title: Normalization of total body and regional sympathetic hyperactivity in heart failure after heart transplantation.
abstract: BACKGROUND
  Sympathetic nerve activity is increased in patients with severe heart failure. Whether this intense sympathoexcitation is normalized after heart transplantation, despite cyclosporine A treatment, is still unsettled. In the present study, regional sympathetic function in 12 patients with severe heart failure, awaiting heart transplantation, was compared with that in 15 heart transplant recipients and 12 healthy subjects.
  
  
  METHODS
  Total and regional sympathetic activity in the heart and kidney were evaluated with isotope dilution, using steady-state infusion of [3H] norepinephrine. Sympathetic nerve traffic to skeletal muscle vascular bed was recorded intraneurally with microneurography.
  
  
  RESULTS
  Total body, cardiac, and renal norepinephrine spillovers were high in the heart failure group (6792 +/- 455, 385 +/- 74, and 1554 +/- 114 pmol/min, respectively) as was muscle sympathetic nerve activity (82 +/- 5 bursts/min). Transplant recipients showed a marked reduction of total body (3200 +/- 307 pmol/min) and renal (747 +/- 169 pmol/min) norepinephrine spillovers and sympathetic nerve firing to skeletal muscle (22 +/- 6 bursts/min), none of which differed from healthy subjects.
  
  
  CONCLUSIONS
  The augmentation of total body and regional sympathetic outflow to the kidney and skeletal muscle vascular beds, associated with a failing heart, was normalized after transplantation. Thus, sympathoexcitation in heart failure is reversible. Furthermore, because all heart transplant recipients received cyclosporine A, the findings do not support the concept that cyclosporine-induced hypertension is mediated by increased sympathetic nerve activity.
authors.affiliation: Department of Cardiology, Sahlgrenska University Hospital, Göteborg, Sweden.
authors.forename: B
authors.initials: B
authors.lastname: Rundqvist
authors.forename: M
authors.initials: M
authors.lastname: Elam
authors.forename: G
authors.initials: G
authors.lastname: Eisenhofer
authors.forename: P
authors.initials: P
authors.lastname: Friberg
mesh_terms: D000328:Adult; D016022:Case-Control Studies; D016572:Cyclosporine / Q000627:therapeutic use; D004594:Electrophysiology; D006329:Heart Conduction System / Q000503:physiopathology; D006333:Heart Failure / Q000503:physiopathology* / Q000601:surgery; D016027:Heart Transplantation / Q000502:physiology*; D006801:Humans; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D007668:Kidney / Q000294:innervation / Q000378:metabolism; D008657:Metabolic Clearance Rate; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000098:blood supply / Q000294:innervation / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism; D009638:Norepinephrine / Q000097:blood / Q000378:metabolism; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D013566:Sympathomimetics / Q000097:blood / Q000378:metabolism; D014316:Tritium
chemical_list: D007166:Immunosuppressive Agents; D013566:Sympathomimetics; D014316:Tritium; D016572:Cyclosporine; D009638:Norepinephrine