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1 Department of Molecular and Cellular Physiology, LSU Health Sciences Center, Shreveport, LA, USA
2 Department of Medicine, Cardiology Section, LSU Health Sciences Center, Shreveport, LA, USA
3 Department of Surgery, LSU Healh Sciences Center, Shreveport, LA, USA
4 Department of Cell Biology and Genetics, Erasmus University Medical Center, Rotterdam, Netherlands Antilles
5 Department of Cell Biology and Genetics, Erasmus University Medical Center, Rotterdam, Netherlands Antilles; Department of Experimental Cardiology, Erasmus University Medical Center, Rotterdam, Netherlands Antilles
6 Division of Cardiovascular and Respiratory Medicine, Department of Internal Medicine, Kobe University Graduate Shool of Medicine, Kobe, Japan
7 Department of Molecular and Cellular Physiology, LSU Health Sciences Center, Shreveport, LA, USA; Department of Medicine, Cardiology Section, LSU Health Sciences Center, Shreveport, LA, USA
* To whom correspondence should be addressed. E-mail: dlefer{at}lsuhsc.edu.
Previous studies indicate that deficiency of endothelial nitric oxide synthase (eNOS)- derived NO exacerbates myocardial reperfusion injury. We hypothesized that overexpression of eNOS would reduce the extent of myocardial ischemia-reperfusion (MI-R) injury. We investigated two distinct strains of transgenic mice overexpressing the eNOS gene (eNOS Tg). Bovine eNOS was overexpressed in one strain (eNOS Tg-Kobe) while the human eNOS gene was overexpressed in the other strain (eNOS Tg- RT). Nontransgenic and eNOS Tg mice were subjected to 30 minutes of coronary artery occlusion followed by 24 hours of reperfusion and the extent of myocardial infarction was determined. Myocardial infarct size was reduced by 33% in the eNOS Tg-Kobe strain (p < 0.05 vs. NTg) and by 32% in the eNOS Tg-RT strain (p < 0.05 vs. NTg). However, post-ischemic cardiac function (cardiac output, fractional shortening) was not improved in the eNOS Tg-Kobe mouse at 24 hours of reperfusion (p = NS vs. NTg). In additional studies, eNOS Tg-Kobe were subjected to 30 min. of MI and 7 days of reperfusion. Fractional shortening and left ventricular dP/dT were measured in eNOS Tg-Kobe and NTg mice and no significant differences in contractility were observed (p = NS) between the eNOS Tg and the NTg controls. Left ventricular end-diastolic pressure was significantly (p < 0.05 vs. NTg) reduced in the eNOS Tg-Kobe strain at 7 days of reperfusion. The cardioprotective effects of eNOS overexpression on myocardial infarct size were ablated by L-NAME (300mg/Kg) pretreatment. Thus, genetic overexpression of eNOS in mice attenuates myocardial infarction following MI-R, but fails to significantly protect against post-ischemic myocardial contractile dysfunction in mice.
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