TRANSITION FROM COMPENSATORY HYPERTROPHY TO DILATED, FAILING LEFT-VENTRICLES IN DAHL SALT-SENSITIVE RATS

To establish an experimental model for studying a specific transitiona l stage from compensatory hypertrophy to heart failure, we studied the pathophysiology of the left ventricle (LV) in Dahl salt-sensitive (DS ) rats fed a high-salt diet. DS rats fed an 8% NaCl diet after the age of 6 wk developed concentric LV hypertrophy at 11 wk, followed by mar ked LV dilatation at 15-20 wk. During the latter stage, the DS rats sh owed labored respiration with LV global hypokinesis. All the DS rats d ied within 1 wk by massive pulmonary congestion. The dissected left ve ntricles revealed chamber dilatation and a marked increase in mass wit hout myocardial necrosis. In contrast, corresponding Dahl salt-resista nt (DR) rats fed the same diet showed neither mortality nor any of the se pathological changes. The in vivo LV end-systolic pressure-volume r elationship shifted to the right with a less steep slope in the failin g DS rats compared with that in age-matched DR rats. Isometric contrac tions of LV papillary muscles isolated from these DS rats showed reduc ed tension development in the failing stage, but normal tension develo pment in the hypertrophied stage. In conclusion, the DS rat fed a high -salt diet is a useful model showing rapidly developing congestive hea rt failure, in which the transition from compensatory hypertrophy to d ecompensatory dilatation of LV is easily and consistently manifested.