title: Growth hormone attenuates myocardial fibrosis in rats with chronic pressure overload-induced left ventricular hypertrophy.
abstract: 1. The role of growth hormone (GH) in cardiac remodelling and function in chronic and persistent pressure overload-induced left ventricular hypertrophy has not been defined. The aim of the present study was to assess short-term GH treatment on left ventricular function and remodelling in rats with chronic pressure overload-induced hypertrophy. 2. Twenty-six weeks after induction of ascending aortic stenosis (AAS), rats were treated with daily subcutaneous injections of recombinant human GH (1 mg/kg per day; AAS-GH group) or saline (AAS-P group) for 14 days. Sham-operated animals served as controls. Left ventricular function was assessed by echocardiography before and after GH treatment. Myocardial fibrosis was evaluated by histological analysis. 3. Before GH treatment, AAS rats presented similar left ventricular function and structure. Treatment of rats with GH after the AAS procedure did not change bodyweight or heart weight, both of which were higher in the AAS groups than in the controls. After GH treatment, posterior wall shortening velocity (PWSV) was lower in the AAS-P group than in the control group. However, in the AAS-GH group, PWSV was between that in the control and AAS-P groups and did not differ significantly from either group. Fractional collagen (% of total area) was significantly higher in the AAS-P and AAS-GH groups compared with control (10.34 +/- 1.29, 4.44 +/- 1.37 and 1.88 +/- 0.88%, respectively; P < 0.05) and was higher still in the AAS-P group compared with the AAS-GH group. 4. The present study has shown that short-term administration of GH to rats with chronic pressure overload-induced left ventricular hypertrophy induces cardioprotection by attenuating myocardial fibrosis.
authors.affiliation: Internal Medicine Department, Botucatu Medical School, Sao Paulo State University, UNESP, Brazil.
authors.forename: Vanessa O
authors.initials: VO
authors.lastname: Moreira
authors.forename: Camila A
authors.initials: CA
authors.lastname: Pereira
authors.forename: Mirella O
authors.initials: MO
authors.lastname: Silva
authors.forename: Sergio L
authors.initials: SL
authors.lastname: Felisbino
authors.forename: Antonio C
authors.initials: AC
authors.lastname: Cicogna
authors.forename: Katashi
authors.initials: K
authors.lastname: Okoshi
authors.forename: Flavio F
authors.initials: FF
authors.lastname: Aragon
authors.forename: Carlos R
authors.initials: CR
authors.lastname: Padovani
authors.forename: Marina P
authors.initials: MP
authors.lastname: Okoshi
authors.forename: Ana V B
authors.initials: AV
authors.lastname: Castro
mesh_terms: D000818:Animals; D001011:Aorta / Q000601:surgery; D001018:Aortic Diseases / Q000150:complications / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D002317:Cardiovascular Agents / Q000008:administration & dosage / Q000494:pharmacology*; D002908:Chronic Disease; D003251:Constriction, Pathologic; D004195:Disease Models, Animal; D004452:Echocardiography; D005355:Fibrosis; D019382:Human Growth Hormone / Q000008:administration & dosage / Q000494:pharmacology*; D017379:Hypertrophy, Left Ventricular / Q000188:drug therapy* / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D007279:Injections, Subcutaneous; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects; D009206:Myocardium / Q000473:pathology*; D051381:Rats; D017208:Rats, Wistar; D011994:Recombinant Proteins / Q000494:pharmacology; D013997:Time Factors; D016277:Ventricular Function, Left / Q000187:drug effects*; D020257:Ventricular Remodeling / Q000187:drug effects*
chemical_list: D002317:Cardiovascular Agents; D011994:Recombinant Proteins; D019382:Human Growth Hormone