title: Lung anabolic activity in patients with chronic heart failure: potential implications for clinical practice.
abstract: OBJECTIVE
  The proteins in the lungs are in constant flux, undergoing degradation and resynthesis. We investigated pulmonary protein and amino acid metabolism, the biochemical basis of the remodeling process, in individuals with chronic heart failure receiving or not receiving β-blocker therapy with bisoprolol (BIS).
  
  
  METHODS
  Clinically stable rehabilitative patients with chronic heart failure, without metabolic diseases or liver/renal failure, and with a stable weight over the preceding 3 mo underwent right heart catheterization, and radial artery cannulation. Mixed central venous and arterial blood samples were drawn simultaneously to calculate the venous-arterial difference of amino acids (pulmonary uptake and release).
  
  
  RESULTS
  Twenty-two patients on BIS therapy and eight not receiving BIS were analyzed. The two groups showed a net pulmonary protein synthesis (i.e., a positive value of phenylalanine [venous-arterial difference] × cardiac index product) and amino acid extraction, the rates of which were significantly lower in patients on BIS therapy. The two groups had pulmonary hypertension (mean pulmonary artery pressure >19 mmHg). Pulmonary vascular resistance was 57% higher in patients not receiving BIS than in those on BIS therapy (6.65 ± 2.90 versus 4.23 ± 1.49 mmHg/L · min⁻¹ · m⁻², P < 0.05). Pulmonary vascular resistance correlated positively with the pulmonary extraction of total essential amino acids (r = +0.4576, P = 0.01) and leucine (r = +0.5083, P = 0.004), the most important amino acid for protein synthesis.
  
  
  CONCLUSIONS
  Patients with chronic heart failure have increased rates of amino acid extraction and pulmonary protein synthesis, suggesting, at least in part, an increased rate of lung remodeling. Therapy with BIS attenuates lung metabolic abnormalities.
authors.affiliation: Servizio di Fisiopatologia Metabolico-Nutrizionale e Nutrizione Clinica, Fondazione S. Maugeri, IRCCS, Istituto Scientifico di Montescano, Montescano, Italy.
authors.forename: Roberto
authors.initials: R
authors.lastname: Aquilani
authors.forename: Maria Teresa
authors.initials: MT
authors.lastname: La Rovere
authors.forename: Oreste
authors.initials: O
authors.lastname: Febo
authors.forename: Paola
authors.initials: P
authors.lastname: Baiardi
authors.forename: Federica
authors.initials: F
authors.lastname: Boschi
authors.forename: Paolo
authors.initials: P
authors.lastname: Iadarola
authors.forename: Simona
authors.initials: S
authors.lastname: Viglio
authors.forename: Maurizia
authors.initials: M
authors.lastname: Dossena
authors.forename: Andria Innocenza
authors.initials: AI
authors.lastname: Bongiorno
authors.forename: Ornella
authors.initials: O
authors.lastname: Pastoris
authors.forename: Manuela
authors.initials: M
authors.lastname: Verri
mesh_terms: D058671:Adrenergic beta-1 Receptor Antagonists / Q000627:therapeutic use; D056151:Airway Remodeling; D000596:Amino Acids / Q000378:metabolism*; D001158:Arteries / Q000378:metabolism; D017298:Bisoprolol / Q000627:therapeutic use; D002908:Chronic Disease; D005260:Female; D006333:Heart Failure / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D006976:Hypertension, Pulmonary / Q000209:etiology / Q000378:metabolism*; D007930:Leucine / Q000378:metabolism; D008168:Lung / Q000098:blood supply / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D014176:Protein Biosynthesis; D014655:Vascular Resistance; D014680:Veins / Q000378:metabolism
chemical_list: D058671:Adrenergic beta-1 Receptor Antagonists; D000596:Amino Acids; D007930:Leucine; D017298:Bisoprolol