The activity of the sympathetic nervous system as reflected both by plasma norepinephrine (NE) and direct neural recordings is increased in patients with congestive heart failure (CHF).1-3 The mechanisms by which stimulation of the sympathetic nervous system is initiated and maintained are not well characterized. The response of the sympathetic nervous system to further stimulation in CHF is often blunted.4-6 No information is currently available concerning ganglionic or preganglionic regulation of sympathetic activity in this disease. It is conceivable that hyperresponsiveness to central or ganglionic stimuli could play a role in the chronically elevated sympathetic tone in heart failure. Alternatively, subnormal responsiveness to such stimuli could help explain the blunted response to further sympathetic stimulation. We performed the current study to investigate whether the sympathetic response to ganglionic stimulation was normal, enhanced or depressed in patients with chronic CHF.
|Original language||English (US)|
|Number of pages||2|
|Journal||The American Journal of Cardiology|
|State||Published - Jan 1 1989|
Bibliographical noteFunding Information:
From the Cardiovascular Division, Hennepin County Medical Center, and University of Minnesota, 701 Park Avenue South, Minneapolis, Minnesota 55415, and the Tobacco and Health Research Institute, University of Kentucky, Lexington, Kentucky. This study was supported by a grant-in-aid from the American Heart Association. Dr. Goldsmith is also the recipient of an Established Investigator award from the American Heart Association. Manuscript received July 28, 1988; revised manuscript received September 26, 1988, and accepted September 30.