Mice lacking inducible nitric oxide synthase have improved left ventricular contractile function and reduced apoptotic cell death late after myocardial infarction
| Autor: | Soeun Ngoy, Wilson S. Colucci, Daniel A. Brenner, Zhonglin Xie, Krishna Singh, Deborah A. Siwik, Douglas B. Sawyer, Carl S. Apstein, Flora Sam, Donny L.F. Chang |
|---|---|
| Rok vydání: | 2001 |
| Předmět: |
medicine.medical_specialty
Physiology Ratón Cell Survival Myocardial Infarction Nitric Oxide Synthase Type II Apoptosis Blood Pressure In Vitro Techniques Ventricular Function Left Nitric oxide Contractility chemistry.chemical_compound Mice Internal medicine medicine In Situ Nick-End Labeling Animals Myocardial infarction Mice Knockout biology business.industry Myocardium Body Weight Stroke Volume Organ Size medicine.disease Immunohistochemistry Myocardial Contraction Survival Analysis Pathophysiology Nitric oxide synthase Mice Inbred C57BL Endocrinology chemistry Circulatory system biology.protein Disease Progression Nitric Oxide Synthase Cardiology and Cardiovascular Medicine business |
| Zdroj: | Circulation research. 89(4) |
| ISSN: | 1524-4571 |
| Popis: | Nitric oxide produced by inducible nitric oxide synthase (NOS2) has been implicated in the pathophysiology of chronic myocardial remodeling and failure. We tested the role of NOS2 in left ventricular (LV) remodeling early (1 month) and late (4 months) after myocardial infarction (MI) in mice lacking NOS2. MI size measured 7 days, 1 month, and 4 months after MI was the same in NOS2 knockout (KO) and wild-type (WT) mice. The LV end-diastolic pressure-volume relationship measured by the isovolumic Langendorff technique showed a progressive rightward shift from 1 to 4 months after MI in WT mice. LV developed pressure measured over a range of LV volumes was reduced at 1 and 4 months after MI in WT mice ( P P P P |
| Databáze: | OpenAIRE |
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