Heart failure in sheep significantly increased resting cardiac sympathetic nerve activity versus normal animals (89 vs 46 bursts/100 heartbeats; P<0.001), but baroreflex control remained undiminished.
Is the increased cardiac sympathetic nerve activity in heart failure due to defective control by arterial baroreceptors in a sheep model?
In a sheep model of heart failure, resting cardiac sympathetic nerve activity is significantly increased, but this elevation is not caused by defective control by arterial baroreceptors.
Absolute Event Rate: 89% vs 46%
p-value: p=<0.001
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.
Watson et al. (Fri,) conducted a other in Heart failure (n=16). Ventricular pacing-induced heart failure vs. Normal unpaced animals was evaluated on Resting cardiac sympathetic nerve activity (bursts/100 heartbeats) (p=<0.001). Heart failure in sheep significantly increased resting cardiac sympathetic nerve activity versus normal animals (89 vs 46 bursts/100 heartbeats; P<0.001), but baroreflex control remained undiminished.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: