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Congestive heart failure in copper-deficient mice.
Laila Elsherif1, Raymond V Ortines, Jack T Saari
1Department of Pharmacology and Toxicology, University of Louisville, Louisville, Kentucky 40202, USA.
Experimental Biology and Medicine (Maywood, N.J.)
|July 24, 2003
Summary
Copper deficiency (CuD) causes significant systolic and diastolic heart dysfunction in mice, progressing to heart failure. This study reveals impaired contractility and relaxation, alongside pathological changes, indicating congestive heart failure in CuD models.
Area of Science:
- Cardiovascular Physiology
- Nutritional Biochemistry
- Pathology
Background:
- Copper deficiency (CuD) is known to induce hypertrophic cardiomyopathy in experimental models.
- The progression from compensated hypertrophy to decompensated heart failure in CuD has not been well-studied.
Purpose of the Study:
- To investigate the contractile and hemodynamic parameters in CuD mouse hearts.
- To determine if heart failure develops subsequent to hypertrophy in CuD.
Main Methods:
- FVB mice dams were fed either a CuD or copper-adequate (CuA) diet from day 3 postpartum.
- Weanling pups received the same diet for 5 weeks (pre- and postweaning).
- Cardiac function was assessed at week 4 via left ventricular catheterization.
Main Results:
- CuD mice exhibited significantly decreased left ventricle systolic pressure and depressed contractility (+dP/dt and -dP/dt).
- Elevated left ventricle end-diastolic pressure and prolonged relaxation indicated diastolic dysfunction.
- CuD hearts showed blunted responses to isoproterenol and morphological changes including collagen and lipid deposition.
Conclusions:
- Copper deficiency leads to both systolic and diastolic cardiac dysfunction in mice.
- Histopathological findings in CuD hearts are consistent with diagnoses of congestive heart failure.
- This study establishes a link between CuD and the development of heart failure.