Esfandiary 2012 Abstract IOC68
Esfandiary A, Pak O, Weissmann N, Sommer N (2012) Mitochondrial respiration in experimental right heart hypertrophy. MiPNet17.08. |
Link: MiPNet17.08 IOC68
Esfandiary A, Pak O, Weissmann N, Sommer N (2012)
Event: IOC68
Right heart failure is the leading cause of death in diseases which induce increased right heart afterload (e.g. pulmonary hypertension). Right heart hypertrophy can compensate for increased afterload, before right heart failure develops. Increased right heart afterload and right heart hypertrophy may induce mitochondrial alterations that determine right heart performance. This study aims to investigate the role of mitochondria in right heart hypertrophy. Right heart hypertrophy was induced in C57Bl6/J wild type mice by pulmonary artery banding (PAB). Control mice received sham surgery. Three weeks later, the development of right heart hypertrophy was evaluated by measurement of right ventricular systolic pressure (RVP) and weight of the right ventricle. Mitochondrial respiration of freshly prepared heart biopsies from the right and left ventricles was quantified by high-resolution respirometry. We used a substrate-inhibitor protocol with pyruvate, ADP, malate, octanoylcarnitine, rotenone, succinate and antimycin A. PAB caused a significant increase in RVP and right ventricular weight in comparison to sham operated animals. Systolic arterial pressure and the ratio of the weight of the left ventricle to body weight were not significantly changed. We could not detect significant differences in respiration of the right ventricular biopsies after PAB compared to sham operation. Thus, respiration was not altered in the right ventricle during right ventricular hypertrophy induced by PAB. Further studies need to be performed to evaluate the role of mitochondrial membrane potential, ROS and other metabolic pathways.
β’ Keywords: Right heart hypertrophy, Right ventricular failure, Cardiac afterload, Heart ratio, Mitochondria, Respiration, PAB (pulmonary artery banding), RVP (right ventricular pressure)
β’ O2k-Network Lab: DE Giessen Weissmann N
Labels:
Organism: Mouse
Tissue;cell: Heart
HRR: Oxygraph-2k