2004
DOI: 10.2174/1570161043476474
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Cardiovascular Control After Spinal Cord Injury

Abstract: Spinal cord injury (SCI) leads to profound haemodynamic changes. Constant outflows from the central autonomic pattern generators modulate the activity of the spinal sympathetic neurons. Sudden loss of communication between these centers and the sympathetic neurons in the intermediolateral thoracic and lumbar spinal cord leads to spinal shock. After high SCI, experimental data demonstrated a brief hypertensive peak followed by bradycardia with escape arrhythmias and marked hypotension. Total peripheral resistan… Show more

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Cited by 55 publications
(45 citation statements)
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“…9 Accordingly, we propose to use an established meta-analytical method for synthesizing observational studies in order to examine the effect of neurological level of injury on various CV outcomes (BP and HR) at rest in individuals with SCI. Potential confounding factors that are thought to affect CV responses, including age, 10,11 sex, 12 duration of SCI [13][14][15][16] and level of fitness, 17 are also considered to obtain adjusted results. We hypothesize that there will be a lesiondependent impairment in CV function, whereby systolic BP (SBP), diastolic BP (DBP) and HR will be lower in those with the highest (cervical (C)) injuries.…”
Section: Introductionmentioning
confidence: 99%
“…9 Accordingly, we propose to use an established meta-analytical method for synthesizing observational studies in order to examine the effect of neurological level of injury on various CV outcomes (BP and HR) at rest in individuals with SCI. Potential confounding factors that are thought to affect CV responses, including age, 10,11 sex, 12 duration of SCI [13][14][15][16] and level of fitness, 17 are also considered to obtain adjusted results. We hypothesize that there will be a lesiondependent impairment in CV function, whereby systolic BP (SBP), diastolic BP (DBP) and HR will be lower in those with the highest (cervical (C)) injuries.…”
Section: Introductionmentioning
confidence: 99%
“…This reaction simulates neurogenic shock and autonomic hyperreflexia in humans. 10,11 Nine studies specifically tested the use of various pharmacologic agents for hemodynamic support in animals with SCIs (Table 1). Mean blood pressure and more specifically, spinal cord blood flow increased significantly using a combination of nimodipine (calcium channel blocker) with epinephrine (vasopressor), dextran (colloid), phenylephrine (vasopressor) and mildly with epinephrine and whole blood.…”
Section: Resultsmentioning
confidence: 99%
“…It is caused by a deafferented spinal cord stimulated by a stimulus triggered mostly by the distention of visceral organs in the pelvic region in injuries over the T5-6 sympathetic splanchnic exit level of the spinal cord. 12 Although AD is described as a symptom complex that develops as a response to a noxious stimulant below the lesion level and is characterized by bradycardia and sudden increase in BP, 13 how much the increase in BP should be and whether a DBP increase is required together with SBP and whether HR changes should accompany the BP increase in order to identify BP elevation as AD are controversial. Some authors describe the SBP increasing more than 20-30 mmHg or 20-30% as a dysreflexic episode [14][15][16][17] while other authors have reported that a decrease of 15% in the HR together with a 30% increase in SBP and DBP may indicate AD, 16 that a BP exceeding 160/90 mmHg 18 or 150/100 mmHg may be a finding of AD, 19 and that a sudden increase in SBP and DBP of 20-40 mmHg and accompanying bradycardia may be a finding of AD.…”
Section: Discussionmentioning
confidence: 99%