Spinal cord injury-induced neuroplasticity within sympathetic pathways causes cardiac dysfunction and increases the susceptibility to life-threatening ventricular arrhythmias. For example, using coronary artery occlusion we documented a dramatic increase in the susceptibility to ventricular tachy-arrhythmias in conscious rats with mid-thoracic spinal cord injury (T5X). Furthermore, using injection of cholera toxin B into the left and right stellate ganglia, as well as pericardial sac, and using the Sholl analyses, we documented that stellate-projecting sympathetic pre-ganglionic neurons within spinal segments T1–T5 as well as cardiac projecting sympathetic post-ganglionic neurons within the stellate ganglia from T5X rats have larger dendritic trees than uninjured rats. The hearts of rats with T5X are also hyper-innervated by tyrosine hydroxylase (TH)-immunoreactive sympathetic axons. These neuroplastic changes are associated with an increased nerve growth factor content within the heart and stellate ganglia. Thus, by using a combination of techniques and lines of evidence, we documented that mid-thoracic spinal cord injury results in cardiac sympathetic hyper-innervation and increased susceptibility to life-threatening ventricular arrhythmias. These results have important implications for understanding the mechanisms responsible for the high mortality rates and incidence of cardiovascular disease in individuals with spinal cord injury.
To read this article in full you will need to make a payment
Purchase one-time access:Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online access
One-time access price info
- For academic or personal research use, select 'Academic and Personal'
- For corporate R&D use, select 'Corporate R&D Professionals'
Subscribe:Subscribe to Autonomic Neuroscience: Basic and Clinical
Already a print subscriber? Claim online access
Already an online subscriber? Sign in
Register: Create an account
Institutional Access: Sign in to ScienceDirect
© 2013 Published by Elsevier Inc.