scholarly journals Is central nervous system processing altered in patients with heart failure?

2004 ◽  
Vol 25 (11) ◽  
pp. 952-962 ◽  
Author(s):  
S DROSEN
2020 ◽  
Author(s):  
Mark Dayer ◽  
David H MacIver ◽  
Stuart D Rosen

The view that chronic heart failure was exclusively a disease of the heart dominated the cardiovascular literature until relatively recently. However, over the last 40 years it has increasingly come to be seen as a multisystem disease. Aside from changes in the sympathetic and parasympathetic nervous systems and the renin-angiotensin-aldosterone system, adaptations to the lungs, muscles and gastrointestinal tract have been clearly documented. It is clear that the brain and CNS are also affected in patients with heart failure, although this is often under recognized. The purpose of this review is to summarize the changes in the structure and biochemical function of the CNS in patients with chronic heart failure and to discuss their potential importance.


2010 ◽  
Vol 31 (7) ◽  
pp. 969-976 ◽  
Author(s):  
Jondavid Menteer ◽  
Paul M. Macey ◽  
Mary A. Woo ◽  
Ashok Panigrahy ◽  
Ronald M. Harper

2003 ◽  
Vol 284 (2) ◽  
pp. R328-R335 ◽  
Author(s):  
Joseph Francis ◽  
Robert M. Weiss ◽  
Alan Kim Johnson ◽  
Robert B. Felder

The Randomized Aldactone Evaluation Study (RALES) demonstrated a substantial clinical benefit to blocking the effects of aldosterone (Aldo) in patients with heart failure. We recently demonstrated that the enhanced renal conservation of sodium and water in rats with heart failure can be reduced by blocking the central nervous system effects of Aldo with the mineralocorticoid receptor (MR) antagonist spironolactone (SL). Preliminary data from our laboratory suggested that central MR might contribute to another peripheral mechanism in heart failure, the release of proinflammatory cytokines. In the present study, SL (100 ng/h for 21 days) or ethanol vehicle (Veh) was administered via the 3rd cerebral ventricle to one group of rats after coronary ligation (CL) or sham CL (Sham) to induce congestive heart failure (CHF). In Veh-treated CHF rats, tumor necrosis factor-α (TNF-α) levels increased during day 1 and continued to increase throughout the 3-wk observation period. In CHF rats treated with SL, started 24 h after CL, TNF-α levels rose initially but retuned to control levels by day 5 after CL and remained low throughout the study. These findings suggest that activation of MR in the central nervous system plays a critical role in regulating TNF-α release in heart failure rats. Thus some of the beneficial effect of blocking MR in heart failure could be due at least in part to a reduction in TNF-α production.


1985 ◽  
Vol 68 (6) ◽  
pp. 659-667 ◽  
Author(s):  
Mark A. Creager ◽  
David P. Faxon ◽  
Susan M. Rockwell ◽  
Haralambos Gavras ◽  
Jay D. Coffman

1. In patients with congestive heart failure, both the sympathetic nervous system and renin-angiotensin system are often stimulated. In order to assess the contribution of the renin-angiotensin system to limb vascular resistance, the forearm haemodynamic response to captopril was studied in 13 patients with heart failure. 2. Seven subjects were studied while supine and during 60° head-up tilt. To eliminate α-adrenergic effects, six additional patients with heart failure were pretreated with intra-arterial phentolamine and then given captopril. Venous occlusion plethysmography was used to determine forearm blood flew and forearm vascular resistance. 3. Tilt did not significantly increase pretreatment plasma renin activity or plasma noradrenaline concentration, nor did it decrease forearm blood flow. Furthermore, captopril did not alter forearm vascular resistance during supine or upright posture. During the phentolamine infusion, however, captopril reduced forearm vascular resistance by 19% (P < 0.05). 4. Despite increased plasma renin activity, captopril did not cause forearm vasodilatation during supine or upright posture in these patients with heart failure. When the contribution of the sympathetic nervous system was eliminated, captopril decreased forearm vascular resistance. Therefore, in patients with congestive heart failure, the sympathetic nervous system is important in limb vasoregulation, and the contribution of the renin-angiotensin system is apparent only after α-adrenergic blockade.


2011 ◽  
Vol 148 (1) ◽  
pp. 53-58 ◽  
Author(s):  
Linda M. Ueno ◽  
Luciano F. Drager ◽  
Ana C.T. Rodrigues ◽  
Maria U.P.B. Rondon ◽  
Wilson Mathias ◽  
...  

2001 ◽  
Vol 281 (5) ◽  
pp. H2241-H2251 ◽  
Author(s):  
Joseph Francis ◽  
Robert M. Weiss ◽  
Shun-Guang Wei ◽  
Alan Kim Johnson ◽  
Terry G. Beltz ◽  
...  

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.


2015 ◽  
Vol 64 (5) ◽  
pp. 351-360 ◽  
Author(s):  
Monica Parry ◽  
Chantelle A. Nielson ◽  
Fiona Muckle ◽  
Sheila O’Keefe-McCarthy ◽  
Rene van Lien ◽  
...  

2006 ◽  
Vol 84 (1) ◽  
pp. 61-66 ◽  
Author(s):  
Richard S.T. Leung ◽  
John S. Floras ◽  
T. Douglas Bradley

Cheyne–Stokes respiration (CSR) is associated with increased mortality among patients with heart failure. However, the specific link between CSR and mortality remains unclear. One possibility is that CSR results in excitation of the sympathetic nervous system. This review relates evidence that CSR exerts acute effects on the autonomic nervous system during sleep, and thereby influences a number of cardiovascular phenomena, including heart rate, blood pressure, atrioventricular conduction, and ventricular ectopy. In patients in sinus rhythm, heart rate and blood pressure oscillate during CSR in association with respiratory oscillations, such that both peak heart rate and blood pressure occur during the hyperpneic phase. Inhalation of CO2 abolishes both CSR and the associated oscillations in heart rate and blood pressure. In contrast, O2 inhalation sufficient to eliminate hypoxic dips has no significant effect on CSR, heart rate, or blood pressure. In patients with atrial fibrillation, ventricular rate oscillates in association with CSR despite the absence of within-breath respiratory arrhythmia. The comparison of RR intervals between the apneic and hyperpneic phases of CSR indicates that this breathing disorder exerts its effect on ventricular rate by inducing cyclical changes in atrioventricular node conduction properties. In patients with frequent ventricular premature beats (VPBs), VPBs occur more frequently during the hyperpneic phase than the apneic phase of CSR. VPB frequency is also higher during periods of CSR than during periods of regular breathing, with or without correction of hypoxia. In summary, CSR exerts multiple effects on the cardiovascular system that are likely manifestations of respiratory modulation of autonomic activity. It is speculated that the rhythmic oscillations in autonomic tone brought about by CSR may ultimately contribute to the sympatho-excitation and increased mortality long observed in patients with heart failure and CSR.


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