Cookies help us deliver our services. By using our services, you agree to our use of cookies. More information

Difference between revisions of "Esfandiary 2012 Abstract IOC68"

From Bioblast
Line 4: Line 4:
|year=2012
|year=2012
|event=IOC68
|event=IOC68
|abstract=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 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 to evaluate the role of mitochondrial membrane potential, ROS and other metabolic pathways need to be performed.
|abstract=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.
|keywords=Right heart hypertrophy, Right ventricular failure, Cardiac afterload, Pulmonary artery banding, Heart ratio, Mitochondria, Respiration, PAB (Pulmonary Artery Banding), RVP (right ventricular pressure)
|keywords=Right heart hypertrophy, Right ventricular failure, Cardiac afterload, Heart ratio, Mitochondria, Respiration, PAB (pulmonary artery banding), RVP (right ventricular pressure)
|mipnetlab=DE Giessen Weissmann N
|mipnetlab=DE Giessen Weissmann N
}}
}}
Line 11: Line 11:
|instruments=Oxygraph-2k
|instruments=Oxygraph-2k
|organism=Mouse
|organism=Mouse
|tissues=Cardiac muscle
}}
}}

Revision as of 07:22, 9 April 2012

Esfandiary A, Pak O, Weissmann N, Sommer N (2012) Mitochondrial respiration in experimental right heart hypertrophy. MiPNet17.08.

Link:

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: Cardiac muscle"Cardiac muscle" is not in the list (Heart, Skeletal muscle, Nervous system, Liver, Kidney, Lung;gill, Islet cell;pancreas;thymus, Endothelial;epithelial;mesothelial cell, Blood cells, Fat, ...) of allowed values for the "Tissue and cell" property. 



HRR: Oxygraph-2k