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1 Department of Anesthesia and Critical Care, Massachusetts General Hospital, Boston, MA, USA; Cardiovascular Research Center in the Cardiology Division of the Department of Medicine, Massachusetts General Hospital, Boston, MA, USA
2 Cardiovascular Research Center in the Cardiology Division of the Department of Medicine, Massachusetts General Hospital, Boston, MA, USA
3 Ultrasound Laboratory in the Cardiology Division of the Department of Medicine, Massachusetts General Hospital, Boston, MA, USA
4 Department of Anesthesia and Critical Care, Massachusetts General Hospital, Boston, MA, USA
5 Department of Pathology, Massachusetts General Hospital, Boston, MA, USA
6 Ultrasound Laboratory in the Cardiology Division of the Department of Medicine, Massachusetts General Hospital, Boston, MA, USA; Cardiovascular Research Center in the Cardiology Division of the Department of Medicine, Massachusetts General Hospital, Boston, MA, USA
* To whom correspondence should be addressed. E-mail: fichinose{at}partners.org.
To investigate the role of endothelial nitric oxide synthase (NOS3) in left ventricular (LV) remodeling induced by chronic pressure-overload, the impact of transverse aortic constriction (TAC) on LV structure and function was compared in wild-type (WT) and NOS3-deficient (NOS3-/-) mice. Before TAC, LV wall thickness, mass, and fractional shortening were similar in the two mouse strains. Twenty-eight days after TAC, both WT
and NOS3-/- mice had increased LV wall thickness and mass, as well as decreased fractional shortening. Although the pressure gradient across the TAC was similar in both strains of mice 28 days after TAC, LV mass and posterior wall thickness were greater in
NOS3-/- than in WT mice, while fractional shortening and the maximum rate of developed LV pressure (dP/dtmax) were less. Diastolic function, as measured by the time constant of isovolumic relaxation (
) and the maximum rate of LV pressure decay
(dP/dtmin), was impaired to a greater extent in NOS3-/- than in WT mice. The degree of myocyte hypertrophy and LV fibrosis was greater in NOS3-/- than in WT mice at 28 days after TAC. Mortality was greater in NOS3-/- than in WT mice 28 days after TAC. Longterm administration of hydralazine normalized the blood pressure and prevented the LV dilation in NOS3-/- mice, but did not prevent the LV hypertrophy, dysfunction, and fibrosis associated with NOS3-deficiency after TAC. These results suggest that the absence of NOS3 augments LV dysfunction and remodeling in a murine model of
chronic pressure-overload.
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