title: [The concentration of atrial natriuretic peptide (ANP) in plasma and atrial tissue of canines with acute heart failure induced by reversible aortic or mitral regurgitation].
abstract: We have established an easily reversible acute heart failure model in beagle canines by reversible aortic or mitral regurgitation (AR or MR). To cause reversible AR, a basket catheter was inserted into the left ventricle from the apex and fixed at the aortic valve in 10 canines. To cause MR, a basket catheter was inserted into the left atrium via the pulmonary vein and fixed at the mitral valve in 10 canines. The regurgitation by AR or MR was caused by extending the tip basket wire, and the recovery from the regurgitation was immediately possible by closing it. Left atrial pressure (LAP), right atrial pressure (RAP) and pulmonary artery pressure (PAP) were increased significantly during AR or MR, and decreased to the normal level after the release of AR or MR. Using these reversible acute heart failure models, the effects of both advancing and restoring acute heart failure by the secretion of ANP were examined by observing the changes of ANP concentration and its molecular forms in the plasma and left atrial tissue in the same canine. Plasma ANP concentration showed a reversible change. In group analysis, plasma ANP concentration did not correlate with LAP or RAP, but in each canine it showed high correlations with LAP (r = 0.70 approximately 0.94, 0.82 +/- 0.07) and RAP (r = 0.60 approximately 0.93, 0.79 +/- 0.08), having a different slope in each regression line. The ANP concentration in the atrial tissue was decreased during AR or MR, but the low level was maintained after AR or MR. The main molecular form of ANP in the plasma was alpha-ANP and that in the tissue was gamma-ANP. In summary, the tissue storage of ANP was decreased because the ANP secretion caused by stimulation of acute heart failure exceeded its production. The ANP secretion was decreased by the subsequent elimination of heart failure, but the production was not stimulated rapidly, because the tissue content remained unchanged.
authors.affiliation: Department of Medicine, Kitasato University, School of Medicine, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Satoh
authors.forename: T
authors.initials: T
authors.lastname: Masuda
authors.forename: N
authors.initials: N
authors.lastname: Hasegawa
authors.forename: F
authors.initials: F
authors.lastname: Marumo
authors.forename: R
authors.initials: R
authors.lastname: Kikawada
mesh_terms: D000208:Acute Disease; D000818:Animals; D001022:Aortic Valve Insufficiency / Q000150:complications*; D009320:Atrial Natriuretic Factor / Q000097:blood / Q000378:metabolism*; D001794:Blood Pressure; D002303:Cardiac Output, Low / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D002851:Chromatography, High Pressure Liquid; D004195:Disease Models, Animal; D004285:Dogs; D006325:Heart Atria / Q000378:metabolism / Q000503:physiopathology; D006439:Hemodynamics; D008944:Mitral Valve Insufficiency / Q000150:complications*; D009206:Myocardium / Q000378:metabolism*; D011863:Radioimmunoassay
chemical_list: D009320:Atrial Natriuretic Factor