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Telemetry and T3 complete transection surgeries for Chapter 2 were completed with aid of Dr. Krassioukov and Dr. West, respectively. T3 complete transection surgeries for Chapter 3 were completed with aid of Dr. Pressure myography experiments for Chapter 3 were completed in collaboration with Dr.


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SCI Individuals Frias for her expertise in animal surgeries and Ray for his technical expertise in animal care. I would like to thank Dr. Laher for, not only for his aid in the pressure myography portion of the experiments, but for his guidance and advice that would be invaluable to me as I further my career in academia.

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Christopher West for his guidance, expertise and patients in all facets of my experiments that I completed during my Masters. You had faith in a potential work study student and 4 years later I was fortunate to complete my Masters with you by my side. You are the definition of a mentor and big brother. Krassioukov for giving me the opportunity to complete my Masters in a truly top tier, world renown spinal cord injury research team.

Your expertise and guidance helped me grow as a researcher which will be forever invaluable in any career path I should take. You inspired me to continue pursuing my career in SCI research. I would like to thank my sister for your undying love and support. Without you, none of this would be possible. You are the biggest inspiration in my life and I love you. In addition to severe motor and sensory dysfunction, SCI disrupts autonomic pathways and consequently perturbs cardiovascular homeostasis.

In comparison with able-bodied AB individuals, people with chronic SCI have a greater propensity to develop cardiovascular dysfunction[1]. Cardiovascular complications in the early stages of thoracic or cervical SCI can be life threatening, and include chronic, persistent hypotension, and cardiac arrest[2]. High thoracic or cervical SCI individuals have an increased propensity for impaired blood pressure control. In addition to chronic hypotension, individuals living with high thoracic or cervical SCI may suffer from recurrent bouts of autonomic dysreflexia or AD a life threatening condition characterized by extreme reflexive spikes in SBP which may result in myocardial infarction, stroke and even sudden death [3].

Specifically, there is a gap in the knowledge in regards to the temporal development of cardiovascular dysfunction post SCI, specifically with regards to diurnal variations in hemodynamics and the development and progression of these spontaneous AD events. Further, resistance vasculature plays a vital role in control of arterial blood pressure, yet there is a gap in knowledge in regards to the time course of morphological and functional adaptations of resistance vasculature after SCI. It would be invaluable to delineate how this swinging of arterial blood pressure post SCI due to chronic, persistent hypotension and spontaneous AD, might influence the structural and functional characteristics of resistance vasculature post SCI.

My dissertation examines the effects of a complete high thoracic SCI in an animal model on diurnal variations in hemodynamics and onset of spontaneous AD. In addition, we look to examine 2 the time course of morphological and functional changes in resistance vasculature after high thoracic SCI. I will review the current knowledge in regards to the autonomic nervous system and autonomic cardiovascular control after SCI.

I will also review the structural and functional parameters of peripheral vasculature in the cardiovascular system and the effects of SCI on peripheral vasculature structure and function.

My Experience at the University of Vermont

The worldwide prevalence of traumatic SCI ranges from 3. This an estimate from recent systematic review by Jazayeri et al with an appreciation that there is more readily available epidemiological data from Canada, Australia, US and other wealthier European countries but lack of appropriate epidemiological data from countries in Asia and Africa. Though the prevalence of SCI is quite low it does however have substantial lifetime economic ie monetary and social consequences[7].

A large fraction of these costs are due to the treatment and control of secondary complications after SCI[8]. Along with motor dysfunction, there are variety of secondary complications that result in a diminished quality of life in individuals living with SCI. Studies have revealed that older patients living with SCI have a higher rate of secondary complications and increased hospital stay[10]. In a study by Anderson individuals with SCI ranked cardiovascular autonomic function among the highest priority even above their locomotor recovery in order to improve their quality of 3 life[11].

Cardiovascular disease is one of the leading causes of morbidity and mortality in chronic SCI[12]. After adjusting for age and sex, individuals with SCI are at a significant increased risk of heart disease and stroke[13].

Cardiovascular Research Institute | College of Medicine | University of Vermont

The probability of developing a cardiovascular disease rises dramatically after injury[1, 12, 14] and individuals experience these complications at a younger age and more frequently than those without SCI[1]. Impaired blood pressure control, heart rate variability, impaired response to exercise and arrhythmias due to loss of autonomic cardiovascular control contribute to the increased risk of cardiovascular disease and stroke in chronic SCI patients[15, 16]. Cell bodies of sympathetic preganglionic neurons lie in the gray matter of the lateral horn and in the gray matter in between the central canal and lateral horn of the spinal cord.

Preganglionic efferent neurons make up the intermediolateral IML column of the spinal cord's thoracolumbar region T1-L2 [18]. Parasympathetic preganglionic efferent neuronal cell bodies are located within the nuclei of four cranial nerves in the brain stem oculomotor, facial, glossopharyngieal and vagus nerve and project from the sacral regions of the spinal cord[19]. Preganglionic efferent fibres with exception of the innervation of the adrenal medulla synaptically end on neurons located in autonomic ganglia. Sympathetic ganglia are divided into two major groups: the paravertebral and prevertebral ganglia[20].

The paravertebral ganglia form the sympathetic trunk, which consists of a series of ganglia located on both sides of the vertebral column, extending from the base of the scull to the sacrum[17, 20]. Prevertebral ganglia lie anterior to the spinal column and in close proximity to the major abdominal arteries[20]. There are four routes the preganglionic sympathetic neurons may take to act on a target[21] refer to Figure 1 : 4 Figure 1: Schematic representation of four routes sympathetic preganglionic neurons may take to act on a target.

Preganglionic axons may terminate in the paravertebral ganglia ganglia within the sympathetic trunk at its level of departure in the spinal cord, it may descend or ascend the sympathetic trunk and synapse on different paravertebral ganglia, or it may move through paravertebral ganglia without synapsing and synapse within the prevertebral ganglia ganglia outside of the sympathetic trunk.

Finally sympathetic preganglionic neurons may also directly innervate target organ e,g chromaffin cells of adrenal medulla.

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Preganglionic sympathetic neurons may also directly innervate chromaffin cells of adrenal medulla. Chromaffin cells are neural crest in origin and many consider these cells as post ganglionic neurons that have shed their processes[22]. Atrial and ventricular cardiac myocytes are innervated by sympathetic axons, while sinoatrial and atrioventricular myocytes receive both parasympathetic and sympathetic innervations. Sympathetic preganglionic efferent fibres stem from spinal segments T1 to T4 and innervate paravertebral ganglia.

Sympathetic post ganglionic fibres originating in paravertebral sympathetic ganglia innervate cardiac myocytes and pacemaker cells in the heart. Blood vessels also receive innervations from the autonomic nervous system and a majority of these blood vessels in the body are heavily innervated by sympathetic neurons. Activation of blood vessels by sympathetic neurons leads to vasoconstriction of arterial beds, increased systemic vascular resistance increased arterial blood pressure and reduced blood flow.

Sympathetic preganglionic projections from the IML column modify peripheral vasculature resistance via activation of smooth muscle[19]. These include arteries, arterioles and veins with post ganglionic sympathetic axons innervating the adventitial media border of the vessels[19]. These include the paraventricular nucleus of the thalamus and the rostral ventral lateral medulla RVLM. They mediate these responses via NO, a neurotransmitter stimulant involved in blood pressure modulation. The paraventricular nucleus of the thalamus is a key modulator of cardiovascular control, as seen by early experiments exposing the PVN to increasing doses of NO via artificial cerebrospinal fluid delivery to the PVN[24].

The RVLM neurons regulate tonic activity of sympathetic preganglionic neurons[25]. This acts on the cell bodies of preganglionic sympathetic neurons in the IML of the thoracolumbar region of the spinal cord, culminating in hypotension and bradychardia[26]. These axons are located within the dorsolateral funinculus of the spinal cord in humans[28].

In the rodent model, the RVLM neurons at the rostrocaudal level of the medulla are bordered rostrally and laterally by the facial nucleus, dorsally by the nucleus ambiguus and medially by the gigantocellular reticular formation and the inferior olivary nuclei[18, ]. RVLM cardiovascular neurons are members of the C1 group of adrenergic neurons that are uniquely distinguished by the presence of the enzyme phenylethanolamine-N-methyltransferase PNMT [32].

The nucleus tract of the solitarius or nucleus solitarius NTS is a key coordinator of cardiovascular autonomic control. The NTS is a series of nuclei consisting of a column of grey matter within the medulla oblongata. The NTS receives input from baroreceptors that sense stretch i. Baroreceptors send afferent inputs to rostral NTS, which is located in the dorsomedial medulla and ipsilateral portion of the commissural sub-nucleus of NTS[33].

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Inhibition of the excitatory projections to the IML of the spinal cord results in a decrease in sympathetic activity and reduction in arterial blood pressure[35]. NTS neurons also relay this signal to the dorsal nucleus of the vagus nerve[34]. These parasympathetic vagal neurons project to the heart's terminal ganglia, slowing the heart rate through pacemaker cells in the heart[17]. Blood pressure is regulated through two important factors: cardiac output and peripheral vascular resistance. The contribution to peripheral vascular resistance is not the same among all the arterial beds in the periphery.

One of the key determinants of arterial blood pressure is associated with the splanchnic circulation. A majority of the sympathetic innervations of the splanchnic organs stem from spinal segments T4-T9 as cholinergic preganglionic neurons. These neurons pass through the greater splanchnic nerves and synapse in the celiac ganglion plexus with post ganglionic adrenergic fibres, which ultimately innervate the target[36, 37].

A smaller number of the sympathetic innervations of the splanchnic organs originate in spinal segments TT12, pass through the lesser and least splanchnic nerves and innervate prevertebral ganglia[36]. Particularly, injury at the sixth thoracic spinal cord segment and above may disrupt descending autonomic pathways of the cardiovascular system that innervate glands, smooth muscle of blood vessels and cardiac muscle[38]. The degree of cardiovascular dysfunction is determined by the level and severity of SCI[39]. Orthostatic Hypotension is a dysregulation of reflexive blood pressure control when shifting from a seated to a standing position[40].

Autonomic Dysreflexia is a life threatening condition characterized by episodes of extreme hypertension due to noxious and non-noxious peripheral stimuli below the level of injury[]. Injury above the sixth thoracic spinal cord segment is associated with disruption of descending autonomic pathways of the cardiovascular system. Inhibition of the excitatory bulbospinal projections that innervate preganglionic sympathetic neurons in the IML of the spinal cord reduce sympathetic activity.

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This reduction of sympathetic activity may lead to decreased tone in arterial blood vessels and activation of vagal nuclei. There is a linear relationship between the decreased number of FG labelled neurons and increased severity of SCI. This large drop in projecting bulbospinal RVLM projections can be attributed to cell death or degeneration, a well known response to axotomy of various neuron populations.

There is also a close correlation with the number of FG retrogradedly labelled neurons in the red nucleus, vestibular nucleus and reticular formation after graded clip compression injury[45, 46] and contusion injury[47]. This loss or decrease in central and peripheral neurogenic tone is commonly associated with acute SCI and referred to as neurogenic shock i. Even though there is some preservation in the myogenic tone, it is not sufficient in maintaining blood pressure following high thoracic or cervical SCI[37].

Of major importance is the loss of sympathetic activity to a significant portion of the peripheral blood vessels in the lower extremities, including the splanchnic circulation. This acute period post SCI is characterized by profound hypotension and disrupted diurnal rhythmicity[48, 49].