title: [Echocardiographic analysis of the effect of different Na+/H+ exchanger inhibitors on left ventricular structure and function in spontaneously hypertensive rats].
abstract: The aim of this study was to analyze by echocardiogram, the action of two Na+/H+ exchange, inhibitors, HOE 642 (HOE) and BIIB 723 (BIIB) on left ventricular (LV) mass and LV systolic function. We studied 16 spontaneously hypertensive rats (SHR), 8 treated with HOE 30 mg/kg/day, 8 with 30 mg/kg/day of BIIB during 30 days and 4 SHR as controls during those 30 days. Results are expressed as mean values +/- SEM. The systolic blood pressure and the echocardiograpic parameters examined did not evidence changes during that period in the controls rats. Even though HOE determined a slight decrease in blood pressure (HOE C: 184 +/- 1.75 mm Hg; HOE 30d: 176.20 +/- 2.60 mm Hg - p < 0.01) which was not detected with BIIB, both drugs provoked an increase of peak systolic stress (HOE C: 166 +/- 29 kdynes/cm2; HOE 30d: 204 +/- 34 kdynes/cm2, p < 0.04; BIIB C: 164 +/- 25.90 kdynes/ cm2; BIIB 30d: 234 +/- 29.30 kdynes/cm2, p < 0.02). HOE and BIIB reduced LV mass after 30 days of administration (HOE C: 612.50 +/- 50 mg; 30d: 452 +/- 37 mg, p < 0.01. BIIB C: 544 +/- 16mg; 30d: 374 +/- 25 mg, p < 0.01). LV endocardial shortening was similar independently of the NHE inhibitors used (HOE C: 62.30 +/- 2.75%; 30d: 65.50 +/- 2.40%, ns. BIIB C: 63.20 +/- 2,39%; 30d 67,20 +/- 1.62%, ns). These data demonstrate that long-treatment with HOE or BIIB produced similar LV mass regression without changes in endocardial fractional shortening in spite of the increase of peak systolic stress. This finding could represent an increased inotropism previously depressed by the development of hypertrophy.
authors.affiliation: Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Médicas, Universidad Nacional de La Plata, Argentina. cicme@atlas.med.unip.edu.ar
authors.forename: Eduardo M
authors.initials: EM
authors.lastname: Escudero
authors.forename: Ana L
authors.initials: AL
authors.lastname: Tufare
authors.forename: Irene L
authors.initials: IL
authors.lastname: Ennis
authors.forename: Carolina D
authors.initials: CD
authors.lastname: Garciarena
authors.forename: Oscar A
authors.initials: OA
authors.lastname: Pinilla
authors.forename: Verónica B
authors.initials: VB
authors.lastname: Carranza
mesh_terms: D000284:Administration, Oral; D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use; D002306:Cardiac Volume / Q000187:drug effects / Q000502:physiology; D004195:Disease Models, Animal; D006146:Guanidines / Q000494:pharmacology* / Q000627:therapeutic use*; D006321:Heart / Q000187:drug effects*; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000187:drug effects / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000139:chemically induced / Q000000981:diagnostic imaging*; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology; D051381:Rats; D011918:Rats, Inbred SHR; D017923:Sodium-Hydrogen Exchangers / Q000037:antagonists & inhibitors*; D013268:Stimulation, Chemical; D013450:Sulfones / Q000627:therapeutic use*; D014463:Ultrasonography; D016277:Ventricular Function, Left / Q000187:drug effects* / Q000502:physiology
chemical_list: D000889:Anti-Arrhythmia Agents; C522118:BIIB 723; D006146:Guanidines; D017923:Sodium-Hydrogen Exchangers; D013450:Sulfones; C093373:cariporide