Journal of neurotrauma
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Journal of neurotrauma · Jun 2015
Characterizing the temporal development of cardiovascular dysfunction in response to spinal cord injury.
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. ⋯ 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.
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Journal of neurotrauma · Jun 2015
Wallerian degeneration in the optic nerve stretch-injury model of TBI: a stereological analysis.
Patients with chronic traumatic encephalopathy (CTE) show loss of central white matter, central gray matter, and cortical gray matter with increasing post-traumatic survival. The majority of experimental studies using animals have, however, discussed only the ultrastructural pathophysiology of injured central white matter leading to secondary axotomy and the formation of axonal terminal bulbs. Using the stretch-injured optic nerve model in adult guinea pigs, the present study provides novel quantitative data concerning Wallerian degeneration of disconnected axonal fragments following secondary axotomy out to 12 weeks after injury to an optic nerve. ⋯ This data suggests that some nerve fibers initiate Wallerian degeneration days and weeks after the initial time of mechanical injury to an optic nerve. The number of intact nerve fibers continues to fall over at least three months after injury in the stretch-injury model of traumatic axonal injury. It is suggested that these novel findings relate to the mechanism(s) whereby central white matter volume decreases over months and years in CTE patients.
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Journal of neurotrauma · Jun 2015
Endogenous nutritive support following traumatic brain injury: peripheral lactate production for glucose supply via gluconeogenesis.
We evaluated the hypothesis that nutritive needs of injured brains are supported by large and coordinated increases in lactate shuttling throughout the body. To that end, we used dual isotope tracer ([6,6-(2)H2]glucose, i.e., D2-glucose, and [3-(13)C]lactate) techniques involving central venous tracer infusion along with cerebral (arterial [art] and jugular bulb [JB]) blood sampling. Patients with traumatic brain injury (TBI) who had nonpenetrating head injuries (n=12, all male) were entered into the study after consent of patients' legal representatives. ⋯ This previously unrecognized mobilization of lactate subserves hepatic and renal gluconeogenesis. As such, a lactate shuttle mechanism indirectly makes substrate available for the body and its essential organs, including the brain, after trauma. In addition, when elevations in arterial lactate concentration occur after TBI, lactate shuttling may provide substrate directly to vital organs of the body, including the injured brain.