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Sympathetic inhibition with clonidine prolongs survival in experimental chronic heart failure
1Department of Cardiology, Cardiovascular Institute and Fu Wai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. zhangy2@ccf.org
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Sympathetic nervous system inhibition with clonidine improved survival in a rat model of congestive heart failure (CHF). This study demonstrates clonidine
Area of Science:
- Cardiology
- Pharmacology
- Physiology
Background:
- Sympathetic nervous system activation is linked to increased mortality in congestive heart failure (CHF).
- Centrally acting sympatholytic agents show hemodynamic benefits in CHF patients.
- The impact of sympathetic inhibition on CHF survival remains unclear.
Purpose of the Study:
- To investigate the effect of sympathetic inhibition using clonidine on survival in a rat model of CHF.
- To assess the long-term efficacy of clonidine in improving survival rates post-myocardial infarction.
Main Methods:
- Myocardial infarction and heart failure were induced in rats via left coronary artery ligation.
- Rats were randomized to receive clonidine (100 microg kg(-1) d(-1)) or placebo for one year.
- Systolic blood pressure, heart rate, and plasma norepinephrine levels were monitored.
Main Results:
- Clonidine treatment significantly reduced systolic blood pressure and heart rate compared to placebo.
- Plasma norepinephrine levels were decreased in the clonidine group.
- One-year survival was significantly improved in clonidine-treated rats (50% vs. 22.6%, P<0.05).
Conclusions:
- Long-term sympathetic inhibition with clonidine enhances survival in a rat model of CHF.
- Clonidine's beneficial effects on survival may be mediated by reduced sympathetic activity.
- These findings suggest potential therapeutic benefits of sympathetic inhibition in CHF.
Abstract:
Activation of the sympathetic nervous system is associated with increased mortality in congestive heart failure (CHF), and inhibition of the sympathetic nervous system by centrally acting sympatholytic agents has been shown to have beneficial effects on hemodynamics in these patients. However, the effect of sympathetic inhibition on survival in CHF is not clear. In the present study, the effect of sympathetic inhibition with clonidine on survival was examined in a rat model of heart failure. Myocardial infarction and heart failure was induced in rats by ligation of the left coronary artery and sham-operated rats served as the control. Two weeks after surgery, the ligated rats were randomly assigned to the clonidine (100 microg kg(-1) d(-1), n=30) group or the placebo (vehicle, n=31) group. All rats were followed daily for a 1-year period or until spontaneous death. Compared with placebo therapy, clonidine treatment reduced systolic blood pressure and heart rate throughout the experimental period. The plasma norepinephrine level determined at the end of the experiment was also reduced. Long-term sympathetic inhibition with clonidine treatment improved 1-year survival (50% vs. 22.6%, P<0.05) after surgery in this rat model of CHF.