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Am J Physiol Heart Circ Physiol (April 13, 2007). doi:10.1152/ajpheart.00147.2007
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Submitted on February 6, 2007
Accepted on April 5, 2007

INCREASED CARDIAC SYMPATHETIC NERVE ACTIVITY IN HEART FAILURE IS NOT DUE TO DESENSITIZATION OF THE ARTERIAL BAROREFLEX

Anna M. D. Watson1, Sally G. Hood1, Rohit Ramchandra1, Robin M McAllen1, and Clive N May1*

1 Systems Neurobiology, Howard Florey Institute, Parkville, Victoria, Australia

* To whom correspondence should be addressed. E-mail: c.may{at}hfi.unimelb.edu.au.

Increased sympathetic drive to the heart worsens prognosis in heart failure, but the level of cardiac sympathetic nerve activity (CSNA) has been assessed only by indirect methods, which do not permit testing whether its control by arterial baroreceptors is defective. To do this, CSNA was measured directly in 16 female sheep, 8 of which had been ventricularly paced at 200-220 beats/min for 4-6 weeks, until their ejection fraction fell to between 35 and 40%. Recording electrodes were surgically implanted in the cardiac sympathetic nerves and after 3 days’ recovery, responses to intravenous phenylephrine and nitroprusside infusions were measured in conscious sheep. Electrophysiological recordings showed that resting CSNA (bursts/100 heart beats) was significantly elevated in heart failure sheep (89±3) compared with normal animals (46±6, P<0.001). This increased CSNA was not accompanied by any increase in the low frequency power of heart rate variability. The baroreceptor- heart rate reflex was significantly depressed in heart failure (maximum gain -3.29±0.56 vs. -5.34±0.66 beats/min/mmHg in normal animals), confirming published findings. In contrast, the baroreflex control of CSNA was undiminished (maximum gain in heart failure -6.33±1.06, vs. -6.03±0.95 %/mmHg in normal sheep). Direct recordings in a sheep model of heart failure thus show that resting CSNA is strikingly increased, but this is not due to defective control by arterial baroreceptors.




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