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Cardiac sympathetic responses to acute vasodilation. Normal ventricular function versus congestive heart failure
1Department of Medicine, Mount Sinai Hospital, University of Toronto, Ontario, Canada.
Circulation
|December 15, 1996
Summary
Heart failure impairs baroreflex control of cardiac sympathetic activity. This study found reduced sympathetic responses to blood pressure changes in heart failure patients, suggesting a key mechanism in the disease.
Area of Science:
- Cardiovascular Physiology
- Autonomic Nervous System Regulation
- Heart Failure Pathophysiology
Background:
- Baroreflex control of cardiac sympathetic activity is not well understood in heart failure.
- Previous research suggests indirect evidence of impaired baroreflex control in heart failure.
Purpose of the Study:
- To investigate the hypothesis that baroreflex control of cardiac sympathetic activity is reduced in patients with heart failure.
- To quantify cardiac sympathetic activity in response to baroreceptor stimulation in heart failure.
Main Methods:
- Utilized the norepinephrine spillover method to measure cardiac sympathetic activity.
- Studied 17 patients with heart failure and 6 healthy controls with normal ventricular function.
- Administered nitroprusside infusion to induce controlled reductions in blood pressure in both groups.
Main Results:
- Nitroprusside caused similar reductions in blood pressure in both normal and heart failure groups.
- Cardiac norepinephrine spillover increased by 98% in normal subjects in response to nitroprusside.
- Heart failure patients showed a significantly smaller increase (28%) in cardiac norepinephrine spillover compared to normal subjects.
Conclusions:
- Patients with heart failure exhibit significantly reduced cardiac sympathetic activity in response to baroreceptor unloading compared to healthy individuals.
- This study provides direct evidence for impaired baroreflex control of cardiac sympathetic activity in heart failure.
- Reduced baroreflex control may contribute to the pathophysiology of heart failure.