RIGHT HEART-FAILURE CHRONICALLY STIMULATES HEAT-SHOCK-PROTEIN-72 IN HEART AND LIVER BUT NOT IN OTHER TISSUES

Objectives: During cardiac failure several ontogenically developed ada ptional mechanisms are activated. Among these, heat-shock proteins (HS P) are expressed in response to stress. The aim of the present study w as to investigate the HSP72 protein expression in lungs, liver, cardia c and skeletal muscles during congestive heart failure (CHF). Methods: CHF was induced in Sprague-Dawley rats by a single intraperitoneal in jection of monocrotaline (50 mg/kg). Two groups of animals emerged: a CHF group (n = 10) with right ventricular hypertrophy, pleural and per itoneal effusions, and an Hypertrophy group (n = 12) with right ventri cular hypertrophy without CHE The data for each group were compared wi th those of control (saline infused) age-matched rats. Lungs, liver, r ight and left ventricles, soleus, extensor digitorum longus and tibial is anterior muscles were excised and analyzed for HSP72 concentration by Western blot analysis using a specific monoclonal antibody. Noradre naline 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 n mol/ventricle, P<0.01) and left (1.10+/-0.09 vs 2.10+/-0.130 nmol/vent ricle, P<0.001) ventricular content of noradrenaline compared to the c ontrol; (2) significant activation of HSP72 concentration in right and left ventricles (39.4+/-1.6 vs 5+/-09% 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 mo dification in HSP72 concentration in lungs and all of the peripheral m uscles considered, The Hypertrophy group showed: (1) unchanged total n oradrenaline tissue content as compared to the control; and (2) unmodi fied HSP72 concentration in all tissues analyzed. Conclusions: The pre sent study demonstrates that CHF, but not compensatory hypertrophy, is a specific stimulus for chronic HSP72 induction in the heart and live r. On the contrary, CHF does not affect HSP in lungs and peripheral mu scles. HSP 72 induction represents an intracellular marker of stress r eaction which can persist chronically.