scholarly journals P2763Increased renal 123I-metaiodobenzylguanidine scintigraphy wash out rate accompanied by muscle sympathetic nerve activity in left ventricular dysfunction patients

2018 ◽  
Vol 39 (suppl_1) ◽  
Author(s):  
O Yoshitaka ◽  
H Murai ◽  
H Tokuhisa ◽  
T Hamaoka ◽  
Y Mukai ◽  
...  
2019 ◽  
pp. 209-217
Author(s):  
Bing Xiao ◽  
Fan Liu ◽  
Jing-Chao Lu ◽  
Fei Chen ◽  
Wei-Na Pei ◽  
...  

The objective of the paper is to determine the influence of IGF-1 deletion on renal sympathetic nerve activity (RSNA), left ventricular dysfunction, and renal function in deoxycorticosterone acetate (DOCA)-salt hypertensive mice. The DOCA-salt hypertensive mice models were constructed and the experiment was classified into WT (Wild-type mice) +sham, LID (Liverspecific IGF-1 deficient mice) + sham, WT + DOCA, and LID + DOCA groups. Enzyme-linked immunosorbent assay (ELISA) was used to detect the serum IGF-1 levels in mice. The plasma norepinephrine (NE), urine protein, urea nitrogen and creatinine, as well as RSNA were measured. Echocardiography was performed to assess left ventricular dysfunction, and HE staining to observe the pathological changes in renal tissue of mice. DOCA-salt induction time-dependently increased the systolic blood pressure (SBP) of mice, especially in DOCA-salt LID mice. Besides, the serum IGF-1 levels in WT mice were decreased after DOCA-salt induction. In addition, the plasma NE concentration and NE spillover, urinary protein, urea nitrogen, creatinine and RSNA were remarkably elevated with severe left ventricular dysfunction, but the creatinine clearance was reduced in DOCA-salt mice, and these similar changes were obvious in DOCA-salt mice with IGF-1 deletion. Moreover, the DOCA-salt mice had tubular ectasia, glomerular fibrosis, interstitial cell infiltration, and increased arterial wall thickness, and the DOCA-salt LID mice were more serious in those aspects. Deletion of IGF-1 may lead to enhanced RSNA in DOCA-salt hypertensive mice, thereby further aggravating left ventricular dysfunction and renal damage.


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Yusuke Mukai ◽  
Hisayoshi Murai ◽  
Tadayuki Hirai ◽  
Takuto Hamaoka ◽  
Yoshitaka Okabe ◽  
...  

Introduction: Atrial fibrillation (AF) is associated with diastolic dysfunction (DD) at a high rate and the presence of left ventricular DD is also associated with increased muscle sympathetic nerve activity (MSNA). Catheter ablation (CA) of AF was reported to improve cardiac function, including the reverse remodeling of left ventricle and atrium. However, little is known about the effect of CA on MSNA and DD in AF patients. Purpose: The purpose of this study was to evaluate the effect of CA on MSNA and DD and the difference in therapeutic effect between two groups with and without DD. Methods: This study was conducted as a prospective, observational study. AF patients who were scheduled for CA were enrolled. The patients were divided into two groups, E/e’ ratio≧11 and <11. We measured blood pressure, HR, body weight, echocardiogram parameters, and MSNA before and 12 weeks after CA. Results: 28 AF patients participated in this study. After CA, in the patients with DD(the group of E/e’≧11, n=12), E/e’ ratio, the MSNA burst incidence(BI) and frequency(BF) were significantly decreased (13.4±2.1 to 10.6±3.0, p<0.01. 64.4±15.8 to 34.0±12.0 bursts/100beats, P<0.01, 39.7±9.3 to 23.5±9.2 bursts/min, p<0.01 respectively). In the patients without DD (the group of E/e’<11, n=16), the BI and BF were significantly decreased (59.7±11.8 to 43.5±11.7 bursts/100beats, P<0.01, 38.1±10.5 to 29.2±8.4 bursts/min, p<0.01 respectively) while there was no difference in E/e’ ratio. Interestingly, in the patients with DD, decrease in BI and BF were more pronounced compared in the patients without DD(-30.4±15.9 to -16.2±11.5 bursts/100beats, P<0.05. -16.3±11.5 to -8.9±13.8 bursts/min, P=0.145 respectively). In both groups, no significant changes were observed in EF and peak acceleration rate of mitral E velocity. Conclusion: CA reduced MSNA in AF patients. In the patients with DD, the reduction of MSNA tended to be more remarkable than without DD. These findings suggest that changes of MSNA might reflect the improvement of DD and reduction of AF burden.


1995 ◽  
Vol 268 (1) ◽  
pp. H218-H225 ◽  
Author(s):  
R. Jung ◽  
M. E. Dibner-Dunlap ◽  
M. A. Gilles ◽  
M. D. Thames

Patients with heart failure exhibit a neurohumoral excitatory state and abnormal baroreflex control of the cardiovascular system. We determined whether arterial baroreflexes are impaired during left ventricular dysfunction (LVD) caused by chronic myocardial infarction in the absence of congestive heart failure and whether abnormal central mechanisms contribute to this impairment. Baroreceptors were stimulated in anesthetized rats with and without LVD by increasing arterial pressure with phenylephrine. Lumbar sympathetic nerve and phrenic nerve activity as well as heart rate were recorded. Rats were divided into different groups based on infarct size. Rats with moderate LVD showed impaired baroreflex control of sympathetic, ventilatory, and heart rate responses. Baroreflex gains were inversely related to the size of the infarct. The central gain for sympathetic nerve activity, obtained by using electrical stimulation of the aortic depressor nerve, also was impaired. Baroreflex control of the cardiorespiratory system is thus impaired in rats with moderate LVD in the absence of congestive heart failure. The attenuated baroreflexes are likely due to abnormal afferent mechanisms, although central mechanisms contribute to the impaired barosympathetic reflex.


2021 ◽  
Vol 15 ◽  
Author(s):  
Edgar Toschi-Dias ◽  
Nicola Montano ◽  
Eleonora Tobaldini ◽  
Patrícia F. Trevizan ◽  
Raphaela V. Groehs ◽  
...  

Sympathetic hyperactivation and baroreflex dysfunction are hallmarks of heart failure with reduced ejection fraction (HFrEF). However, it is unknown whether the progressive loss of phasic activity of sympathetic nerve bursts is associated with baroreflex dysfunction in HFrEF patients. Therefore, we investigated the association between the oscillatory pattern of muscle sympathetic nerve activity (LFMSNA/HFMSNA) and the gain and coupling of the sympathetic baroreflex function in HFrEF patients. In a sample of 139 HFrEF patients, two groups were selected according to the level of LFMSNA/HFMSNA index: (1) Lower LFMSNA/HFMSNA (lower terciles, n = 46, aged 53 ± 1 y) and (2) Higher LFMSNA/HFMSNA (upper terciles, n = 47, aged 52 ± 2 y). Heart rate (ECG), arterial pressure (oscillometric method), and muscle sympathetic nerve activity (microneurography) were recorded for 10 min in patients while resting. Spectral analysis of muscle sympathetic nerve activity was conducted to assess the LFMSNA/HFMSNA, and cross-spectral analysis between diastolic arterial pressure, and muscle sympathetic nerve activity was conducted to assess the sympathetic baroreflex function. HFrEF patients with lower LFMSNA/HFMSNA had reduced left ventricular ejection fraction (26 ± 1 vs. 29 ± 1%, P = 0.03), gain (0.15 ± 0.03 vs. 0.30 ± 0.04 a.u./mmHg, P &lt; 0.001) and coupling of sympathetic baroreflex function (0.26 ± 0.03 vs. 0.56 ± 0.04%, P &lt; 0.001) and increased muscle sympathetic nerve activity (48 ± 2 vs. 41 ± 2 bursts/min, P &lt; 0.01) and heart rate (71 ± 2 vs. 61 ± 2 bpm, P &lt; 0.001) compared with HFrEF patients with higher LFMSNA/HFMSNA. Further analysis showed an association between the LFMSNA/HFMSNA with coupling of sympathetic baroreflex function (R = 0.56, P &lt; 0.001) and left ventricular ejection fraction (R = 0.23, P = 0.02). In conclusion, there is a direct association between LFMSNA/HFMSNA and sympathetic baroreflex function and muscle sympathetic nerve activity in HFrEF patients. This finding has clinical implications, because left ventricular ejection fraction is less in the HFrEF patients with lower LFMSNA/HFMSNA.


Sign in / Sign up

Export Citation Format

Share Document