title: Arterial baroreceptor and cardiopulmonary reflex control of sympathetic outflow in human heart failure.
abstract: Several observations indicate that the arterial baroreflex control of sympathetic nerve activity is preserved, even in advanced heart failure. These include: (1) augmentation of muscle sympathetic nerve activity burst amplitude and duration following a premature beat; (2) rapid recognition of changes in blood pressure induced by ventricular arrhythmias; (3) muscle sympathetic alternans and a steep inverse relationship between changes in diastolic pressure and the subsequent sympathetic burst amplitude during pulsus alternans; (4) similar inhibition of muscle sympathetic nerve activity in subjects with normal and impaired left ventricular systolic function by increases in intrathoracic aortic transmural pressure; (5) documentation, by cross-spectral analysis, of similar gain in the transfer function between blood pressure and muscle sympathetic nerve activity in these two groups; and (6) during sodium nitroprusside infusion, similar reflex increases in total body norepinephrine spillover in normal and heart-failure subjects. When nonhypotensive lower-body negative pressure was applied to test the hypothesis that selective reduction of atrial and pulmonary pressures would exert a cardiac sympathoinhibitory response in heart failure, there was no effect in control subjects, but cardiac norepinephrine spillover fell by 25% (P < .05) in those with systolic dysfunction. In summary, human heart failure is characterized by a rapidly responsive and sensitive arterial baroreflex, and by activation of a cardiac sympathoexcitatory reflex related to increased cardiopulmonary filling pressures.
authors.affiliation: Mount Sinai Hospital, University Health Network, Department of Medicine, University of Toronto, Toronto, Canada M5G 1X5. john.floras@utoronto.ca
authors.forename: J S
authors.initials: JS
authors.lastname: Floras
mesh_terms: D001158:Arteries / Q000294:innervation*; D017704:Baroreflex / Q000502:physiology*; D002303:Cardiac Output, Low / Q000503:physiopathology*; D006321:Heart / Q000503:physiopathology*; D006801:Humans; D008168:Lung / Q000503:physiopathology*; D013564:Sympathetic Nervous System / Q000503:physiopathology*