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Vascular sympathetic nerve function in congestive heart failure
1Division of Cardiology, Pennsylvania State University, College of Medicine, Milton S. Hershey Medical Center, Hershey 17033.
Insights
In congestive heart failure, rats with heart damage did not show intrinsic sympathetic nerve defects in pulmonary arteries. Increased nerve activity or reduced norepinephrine clearance are likely causes of higher norepinephrine levels.
Area of Science:
- Cardiovascular Physiology
- Neuropharmacology
- Heart Failure Pathophysiology
Background:
- Congestive heart failure is associated with increased sympathetic nerve activity and elevated plasma norepinephrine levels.
- The contribution of intrinsic sympathetic nerve abnormalities within the vasculature to enhanced vascular tone in heart failure remains unclear.
Purpose of the Study:
- To investigate whether intrinsic abnormalities in sympathetic nerve function of pulmonary arteries contribute to enhanced vascular tone in a rat model of congestive heart failure.
Main Methods:
- Chronic myocardial infarction was induced in rats via coronary artery ligation.
- Excised pulmonary arteries were superfused with 3H-norepinephrine and stimulated electrically at varying frequencies (2, 4, 8, 16 Hz).
- 3H-norepinephrine overflow was measured to assess sympathetic nerve function.
Main Results:
- Electrically evoked 3H-norepinephrine overflow was similar between sham and infarct vessels at most frequencies.
- However, infarct vessels showed a significant reduction in 3H overflow at the highest frequency (16 Hz).
- Frequency-response curves for infarct vessels shifted leftward, suggesting increased sympathetic nerve sensitivity.
Conclusions:
- Intrinsic sympathetic nerve abnormalities in pulmonary arteries are unlikely to be the primary cause of elevated plasma norepinephrine in congestive heart failure.
- Increased sympathetic nerve activity or reduced norepinephrine clearance are more probable explanations for heightened vascular tone in this condition.
Abstract:
To determine if intrinsic abnormalities of sympathetic nerve function might contribute to enhanced vascular tone in congestive heart failure, chronic myocardial infarction (infarct) was produced in rats by coronary artery ligation 9 to 10 months previously for comparison with animals subjected to sham operation (sham). The excised pulmonary artery, preincubated with 3H-norepinephrine (NE) was superfused, and stimulated electrically at 2, 4, 8 and 16 Hz. The nonnormalized data at each frequency for electrically evoked 3H overflow in excess of basal outflow was similar in sham and infarct vessels (difference not significant); however, the shape of the frequency-response curves was different. The 3H overflow/pulse from sham vessels was constant between 2 and 16 Hz; however, for the infarct vessels there was a significant reduction (p less than 0.05) at the highest frequency (16 Hz). Because of an 18.4% lower peak 3H overflow at 16 Hz (difference not significant), the infarct frequency-response curve shifted significantly (4 and 8 Hz, p less than 0.025 and p less than 0.01) to the left when data were expressed as a percent of peak percent 3H overflow, suggesting an increased sensitivity of the system. These data suggest that an intrinsic vascular sympathetic nerve abnormality is not a major cause of the increased plasma NE in congestive heart failure; increased nerve activity or decreased clearance of NE may be more important.