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Infarct size and nitric oxide synthase in murine myocardium
M S Sumeray1, D D Rees, D M Yellon
1The Hatter Institute, Department of Academic and Clinical Cardiology, University College Hospital, Grafton Way, London, WC1E 6DB, UK.
Journal of Molecular and Cellular Cardiology
|February 1, 2000
Summary
Endothelial nitric oxide synthase (eNOS) protects the heart from injury after reperfusion. Mice lacking eNOS experienced larger infarcts, suggesting a protective role for eNOS in myocardial ischemia-reperfusion injury.
Area of Science:
- Cardiovascular Research
- Molecular Cardiology
- Ischemia-Reperfusion Injury
Background:
- The role of nitric oxide (NO) in myocardial ischemia-reperfusion (I/R) injury is debated, with potential for both harmful and beneficial effects.
- Nitric oxide synthase (NOS) exists as two constitutive isoforms: endothelial (eNOS) and neuronal (nNOS).
Purpose of the Study:
- To investigate the distinct roles of eNOS and nNOS in myocardial I/R injury using knockout mouse models.
- To determine the protective or detrimental effects of eNOS and nNOS during cardiac I/R.
Main Methods:
- Comparison of wild-type (WT), eNOS knockout (eNOS KO), and nNOS knockout (nNOS KO) mouse hearts subjected to 30 minutes of global ischemia and 30 minutes of reperfusion.
- Langendorff perfusion system used to assess recovery of contractile function (force-rate product) and infarct size (planimetry).
Main Results:
- Recovery of contractile function did not significantly differ between WT, eNOS KO, and nNOS KO groups.
- eNOS KO hearts exhibited significantly larger infarct sizes (41%) compared to WT (33%) and nNOS KO (30%) hearts (P<0.05).
Conclusions:
- Endothelial nitric oxide synthase (eNOS) plays a protective role against myocardial ischemia-reperfusion injury in murine models.
- These findings suggest potential clinical implications for pharmacotherapies targeting eNOS to enhance myocardial protection.