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Cardiac sympathetic neuronal function in left ventricular volume and pressure overload
G A Somsen1, E A Dubois, K Brandsma
1Department of Cardiology, Academic Medical Center, University of Amsterdam, The Netherlands.
Cardiovascular Research
|January 1, 1996
Summary
Mechanical overload in rabbits enhances cardiac sympathetic activity, leading to noradrenaline depletion and reduced beta-adrenoceptors, even in early heart failure. This suggests altered sympathetic function, not dysfunction, in overloaded hearts.
Area of Science:
- Cardiology
- Neurocardiology
- Physiology
Background:
- Cardiac sympathetic neuronal function is altered in heart failure.
- Controversy exists regarding neurohormonal changes in pressure and volume overloaded hearts.
Purpose of the Study:
- To assess the effects of mechanical overload on cardiac sympathetic neuronal function and beta-adrenoceptor density in rabbits.
- To relate these changes to left ventricular function.
Main Methods:
- Induction of left ventricular volume overload via aortic valve perforation.
- Induction of pressure overload by suprarenal aortic banding in rabbits.
- Sham operations served as controls.
Main Results:
- Cardiac overload increased left ventricular weight and end-diastolic diameter.
- Myocardial noradrenaline concentration and beta-adrenoceptor density were significantly reduced in overloaded hearts.
- No significant changes in fractional shortening or myocardial [123I]-MIBG uptake were observed.
Conclusions:
- Cardiac volume and pressure overload enhance sympathetic activity, evidenced by noradrenaline depletion and beta-adrenoceptor downregulation.
- No cardiac neuronal dysfunction was detected, even in early heart failure stages.