Spinal cord injury (SCI) is associated with rapid and sustained impairments in cardiovascular function that ultimately cause an early onset of cardiovascular disease. We know remarkably little about the temporal progression of cardiovascular disturbances, but such an understanding is critical to inform clinical management and develop appropriate intervention strategies. To characterize the cardiovascular response to SCI, six male Wistar rats were instrumented with telemetry and assessed for continuous arterial blood pressure (BP), core body temperature, and heart rate (HR) 7 days before and up to 28 days after T3 SCI. Hemodynamic variables were averaged day by day and hour by hour. Spontaneously occurring autonomic dysreflexia (AD) was characterized by applying a novel algorithm to continuous BP and HR data, and induced AD was assessed weekly via the BP response to colorectal distension. Systolic BP was reduced at all time points after SCI compared with before SCI (p<0.003), except at 4 and 6 days post-injury. Core body temperature was reduced at 2 days post-SCI only (p=0.001). The nocturnal dip in BP and temperature observed pre-SCI was absent during the first 14 days post-SCI, but returned from 21 days post-SCI on (p<0.024). The frequency and severity of spontaneously occurring AD events were significantly less between days 6 and 10 post-SCI compared all other time points (p<0.037). The pressor response to colorectal distension was greater at 14, 21, and 28 days post-SCI compared with at 7 days post-SCI (all p<0.004). In conclusion, SCI induces rapid and profound alterations in basal hemodynamics and diurnal rhythms that partially recover by 14 days post-SCI. AD, on the other hand, is acutely present post-SCI, but the frequency and severity of AD events increase substantially from 14 days post-SCI on.
Cardiovascular disease is the leading cause of death for individuals with spinal cord injury (SCI). Because of a lack of a standardized and accessible animal model for cardiovascular disease after SCI, few laboratories have conducted pre-clinical trials aimed at reinstating descending cardiovascular control. Here, we utilized common contusion methodology applied to the midline of the upper-thoracic cord of adult Wistar rats accompanied with telemetric blood pressure monitoring and FluoroGold retrograde neuronal tracing, as well as lesion site and lumbrosacral afferent immunohistochemistry. We demonstrate widespread cardiovascular (i.e., impaired resting hemodynamics, autonomic dysreflexia) and hindlimb dysfunction at 1 month post-injury. Further, we provide a description of the neuroanatomical changes that accompany cardiovascular abnormalities. Specifically, we describe 1) the injury site including white matter sparing as well as lesion volume, and their correlations to cardiovascular as well as motor outcomes; 2) the severity of injury-dependent changes in sympathoexcitatory medullary neuron spinal connectivity, as measured using FluoroGold tracing; and 3) the extent of aberrant afferent plasticity within the lumbosacral region of the spinal cord, which has been linked to the development of autonomic dysreflexia. We believe that this model, which utilizes equipment common to numerous SCI laboratories, can serve as a research standard for studies specifically aimed at investigating autonomic neuroprotective and regenerative strategies following SCI.
Cardiovascular disease is one of the leading causes of morbidity and mortality in the spinal cord injury (SCI) population. SCI may disrupt autonomic cardiovascular homeostasis, which can lead to persistent hypotension, irregular diurnal rhythmicity, and the development of autonomic dysreflexia (AD). There is currently no software available to perform automated detection and evaluation of cardiovascular autonomic dysfunction(s) such as those generated from 24 h ambulatory blood pressure monitoring (ABPM) recordings in the clinical setting. The objective of this study is to compare the efficacy of a novel 24 h ABPM Autonomic Dysfunction Detection Software against manual detection and to use the software to demonstrate the relationships between level of injury and the degree of autonomic cardiovascular impairment in a large cohort of individuals with SCI. A total of 46 individuals with cervical (group 1, n = 37) or high thoracic (group 2, n = 9) SCI participated in the study. Outcome measures included the frequency and severity of AD, frequency of hypotensive events, and diurnal variations in blood pressure and heart rate. There was good agreement between the software and manual detection of AD events (Bland-Altman limits of agreement = ±1.458 events). Cervical SCI presented with more frequent (p = 0.0043) and severe AD (p = 0.0343) than did high thoracic SCI. Cervical SCI exhibited higher systolic and diastolic blood pressure during the night and lower heart rate during the day than high thoracic SCI. In conclusion, our ABPM AD Detection Software was equally as effective in detecting the frequency and severity of AD and hypotensive events as manual detection, suggesting that this software can be used in the clinical setting to expedite ABPM analyses.
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