Increased cardiac sympathetic nerve activity in heart failure is not due to desensitization of the arterial baroreflex

A. M.D. Watson, S. G. Hood, R. Ramchandra, R. M. McAllen, C. N. May

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Abstract

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 of 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 wk, 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 the responses to intravenous phenylephrine and nitroprusside infusions were measured in conscious sheep. Electrophysiological recordings showed that resting CSNA (bursts/100 heartbeats) 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-1·mmHg-1 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%max/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.

Original languageEnglish
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume293
Issue number1
DOIs
Publication statusPublished - 1 Jul 2007
Externally publishedYes

Keywords

  • Baroreceptors
  • Pacing
  • Spectral analysis

Cite this

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title = "Increased cardiac sympathetic nerve activity in heart failure is not due to desensitization of the arterial baroreflex",
abstract = "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 of 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 wk, 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 the responses to intravenous phenylephrine and nitroprusside infusions were measured in conscious sheep. Electrophysiological recordings showed that resting CSNA (bursts/100 heartbeats) 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-1·mmHg-1 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{\%}max/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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Increased cardiac sympathetic nerve activity in heart failure is not due to desensitization of the arterial baroreflex. / Watson, A. M.D.; Hood, S. G.; Ramchandra, R.; McAllen, R. M.; May, C. N.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 293, No. 1, 01.07.2007.

Research output: Contribution to journalArticleResearchpeer-review

TY - JOUR

T1 - Increased cardiac sympathetic nerve activity in heart failure is not due to desensitization of the arterial baroreflex

AU - Watson, A. M.D.

AU - Hood, S. G.

AU - Ramchandra, R.

AU - McAllen, R. M.

AU - May, C. N.

PY - 2007/7/1

Y1 - 2007/7/1

N2 - 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 of 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 wk, 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 the responses to intravenous phenylephrine and nitroprusside infusions were measured in conscious sheep. Electrophysiological recordings showed that resting CSNA (bursts/100 heartbeats) 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-1·mmHg-1 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%max/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.

AB - 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 of 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 wk, 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 the responses to intravenous phenylephrine and nitroprusside infusions were measured in conscious sheep. Electrophysiological recordings showed that resting CSNA (bursts/100 heartbeats) 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-1·mmHg-1 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%max/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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KW - Pacing

KW - Spectral analysis

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DO - 10.1152/ajpheart.00147.2007

M3 - Article

VL - 293

JO - American Journal of Physiology - Heart and Circulatory Physiology

JF - American Journal of Physiology - Heart and Circulatory Physiology

SN - 0363-6135

IS - 1

ER -