Temporal Dystrophic Remodeling within the Intrinsic Cardiac Nervous System of the Streptozotocin Diabetic Rat Model
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Date
2012-03-12
Authors
Menard, Chantalle
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Abstract
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.
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medicine