title: Peripheral chemoreflex activation contributes to sympathetic baroreflex impairment in chronic heart failure.
abstract: BACKGROUND
  Chemoreflex-mediated sympathetic activation contributes to both initiation and progression of chronic heart failure (CHF).
  
  
  METHODS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Institut National de la Sante et de la Recherche Médicale, UMR-1048, Institut des Maladies Métaboliques et Cardiovasculaires, Toulouse, France. fabien.despas@univtlse3.fr
authors.forename: Fabien
authors.initials: F
authors.lastname: Despas
authors.forename: Elisabeth
authors.initials: E
authors.lastname: Lambert
authors.forename: Angelica
authors.initials: A
authors.lastname: Vaccaro
authors.forename: Marc
authors.initials: M
authors.lastname: Labrunee
authors.forename: Nicolas
authors.initials: N
authors.lastname: Franchitto
authors.forename: Marine
authors.initials: M
authors.lastname: Lebrin
authors.forename: Michel
authors.initials: M
authors.lastname: Galinier
authors.forename: Jean-Michel
authors.initials: JM
authors.lastname: Senard
authors.forename: Gavin
authors.initials: G
authors.lastname: Lambert
authors.forename: Murray
authors.initials: M
authors.lastname: Esler
authors.forename: Atul
authors.initials: A
authors.lastname: Pathak
mesh_terms: D017704:Baroreflex / Q000187:drug effects / Q000502:physiology*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002628:Chemoreceptor Cells / Q000502:physiology*; D002908:Chronic Disease; D004311:Double-Blind Method; D006333:Heart Failure / Q000188:drug therapy / Q000503:physiopathology*; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000294:innervation; D010100:Oxygen / Q000008:administration & dosage; D010102:Oxygen Inhalation Therapy; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000503:physiopathology*
chemical_list: D010100:Oxygen