-risk: 24.7+/-1.69%, P<0.01 vs. control), associated with a 10-fold increase of myocardial endothelial nitric oxide synthase above the control value. Protection afforded by BNP was abolished by L-NAME but not by SMT, suggesting the involvement of putative endothelial but not inducible nitric oxide synthase activation. CONCLUSIONS: We conclude that natriuretic peptide/NOS/NO signaling may constitute an important injury-limiting mechanism in myocardium.
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Authors | Binhui Ren, Yi Shen, Hongtao Shao, Jianjun Qian, Haiwei Wu, Hua Jing |
Journal | Clinica chimica acta; international journal of clinical chemistry
(Clin Chim Acta)
Vol. 377
Issue 1-2
Pg. 83-7
(Feb 2007)
ISSN: 0009-8981 [Print] Netherlands |
PMID | 17026975
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Enzyme Inhibitors
- Natriuretic Peptide, Brain
- Nitric Oxide Synthase Type III
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Topics |
- Animals
- Dose-Response Relationship, Drug
- Enzyme Inhibitors
(pharmacology)
- Male
- Myocardial Infarction
(drug therapy, enzymology, pathology)
- Natriuretic Peptide, Brain
(pharmacology)
- Nitric Oxide Synthase Type III
(antagonists & inhibitors, metabolism)
- Rats
- Rats, Sprague-Dawley
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