Myocardial mitochondrial dysfunction in mice lacking adiponectin receptor 1.

Hypoadiponectinemia is an independent predictor of cardiovascular disease, impairs mitochondrial function in skeletal muscle, and has been linked to the pathogenesis of Type 2 diabetes. In models of Type 2 diabetes, myocardial mitochondrial function is impaired, which is improved by increasing serum adiponectin levels. We aimed to define the roles of adiponectin receptor 1 (AdipoR1) and 2 (AdipoR2) in adiponectin-evoked regulation of mitochondrial function in the heart.

Myocardial mitochondrial and contractile function are preserved in mice lacking adiponectin.

Adiponectin deficiency leads to increased myocardial infarct size following ischemia reperfusion and to exaggerated cardiac hypertrophy following pressure overload, entities that are causally linked to mitochondrial dysfunction. In skeletal muscle, lack of adiponectin results in impaired mitochondrial function. Thus, it was our objective to investigate whether adiponectin deficiency impairs mitochondrial energetics in the heart.

Mitochondrial reactive oxygen species production and respiratory complex activity in rats with pressure overload-induced heart failure.

We investigated the impact of cardiac reactive oxygen species (ROS) during the development of pressure overload-induced heart failure. We used our previously described rat model where transverse aortic constriction (TAC) induces compensated hypertrophy after 2 weeks, heart failure with preserved ejection fraction at 6 and 10 weeks, and heart failure with systolic dysfunction after 20 weeks. We measured mitochondrial ROS production rates, ROS damage and assessed the therapeutic potential of in vivo antioxidant therapies.

Echocardiography alone allows the determination of heart failure stages in rats with pressure overload.

Background: There is currently no standard for the assessment of contractile function in animals. We aimed to determine whether transthoracic echocardiography in rats with chronic pressure overload allows determining the stage of hypertrophy and heart failure (HF).

Methods: Pressure overload was created by placement of a metal clip around the thoracic aorta at a weight of 40 to 50 g.

Pressure overload differentially affects respiratory capacity in interfibrillar and subsarcolemmal mitochondria.

Years ago a debate arose as to whether two functionally different mitochondrial subpopulations, subsarcolemmal mitochondria (SSM) and interfibrillar mitochondria (IFM), exist in heart muscle. Nowadays potential differences are often ignored. Presumably, SSM are providing ATP for basic cell function, whereas IFM provide energy for the contractile apparatus.

Alterations in mitochondrial function in cardiac hypertrophy and heart failure.

Normal cardiac function requires high and continuous supply with ATP. As mitochondria are the major source of ATP production, it is apparent that mitochondrial function and cardiac function need to be closely related to each other. When subjected to overload, the heart hypertrophies.

Targeted metabolic imaging to improve the management of heart disease.

Tracer techniques are powerful methods for assessing rates of biological processes in vivo. A case in point is intermediary metabolism of energy providing substrates, a central feature of every living cell. In the heart, the tight coupling between metabolism and contractile function offers an opportunity for the simultaneous assessment of cardiac performance at different levels in vivo: coronary flow, myocardial perfusion, oxygen delivery, metabolism, and contraction.

Exercise can induce temporary mitochondrial and contractile dysfunction linked to impaired respiratory chain complex activity.

Exercise is considered to elicit a physiological response of the heart. Previous studies investigated the influence of repetitive exercise only at the end of the training period. We assessed the impact of 2 exercise protocols, differing in their treadmill inclination, on cardiac and mitochondrial function at different times during the training period.