Research Paper Volume 2, Issue 11 pp 843—853
Activation of mitochondrial energy metabolism protects against cardiac failure
Figure 2. Activation of mitochondrial metabolism improves cardiac function following doxorubicin-induced cardio-myopathy. (A) Maximum rate of pressure development in the left ventricle (dP/dtmax), (B) left-ventricular maximum rate of pressure decrease (dP/dtmin), (C) end-systolic pressure (Pes), (D) end-systolic volume (Ves), (E) end-diastolic pressure (Ped), (F) end-diastolic volume (Ved), (G) time constant of isovolumetric left ventricular pressure decline (tau, τ). (H) stroke work, (I) stroke volume, (J) cardiac output, (K) ejection fraction, and (L) heart rate in wild-type vs. frataxin-transgenic animals following administration of doxorubicin. Grey bars depict wild-type litter mates, white bars frataxin-transgenic mice (n=6 each).