Date of Award

Fall 2016

Document Type


Degree Name

Master of Science (MS)


Biomedical Engineering

First Advisor

Schmit, Brian D.

Second Advisor

Toth, Jeffrey M.

Third Advisor

LaDisa, John


The purpose of this study was to determine whether there are histological changes in the microvasculature of rat skeletal muscle following chronic spinal cord injury both above and below the level of injury. This study is important because microvascular structure likely impacts muscle performance and cardiovascular health. To the best of our knowledge, this is the only study to investigate microvascular structure within rat skeletal muscle after spinal cord injury. We hypothesized structural remodeling would occur in both the myofibers and microvasculature, which would then manifest in differences in myofiber cross sectional area and microvascular diameter, wall thickness, wall to lumen ratio, and wall cross sectional area. Changes in sympathetic tone and reduced muscular activity following spinal cord injury may induce microvascular structural remodeling. Initially after injury, sympathetic activity below the level of injury is diminished. Over time, neuroplasticity results in recovery of sympathetic tone, which increases vascular smooth muscle contraction and may lead to alterations in vasculature structure. In addition, the spinal lesion leads to loss of descending drive, which causes physical deconditioning below the level of injury. Physical deconditioning is known to induce vascular remodeling, and effects may be opposite of those associated with increased sympathetic tone. We conducted a test of vascular remodeling in a rat contusion model of spinal cord injury. Ten adult female rats were evenly divided into control and spinal cord injury groups. Severe spinal cord injury was induced using a controlled weight drop onto the spinal cord, resulting in a contusion injury. After a 90 day survival period, the biceps brachii, triceps brachii, tibialis cranialis, and soleus muscles were removed, processed, and stained with Verhoeff van Gieson elastin and hematoxylin and eosin stains for histological analysis. Ultrastructural features of the myofibers and non-capillary microvessels were quantified. There was no significant difference between spinal cord injury and control skeletal muscles with regards to muscle cross sectional area, myofiber cross sectional area, microvascular diameter, wall thickness, wall to lumen ratio, or wall cross sectional area. Results indicated similar myofiber integrity and microvascular structure between control and spinal cord injury groups above and below level of injury. While results did not support our original hypothesis, the findings also did not contradict previous studies. Following chronic spinal cord injury, recovery of spontaneous muscle activation and sympathetic activity may maintain integrity of skeletal muscle and associated microvasculature. Future research could assess microvascular function post spinal cord injury and identify an alternate animal model to study effects of spinal cord injury on muscle atrophy and associated microvasculature changes.