scholarly journals Renal, Cardiac, and Autonomic Effects of Catheter-Based Renal Denervation in Ovine Heart Failure

Hypertension ◽  
2021 ◽  
Author(s):  
Lindsea C. Booth ◽  
R. Anethra U. de Silva ◽  
Roberto B. Pontes ◽  
Song T. Yao ◽  
Sally G. Hood ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Renal Denervation ◽  
Controlled Study ◽  
Nervous Control ◽  
Water Excretion ◽  
Beneficial Effects ◽  
Parasympathetic Control ◽  
Rapid Ventricular Pacing ◽  
Autonomic Nervous Control

A growing number of clinical studies suggest that in heart failure renal denervation (RDN) has beneficial effects on the autonomic control of the heart. There is also experimental evidence that surgical RDN improves sodium handling and clearance in heart failure. The aim of this study was to determine the effects of catheter-based RDN on the sympathetic and parasympathetic control of the heart, and salt and water handling capacity of the kidneys, in sheep with established heart failure. A randomized, controlled study was conducted in 10 sheep with heart failure (ejection fraction<40%) induced by rapid ventricular pacing. Sheep underwent either bilateral RDN using the Symplicity denervation system or sham denervation and were studied 1 and 6 weeks after RDN. In established ovine heart failure, at 6 weeks after catheter-based RDN, heart rate significantly decreased, estimates of resting and maximal parasympathetic control of heart rate increased, and cardiac sympathetic nerve activity decreased. Compared with sham denervation, there was an increase in the resting sodium and water excretion 6 weeks after catheter-RDN and an improved ability of the kidneys to excrete a nonhypertensive saline load. After catheter-based RDN, renal norepinephrine levels were reduced by 70% compared with sham denervation. In established heart failure, RDN induced a beneficial shift in both arms of the autonomic nervous control of the heart and improved the ability of the kidneys to excrete sodium and water. Thus, effective catheter-based RDN may be beneficial to both the heart and kidneys in heart failure.

Characterization of baroreflex impairment in conscious dogs with pacing-induced heart failure

1993 ◽  
Vol 265 (5) ◽  
pp. R1132-R1140 ◽  
Author(s):  
N. B. Olivier ◽  
R. B. Stephenson
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Peripheral Resistance ◽  
Open Loop ◽  
Ventricular Pacing ◽  
Baroreflex Control ◽  
Rapid Ventricular Pacing ◽  
Reflex Control

Open-loop baroreflex responses were evaluated in eight conscious dogs before and during congestive heart failure to determine the effects of failure on baroreflex control of blood pressure, heart rate, cardiac output, and total peripheral resistance. Heart failure was induced by rapid ventricular pacing. Baroreflex function was determined by calculation of the range and gain of the open-loop stimulus-response relationships for the effect of carotid sinus pressure on blood pressure, heart rate, cardiac output, and total peripheral resistance. The range and gain of blood pressure responses were substantially reduced as early as 3 days after induction of heart failure (161 +/- 6 to 99 +/- 8 mmHg and -2.7 +/- 0.3 to -1.5 +/- 0.1, respectively) and remained depressed for the 21 days of heart failure. This depression in baroreflex control of blood pressure was associated with similar depressions in reflex range and gain for heart rate (125 +/- 9 to 78 +/- 11 beats/min and -2.05 +/- 0.2 to -1.16 +/- 0.2 beats/min, respectively) and cardiac output (1.74 +/- 0.2 to 0.46 +/- 0.2 l/min and -0.81 +/- 0.02 to -0.027 +/- 0.008 l/min, respectively). The group-averaged range and gain for reflex control of vascular resistance were not altered by heart failure. In three dogs, discontinuation of rapid ventricular pacing led to resolution of heart failure within 7 days and partial restoration of the range and gain of reflex control of blood pressure. We conclude that heart failure reversibly depresses baroreflex control of blood pressure principally through a concurrent reduction in reflex control of cardiac output, whereas reflex control of vascular resistance is not consistently affected.

Heart rate determines the beneficial effects of beta-blockers on cardiovascular outcomes in patients with heart failure and atrial fibrillation

2019 ◽  
Vol 42 (11) ◽  
pp. 1716-1725 ◽  
Author(s):  
Athanasius Wrin Hudoyo ◽  
Hiroki Fukuda ◽  
Miki Imazu ◽  
Kazuhiro Shindo ◽  
Haiying Fu ◽  
...  
Keyword(s):  
Heart Failure ◽  
Atrial Fibrillation ◽  
Heart Rate ◽  
Beta Blockers ◽  
Cardiovascular Outcomes ◽  
Beneficial Effects ◽  
Patients With Heart Failure

scholarly journals Alterations in autonomic nervous control of heart rate among tourists at 2700 and 3700m above sea level

2001 ◽  
Vol 12 (1) ◽  
pp. 8-12 ◽  
Author(s):  
Masaki Kanai ◽  
Fumio Nishihara ◽  
Tatsuya Shiga ◽  
Hitoshi Shimada ◽  
Shigeru Saito
Keyword(s):  
Heart Rate ◽  
Sea Level ◽  
Nervous Control ◽  
Autonomic Nervous ◽  
Autonomic Nervous Control

scholarly journals Ca2+ clock malfunction in a canine model of pacing-induced heart failure

2010 ◽  
Vol 299 (6) ◽  
pp. H1805-H1811 ◽  
Author(s):  
Tetsuji Shinohara ◽  
Hyung-Wook Park ◽  
Seongwook Han ◽  
Mark J. Shen ◽  
Mitsunori Maruyama ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Canine Model ◽  
Optical Recording ◽  
Crista Terminalis ◽  
Rate Acceleration ◽  
Intracellular Ca ◽  
Ectopic Beats ◽  
Rapid Ventricular Pacing

The mechanisms of sinoatrial node (SAN) dysfunction in heart failure (HF) remain unclear. We hypothesized that impaired rhythmic spontaneous sarcoplasmic reticulum Ca2+ release (Ca2+ clock) plays an important role in SAN dysfunction in HF. HF was induced in canine hearts by rapid ventricular pacing. The location of pacemaking sites was determined in vivo using computerized electrical mapping in acute open-chest preparations (normal, n = 3; and HF, n = 4). Isoproterenol (Iso, 0.2 μg·kg−1·min−1) infusion increased heart rate and shifted the pacemaking site to the superior SAN in all normal hearts. However, in failing hearts, Iso did not induce superior shift of the pacemaking site despite heart rate acceleration. Simultaneous optical recording of intracellular Ca2+ and membrane potential was performed in Langendorff-perfused isolated right atrium (RA) preparations from normal ( n = 7) and failing hearts ( n = 6). Iso increased sinus rate, enhanced late diastolic Ca2+ elevation (LDCAE), and shifted the pacemaking sites to the superior SAN in all normal but in none of the HF RAs. Caffeine (2 ml, 20 mmol/l) caused LDCAE and increased heart rate in four normal RAs but in none of the three HF RAs. Iso induced ectopic beats from lower crista terminalis in five of six HF RAs. These ectopic beats were suppressed by ZD-7288, a specific pacemaker current ( If) blocker. We conclude that HF results in the suppression of Ca2+ clock, resulting in the unresponsiveness of superior SAN to Iso and caffeine. HF also increases the ectopic pacemaking activity by activating the If at the latent pacemaking sites in lower crista terminalis.

Renal denervation ameliorates the risk of ventricular fibrillation in overweight and heart failure

EP Europace ◽  
2020 ◽  
Vol 22 (4) ◽  
pp. 657-666 ◽  
Author(s):  
Shinya Yamada ◽  
Li-Wei Lo ◽  
Yu-Hui Chou ◽  
Wei-Lun Lin ◽  
Shih-Lin Chang ◽  
...  
Keyword(s):  
Heart Failure ◽  
Body Weight ◽  
Ventricular Fibrillation ◽  
Renal Denervation ◽  
Electrophysiological Study ◽  
Ventricular Myocardium ◽  
Control Group ◽  
Diet Control ◽  
Rapid Ventricular Pacing ◽  
Ventricular Fibrosis

Abstract Aims Both obesity and heart failure (HF) are associated with sudden cardiac death. The current study aimed to investigate the effects of overweight and HF on the substrate for ventricular fibrillation (VF), and whether renal denervation (RDN) can protect the heart from sympathetic activation and cardiac remodelling in HF rabbits fed with high-fat diet (HFD). Methods and results Twenty-four rabbits randomized into control group fed with regular diet (Control), HFD, HFD-HF, and HFD-HF-RDN groups. Rapid ventricular pacing of 400 b.p.m. for 4 weeks was applied in HFD-HF and HFD-HF-RDN. Surgical and chemical RDNs were approached through bilateral retroperitoneal flank incisions in HFD-HF-RDN. All rabbits received electrophysiological study and a VF inducibility test. The ventricular myocardium was harvested for trichrome stain. After 3 months, mean body weight was heavier in HFD, compared with control (3.5 ± 0.1 kg vs. 2.6 ± 0.1 kg, P &lt; 0.01). No differences in body weight among the three groups fed with HFD were observed. The ventricular refractory periods were longer in HFD-HF and HFD-HF-RDN than in control. An extension of ventricular fibrosis was observed in HFD and HFD-HF compared with control, and the degree of ventricular fibrosis was suppressed in HFD-HF-RDN compared with HFD-HF. The level of tyrosine hydroxylase staining was reduced in HFD-HF-RDN compared with HFD and HFD-HF. Importantly, VF inducibility was lower in HFD-RDN-HF (10 ± 4%), when compared with those in HFD-HF (58 ± 10%, P &lt; 0.01) and HFD (42 ± 5%, P &lt; 0.05), respectively. Conclusion Our results suggest that overweight and HF increase sympathetic activity, structural remodelling, and VF inducibility, but RDN prevents them.

Central mineralocorticoid receptor blockade improves volume regulation and reduces sympathetic drive in heart failure

2001 ◽  
Vol 281 (5) ◽  
pp. H2241-H2251 ◽  
Author(s):  
Joseph Francis ◽  
Robert M. Weiss ◽  
Shun-Guang Wei ◽  
Alan Kim Johnson ◽  
Terry G. Beltz ◽  
...  
Keyword(s):  
Heart Failure ◽  
Central Nervous System ◽  
Nervous System ◽  
Volume Regulation ◽  
Critical Role ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
Water Excretion ◽  
Beneficial Effects ◽  
The Central Nervous System

The mineralocorticoid (MC) receptor antagonist spironolactone (SL) improves morbidity and mortality in patients with congestive heart failure (CHF). We tested the hypothesis that the central nervous system actions of SL contribute to its beneficial effects. SL (100 ng/h for 28 days) or ethanol vehicle (VEH) was administered intracerebroventricularly or intraperitoneally to rats with CHF induced by coronary artery ligation (CL) and to SHAM-operated controls. The intracerebroventricular SL treatment prevented the increase in sodium appetite and the decreases in sodium and water excretion observed within a week of CL in VEH-treated CHF rats. Intraperitoneal SL also improved volume regulation in the CHF rats, but only after 3 wk of treatment. Four weeks of SL treatment, either intracerebroventricularly or intraperitoneally, ameliorated both the increase in sympathetic drive and the impaired baroreflex function observed in VEH-treated CHF rats. These findings suggest that activation of MC receptors in the central nervous system plays a critical role in the altered volume regulation and augmented sympathetic drive that characterize clinical heart failure.

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