title: Right heart failure chronically stimulates heat shock protein 72 in heart and liver but not in other tissues.
abstract: OBJECTIVE
  During cardiac failure several ontogenically developed adaptional mechanisms are activated. Among these, heat-shock proteins (HSP) are expressed in response to stress. The aim of the present study was to investigate the HSP72 protein expression in lungs, liver, cardiac and skeletal muscles during congestive heart failure (CHF).
  
  
  METHODS
  CHF was induced in Sprague-Dawley rats by a single intraperitoneal injection of monocrotaline (50 mg/kg). Two groups of animals emerged: a CHF group (n = 10) with right ventricular hypertrophy, pleural and peritoneal effusions, and an Hypertrophy group (n = 12) with right ventricular hypertrophy without CHF. The data for each group were compared with those of control (saline infused) age-matched rats. Lungs, liver, right and left ventricles, soleus, extensor digitorum longus and tibialis anterior muscles were excised and analyzed for HSP72 concentration by Western blot analysis using a specific monoclonal antibody. Noradrenaline levels in the heart were also measured using HPLC.
  
  
  RESULTS
  The CHF group showed: (1) reduced right (0.460 +/- 0.090 vs 0.830 +/- 0.070 nmol/ventricle, P < 0.01) and left (1.10 +/- 0.09 vs 2.10 +/- 0.130 nmol/ventricle, P < 0.001) ventricular content of noradrenaline compared to the control; (2) significant activation of HSP72 concentration in right and left ventricles (39.4 +/- 1.6 vs 5 +/- 0.9% and 13 +/- 1.2 vs 3.5 +/- 0.6%, P < 0.001 both) and in the liver (39.8 +/- 11 vs 6 +/- 2%, P < 0.001); (3) no modification in HSP72 concentration in lungs and all of the peripheral muscles considered. The Hypertrophy group showed: (1) unchanged total noradrenaline tissue content as compared to the control; and (2) unmodified HSP72 concentration in all tissues analyzed.
  
  
  CONCLUSIONS
  The present study demonstrates that CHF, but not compensatory hypertrophy, is a specific stimulus for chronic HSP72 induction in the heart and liver. On the contrary, CHF does not affect HSP in lungs and peripheral muscles. HSP 72 induction represents an intracellular marker of stress reaction which can persist chronically.
authors: Fondazione Salvatore Maugeri, Centro di Fisiopatologia Cardiovascolare, Gussago, Brescia, Italy.
authors: L
authors: L
authors: Comini
authors: G
authors: G
authors: Gaia
authors: S
authors: S
authors: Curello
authors: C
authors: C
authors: Ceconi
authors: E
authors: E
authors: Pasini
authors: M
authors: M
authors: Benigno
authors: T
authors: T
authors: Bachetti
authors: R
authors: R
authors: Ferrari
mesh_terms: D000818:Animals; D001345:Autoradiography; D015153:Blotting, Western; D005260:Female; D050884:HSP72 Heat-Shock Proteins; D006333:Heart Failure / Q000378:metabolism*; D006360:Heat-Shock Proteins / Q000378:metabolism*; D017380:Hypertrophy, Right Ventricular / Q000378:metabolism*; D008099:Liver / Q000737:chemistry / Q000378:metabolism*; D008168:Lung / Q000737:chemistry; D016686:Monocrotaline; D018482:Muscle, Skeletal / Q000737:chemistry; D009206:Myocardium / Q000737:chemistry / Q000378:metabolism*; D009638:Norepinephrine / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins; D016686:Monocrotaline; D009638:Norepinephrine