scholarly journals Does lipid-lowering medication improve cardiac sympathetic nerve integrity?

2020 ◽  
Author(s):  
Rudolf A. Werner ◽  
James T. Thackeray ◽  
Frank M. Bengel
Keyword(s):  
Sympathetic Nerve ◽  
Lipid Lowering ◽  
Cardiac Sympathetic Nerve

Long-term serial changes of cardiac sympathetic nerve dysfunction in acute decompensated heart failure patients with reduced, mid-range and preserved left ventricular ejection fraction

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
M Seo ◽  
T Yamada ◽  
T Watanabe ◽  
T Morita ◽  
Y Furukawa ◽  
...  
Keyword(s):  
Heart Failure ◽  
Sympathetic Nerve ◽  
Acute Decompensated Heart Failure ◽  
Decompensated Heart Failure ◽  
Left Ventricular Ejection ◽  
Mibg Imaging ◽  
Cardiac Sympathetic Nerve ◽  
Heart Failure Hospitalization ◽  
Nerve Dysfunction

Abstract Background Cardiac sympathetic nerve dysfunction, which is assessed by I-123 metaiodobenzylguanidine (MIBG) imaging, is associated with the poor outcomes in patients with chronic heart failure (CHF). Serial evaluation of cardiac MIBG imaging was shown to be useful for predicting adverse outcome in CHF. However, there was no information available on long-term serial changes of cardiac sympathetic nerve dysfunction after discharge of acute decompensated heart failure (ADHF) hospitalization. Purpose We aimed to clarify the serial change of cardiac MIBG imaging parameter in long-term after discharge of heart failure hospitalization, especially relating to HFrEF (LVEF<40%), HFmrEF (40%≤LVEF<50%) and HFpEF (LVEF≥50%). Methods We studied 112 patients (HFrEF; n=44, HFmrEF; n=23 and HFpEF; n=45) who were admitted for ADHF, discharged with survival and without heart failure hospitalization during follow-up period. All patients underwent cardiac MIBG imaging at the timing of discharge, in 6–12 months and in 18–24 months after discharge. The cardiac MIBG heart to mediastinum ratio (H/M) was calculated on the early image and the delayed image (late H/M). The cardiac MIBG washout rate (WR) was calculated from the early and delayed planar images after taking radioactive decay of I-123 into consideration. Results In HFrEF patients, late H/M was significantly improved from discharge to 6–12 months data (1.60±0.24 vs 1.75±0.31, p<0.0001). Late H/M of HFmrEF patients was also significantly improved from discharge to 18–24 months data (1.71±0.27 vs 1.84±0.29 p=0.043). On the other hand, late H/M of HFpEF patients was not significantly changed. As for WR, WR in HFrEF and HFmrEF patients was significantly improved from discharge to 18–24 months data, although WR of HFpEF was not significantly changed. Conclusion The improvement in cardiac sympathetic nerve dysfunction was observed in patients with HFrEF and HFmrEF, not in HFpEF, after the discharge of acute heart failure hospitalization. Funding Acknowledgement Type of funding source: None

Effects of Ketamine on In Vivo Cardiac Sympathetic Nerve Endings

2001 ◽  
Vol 38 ◽  
pp. S39-S42 ◽  
Author(s):  
Hirotoshi Kitagawa ◽  
Toji Yamazaki ◽  
Tsuyoshi Akiyama ◽  
Hidezo Mori ◽  
Kenji Sunagawa
Keyword(s):  
Sympathetic Nerve ◽  
Nerve Endings ◽  
Cardiac Sympathetic Nerve

scholarly journals Alterations by Norepinephrine of Cardiac Sympathetic Nerve Terminal Function and Myocardial β-Adrenergic Receptor Sensitivity in the Ferret

Circulation ◽  
2000 ◽  
Vol 102 (1) ◽  
pp. 96-103 ◽  
Author(s):  
Chang-seng Liang ◽  
Naomi Kenmotsu Rounds ◽  
Erdan Dong ◽  
Suzanne Y. Stevens ◽  
Junya Shite ◽  
...  
Keyword(s):  
Nerve Terminal ◽  
Sympathetic Nerve ◽  
Adrenergic Receptor ◽  
Cardiac Sympathetic Nerve ◽  
Receptor Sensitivity ◽  
Sympathetic Nerve Terminal

scholarly journals ACE inhibition improves cardiac NE uptake and attenuates sympathetic nerve terminal abnormalities in heart failure

1999 ◽  
Vol 277 (4) ◽  
pp. H1609-H1617 ◽  
Author(s):  
Hiroya Kawai ◽  
Tai-Hwang M. Fan ◽  
Erdan Dong ◽  
Rizwan A. Siddiqui ◽  
Akito Yatani ◽  
...  
Keyword(s):  
Heart Failure ◽  
Tyrosine Hydroxylase ◽  
Nerve Terminal ◽  
Ace Inhibitors ◽  
Sympathetic Nerve ◽  
Ace Inhibition ◽  
Inotropic Response ◽  
Cardiac Sympathetic Nerve ◽  
Beneficial Effects ◽  
Sympathetic Nerve Terminal

Cardiac sympathetic nerve terminal dysfunction plays an important role in the downregulation of myocardial β-adrenoceptors in heart failure. To determine whether chronic angiotensin-converting enzyme (ACE) inhibition improved cardiac sympathetic nerve terminal function and hence increased myocardial β-adrenergic responsiveness, we administered ACE inhibitors to dogs with chronic right-sided heart failure (RHF) produced by tricuspid avulsion and pulmonary artery constriction. The RHF animals exhibited fluid retention, elevated right heart filling pressures, blunted inotropic response to isoproterenol, and reduced β-adrenoceptor density. These changes were accompanied by decreases in right ventricular norepinephrine (NE) uptake and neuronal NE histofluorescence and tyrosine hydroxylase immunoreactive profiles. ACE inhibitors had no effect on the production of heart failure but greatly reduced the attenuation of cardiac NE uptake, neuronal NE histofluorescence, and tyrosine hydroxylase immunoreactive profiles. ACE inhibition also improved the inotropic response to isoproterenol and restored myocardial β-adrenoceptor density. The changes probably are caused by reduction of cardiac NE release by ACE inhibition and may contribute to the beneficial effects of ACE inhibitor therapy in patients with chronic heart failure.

scholarly journals Clinical Usefulness of 123I-Metaiodobenzylguanidine Myocardial Scintigraphy in Diabetic Patients With Cardiac Sympathetic Nerve Dysfunction.

1995 ◽  
Vol 59 (9) ◽  
pp. 599-607 ◽  
Author(s):  
Hajime Miyanaga ◽  
Satoshi Yoneyama ◽  
Tadaaki Kamitani ◽  
Shingo Kawasaki ◽  
Toru Takahashi ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Myocardial Scintigraphy ◽  
Clinical Usefulness ◽  
Diabetic Patients ◽  
Cardiac Sympathetic Nerve ◽  
Nerve Dysfunction

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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