Temporal Dystrophic Remodeling within the Intrinsic Cardiac Nervous System of the Streptozotocin Diabetic Rat Model
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There is significant evixdence to support the existence of “diabetic cardiomyopathy,” described as heart failure (HF) in diabetic individuals in the absence of obstructive coronary disease and hypertension. The underlying pathogenesis is only partially understood, but alterations in the autonomic nervous system’s (ANS) control of cardiac function have been implicated. An important component of the cardiac ANS is the intrinsic cardiac nervous system (ICNS). The ICNS behaves as a neuronal modulator of cardiac function, and has been called the “little brain on the heart”. While there have been several investigations into the effects of diabetes on extracardiac neurons, little is known about the alterations that occur in the ICNS. It is proposed that high glucose concentrations induce toxicity via oxidative stress, resulting in neuronal dystrophy and dysfunction. Our first aim was therefore to confirm that a process of dystrophic remodeling occurs within the ICNS of diabetic hearts. Our second aim was to examine the role of oxidative stress in the pathogenesis of neuronal dystrophy. Our preliminary data indicated that neuronal dystrophy occurs in the ICNS neurons of streptozotocin (STZ)-diabetic rats, and accumulates temporally within the disease process. It was also determined that an increase in reactive oxygen species (ROS) occurs in the neuronal processes of diabetic rats, indicating an association between oxidative stress and the development of a dystrophy. While our preliminary work provides novel insight for diabetes and cardiac research, more investigations are needed to further examine neuronal dysfunction and cell death, and to prove a causative role for oxidative stress in the development of dystrophy.