FIG. 3.

Greater DOX-induced LV dysfunction and dilatation in DNsGCα1^tg/+ than in WT mice. After 8 weeks of DOX treatment, LVID_ES and LVID_ED were increased (A, B) and FS decreased (C) in DNsGCα1^tg/+, but not in WT, mice (n = 20 each). After 12 weeks of DOX administration, systolic dysfunction and dilatation were more pronounced in DNsGCα1^tg/+ than in WT mice. ^†p < 0.05 versus baseline and *p < 0.05 versus WT (same time point). DNsGCα1^tg/+, mice with cardiomyocyte-specific expression of a dominant negative mutation of sGCα1; LVID_ES, left ventricular end-systolic internal diameter; LVID_ED, left ventricular end-diastolic internal diameter; FS, fractional shortening.