scholarly journals Long-term course and cardiac sympathetic nerve activity in patients with hypertrophic cardiomyopathy.

Heart ◽  
1992 ◽  
Vol 67 (2) ◽  
pp. 155-160 ◽  
Author(s):  
M Shimizu ◽  
N Sugihara ◽  
Y Kita ◽  
K Shimizu ◽  
Y Horita ◽  
...  
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Cardiac Sympathetic Nerve ◽  
Nerve Activity ◽  
Cardiac Sympathetic Nerve Activity

scholarly journals Effect of stellate ganglionectomy on basal cardiovascular function and responses to β1-adrenoceptor blockade in the rat

2008 ◽  
Vol 295 (6) ◽  
pp. H2447-H2454 ◽  
Author(s):  
Misa Yoshimoto ◽  
Erica A. Wehrwein ◽  
Martin Novotny ◽  
Greg M. Swain ◽  
David L. Kreulen ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Cardiac Function ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Sympathetic Nerves ◽  
Sympathetic Denervation ◽  
Cardiac Sympathetic Nerve ◽  
Nerve Activity ◽  
Cardiac Sympathetic Nerve Activity

Cardiac sympathetic nerve activity is an important short-term controller of cardiac function and arterial pressure. Studies also suggest that long-term increases in cardiac sympathetic nerve activity may contribute to hypertension, coronary artery disease, and cardiac remodeling in heart failure. However, our understanding of the role of cardiac sympathetic nerves in chronic models of cardiovascular disease has been limited by inadequate experimental approaches. The present study was conducted to develop a surgical method to surgically denervate the sympathetic nerves of the rat heart for long-term cardiovascular studies. We characterized the effect of cardiac sympathetic denervation on basal levels of mean arterial pressure (MAP) and heart rate (HR) and the responses to a chronic administration of atenolol, a β1-adrenoceptor antagonist. Rats were instrumented with telemetry transmitters for continuous recording of MAP and HR. After a 4-day baseline period, the rats were subjected to bilateral stellate ganglionectomy (SGX; n = 9) or sham surgery (Sham; n = 8). Seven days following SGX or Sham, the rats were administered atenolol for 5 days, followed by a 7-day recovery period. Following a transient decrease, SGX had no effect on basal MAP but decreased HR compared with baseline and Sham rats. Five days of atenolol treatment decreased MAP similarly in SGX and Sham rats. Atenolol resulted in a marked bradycardia in Sham rats but had a neglible effects on HR in SGX rats. The measurement of the content of cardiac catecholamines in all cardiac chambers at the end of the study verified a successful sympathetic denervation. This study confirms that bilateral SGX is a useful method to study the contribution of cardiac sympathetic nerves on the regulation of cardiac function. Moreover, these results suggest that cardiac sympathetic nerves are relatively unimportant in maintaining the basal level of MAP or the depressor response to atenolol in conscious, unrestrained rats.

scholarly journals Both central command and exercise pressor reflex activate cardiac sympathetic nerve activity in decerebrate cats

2009 ◽  
Vol 296 (4) ◽  
pp. H1157-H1163 ◽  
Author(s):  
Hirotsugu Tsuchimochi ◽  
Shawn G. Hayes ◽  
Jennifer L. McCord ◽  
Marc P. Kaufman
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Ventral Root ◽  
Central Command ◽  
Cardiac Sympathetic Nerve ◽  
Nerve Activity ◽  
Exercise Pressor Reflex ◽  
Cardiac Sympathetic Nerve Activity ◽  
Pressor Reflex ◽  
Decerebrate Cats

Both static and dynamic exercise are known to increase cardiac pump function as well as arterial blood pressure. Feedforward control by central command and feedback control by the exercise pressor reflex are thought to be the neural mechanisms causing these effects during exercise. It remains unknown as to how each mechanism activates cardiac sympathetic nerve activity (CSNA) during exercise, especially at its onset. Thus we examined the response of CSNA to stimulation of the mesencephalic locomotor region (MLR, i.e., central command) and to static muscle contraction of the triceps surae muscles or stretch of the calcaneal tendon in decerebrate cats. We found that MLR stimulation immediately increased CSNA, which was followed by a gradual increase in heart rate, mean arterial pressure, and ventral root activity in a stimulus intensity-dependent manner. The latency of the increase in CSNA from the onset of MLR stimulation ranged from 67 to 387 ms. Both static contraction and tendon stretch also rapidly increased CSNA. Their latency from the development of tension in response to ventral root stimulation ranged from 78 to 670 ms. These findings suggest that both central command and the muscle mechanoreflex play a role in controlling cardiac sympathetic outflow at the onset of exercise.

scholarly journals Adrenomedullin increases cardiac sympathetic nerve activity in normal conscious sheep

2005 ◽  
Vol 187 (2) ◽  
pp. 275-281 ◽  
Author(s):  
C J Charles ◽  
D L Jardine ◽  
M G Nicholls ◽  
A M Richards
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Vehicle Control ◽  
Cardiac Sympathetic Nerve ◽  
Burst Frequency ◽  
Nerve Activity ◽  
Cardiac Sympathetic Nerve Activity ◽  
Conscious Sheep

The sympathetic nervous system and adrenomedullin (AM) both participate in the regulation of cardiac and circulatory function but their interaction remains uncertain. We have examined the effects of AM on cardiac sympathetic nerve activity (CSNA) and hemodynamics and contrasted these effects with pressure-matched nitro-prusside (NP) administration in normal conscious sheep. Compared with vehicle control, arterial pressure fell similarly with AM (P=0.04) and NP (P<0.001). Heart rate rose in response to both AM (P<0.001) and NP (P=0.002) but the rise with AM was significantly greater than that induced by NP (P<0.001). Cardiac output increased in response to AM compared with both control and NP (both P<0.001). CSNA burst frequency (bursts/min) were increased in response to both AM (P<0.001) and NP (P=0.005) with the rise in burst frequency being greater with AM compared with NP (P<0.001). CSNA burst area/min was also raised by both AM (P=0.03) and NP (P=0.002) with a trend for burst area being greater with AM than NP (P=0.07). CSNA burst incidence (bursts/100 beats) showed no significant differences between any treatment day. In conclusion, we have demonstrated that AM is associated with a greater increase in CSNA and heart rate for a given change in arterial pressure than seen with the classic balanced vasodilator NP.

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