Literature DB >> 22241144

Peripheral chemoreflex activation contributes to sympathetic baroreflex impairment in chronic heart failure.

Fabien Despas1, Elisabeth Lambert, Angelica Vaccaro, Marc Labrunee, Nicolas Franchitto, Marine Lebrin, Michel Galinier, Jean-Michel Senard, Gavin Lambert, Murray Esler, Atul Pathak.   

Abstract

BACKGROUND: Chemoreflex-mediated sympathetic activation contributes to both initiation and progression of chronic heart failure (CHF).
METHOD: To study the direct role of increased peripheral chemosensitivity in reducing sympathetic baroreflex function in CHF patients, we compared sympathetic baroreflex function, assessed by the slope of the relationship between muscle sympathetic nerve activity (MSNA) and DBP, in CHF patients with augmented (n = 18) and normal (n = 20) peripheral chemosensitivity. Using a double-blind, randomized, vehicle-controlled study, we examined the effect of chemoreflex deactivation (by breathing 100% oxygen for 15 min) on sympathetic baroreflex function in CHF patients with elevated and with normal chemosensitivity.
RESULTS: Baseline MSNA was elevated (60.6 ± 3.2 vs. 48.9 ± 3.7 bursts/min, P < 0.05) and sympathetic baroreflex function impaired (3.06 ± 0.55 vs. 5.51 ± 0.69 % bursts/mmHg, P < 0.05) in CHF patients with augmented peripheral chemosensitivity compared with controls. Administration of 100% oxygen led to a significant decrease in MSNA (from 60.5 ± 3.2 to 52.6 ± 3.2 bursts/min, P < 0.001) and increase in sympathetic baroreflex (from 2.95 ± 0.56 to 6.18 ± 0.77, P < 0.001) in CHF patients with enhanced chemoreflex sensitivity. In contrast, neither room air nor 100% oxygen changed MSNA, hemodynamics or sympathetic baroreflex function in CHF patients with normal chemosensitivity.
CONCLUSION: We report for the first time that increased peripheral chemoreflex sensitivity directly decreases sympathetic baroreflex function in CHF patients. This interaction contributes to sympathetic overactivity and blunted sympathetic baroreflex function of CHF patients and may explain how chemoreceptors contribute to the bad prognosis of CHF patients.

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Year:  2012        PMID: 22241144     DOI: 10.1097/HJH.0b013e328350136c

Source DB:  PubMed          Journal:  J Hypertens        ISSN: 0263-6352            Impact factor:   4.844


  29 in total

1.  Divergent muscle sympathetic responses to dynamic leg exercise in heart failure and age-matched healthy subjects.

Authors:  Catherine F Notarius; Philip J Millar; Hisayoshi Murai; Beverley L Morris; Susan Marzolini; Paul Oh; John S Floras
Journal:  J Physiol       Date:  2014-12-15       Impact factor: 5.182

2.  Effect of bilateral carotid body resection on cardiac baroreflex control of blood pressure during hypoglycemia.

Authors:  Jacqueline K Limberg; Jennifer L Taylor; Michael T Mozer; Simmi Dube; Ananda Basu; Rita Basu; Robert A Rizza; Timothy B Curry; Michael J Joyner; Erica A Wehrwein
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Review 7.  Role of neurotransmitter gases in the control of the carotid body in heart failure.

Authors:  Harold D Schultz; Rodrigo Del Rio; Yanfeng Ding; Noah J Marcus
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Review 8.  Sympathetic Activation in Chronic Heart Failure: Potential Benefits of Interventional Therapies.

Authors:  Kamila Lachowska; Marcin Gruchała; Krzysztof Narkiewicz; Dagmara Hering
Journal:  Curr Hypertens Rep       Date:  2016-07       Impact factor: 5.369

Review 9.  Carotid body modulation in systolic heart failure from the clinical perspective.

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Journal:  J Physiol       Date:  2016-04-13       Impact factor: 5.182

Review 10.  Pathophysiology and potential clinical applications for testing of peripheral chemosensitivity in heart failure.

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