Diffuse prolonged depression of cerebral oxidative metabolism following concussive brain injury in the rat: a cytochrome oxidase histochemistry study

Hovda, David A.; Yoshino, Atsuo; Kawamata, Tatsuro; Katayama, Yoichi; Becker, Donald P.

doi:10.1016/0006-8993(91)91429-5

Cited by 223 publications

(124 citation statements)

References 57 publications

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“…However, decrease in CBF may not be problematic if, following TBI, baseline CMRO 2 is low and there is a compensatory increase in oxygen extraction fraction [70]. Regional alterations of brain metabolism, reduction in metabolic rates and energy crisis have been demonstrated in adult patients after TBI [71][72][73]. Although the incidence of cerebral ischemia was reported to be low (1% when using oxygen extraction fraction and cerebral venous oxygen content, and 2.4% when using microdialysis technique), the incidence of metabolic crisis (elevated lactate/pyruvate ratio) following TBI was high (25%) [74].…”

Section: Cerebrovascular Physiology After Tbi Altered Cerebral Blood mentioning

confidence: 99%

Cerebral Blood Flow and Autoregulation After Pediatric Traumatic Brain Injury

Udomphorn

Armstead

Vavilala

2008

Pediatric Neurology

132

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Traumatic brain injury is a global health concern and is the leading cause of traumatic morbidity and mortality in children. Despite a lower overall mortality than in adult traumatic brain injury, the cost to society from the sequelae of pediatric traumatic brain injury is very high. Predictors of poor outcome after traumatic brain injury include altered systemic and cerebral physiology, including altered cerebral hemodynamics. Cerebral autoregulation is often impaired following traumatic brain injury and may adversely impact poor outcome. Although altered cerebrovascular hemodynamics early after traumatic brain injury may contribute to disability in children, there is a paucity of information regarding changes in cerebral blood flow and cerebral autoregulation after pediatric traumatic brain injury. In this article, we discuss normal pediatric cerebral physiology and cerebrovascular pathophysiology following pediatric traumatic brain injury.

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Section: Cerebrovascular Physiology After Tbi Altered Cerebral Blood mentioning

confidence: 99%

Cerebral Blood Flow and Autoregulation After Pediatric Traumatic Brain Injury

Udomphorn

Armstead

Vavilala

2008

Pediatric Neurology

132

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“…Although a number of mechanisms are likely to contribute to this impairment and dysfunction following mild TBI, the exact mechanism for this increased vulnerability and an understanding of this posttraumatic pathobiology remain speculative. Nevertheless, the results of experimental studies have indicated that ion dyshomeostasis 19,83 and metabolic alterations 36,37,97 persist for days following concussive TBI, without creating overt morphological damage, and may represent the pathological basis for an increased vulnerability.…”

Section: J Neurosurg / Volume 95 / November 2001mentioning

confidence: 99%

Mild head injury increasing the brain's vulnerability to a second concussive impact

Laurer¹,

Bareyre²,

Lee³

et al. 2001

Journal of Neurosurgery

289

237

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Object. Mild, traumatic repetitive head injury (RHI) leads to neurobehavioral impairment and is associated with the early onset of neurodegenerative disease. The authors developed an animal model to investigate the behavioral and pathological changes associated with RHI. Methods. Adult male C57BL/6 mice were subjected to a single injury (43 mice), repetitive injury (two injuries 24 hours apart; 49 mice), or no impact (36 mice). Cognitive function was assessed using the Morris water maze test, and neurological motor function was evaluated using a battery of neuroscore, rotarod, and rotating pole tests. The animals were also evaluated for cardiovascular changes, blood—brain barrier (BBB) breakdown, traumatic axonal injury, and neurodegenerative and histopathological changes between 1 day and 56 days after brain trauma. No cognitive dysfunction was detected in any group. The single-impact group showed mild impairment according to the neuroscore test at only 3 days postinjury, whereas RHI caused pronounced deficits at 3 days and 7 days following the second injury. Moreover, RHI led to functional impairment during the rotarod and rotating pole tests that was not observed in any animal after a single impact. Small areas of cortical BBB breakdown and axonal injury, observed after a single brain injury, were profoundly exacerbated after RHI. Immunohistochemical staining for microtubule-associated protein—2 revealed marked regional loss of immunoreactivity only in animals subjected to RHI. No deposits of β-amyloid or tau were observed in any brain-injured animal. Conclusions. On the basis of their results, the authors suggest that the brain has an increased vulnerability to a second traumatic insult for at least 24 hours following an initial episode of mild brain trauma.

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“…1 Multiple primary and secondary injury cascades are involved in TBI, which result in delayed neuronal dysfunction, synapse loss, and cell death. [2][3][4][5][6][7][8][9] These secondary injury cascades can occur very rapidly, within minutes or hours after the trauma and last for days or weeks. Although there are many different factors, most researchers believe that pharmacologic intervention following trauma can disrupt these cascades and result in a more positive outcome.…”

mentioning

confidence: 99%

Dose- and Time-Dependent Neuroprotective Effects of Pycnogenol^® following Traumatic Brain Injury

Ansari

Roberts

2013

Journal of Neurotrauma

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After traumatic brain injury (TBI), both primary and secondary injury cascades are initiated, leading to neuronal death and cognitive dysfunction. We have previously shown that the combinational bioflavonoid, PycnogenolÒ (PYC), alters some secondary injury cascades and protects synaptic proteins when administered immediately following trauma. The purpose of the present study was to explore further the beneficial effects of PYC and to test whether it can be used in a more clinically relevant fashion. Young adult male Sprague-Dawley rats were subjected to a unilateral moderate/severe cortical contusion. Subjects received a single intravenous (i.v.) injection of PYC (1, 5, or 10 mg/kg) or vehicle, with treatment initiated at 15 min, 2 h, or 4 h post injury. All rats were killed at 96 h post TBI. Both the cortex and hippocampus ipsilateral and contralateral to the injury were evaluated for possible changes in oxidative stress (thiobarbituric acid reactive species; TBARS) and both pre-and post-synaptic proteins (synapsin-I, synaptophysin, drebrin, post synaptic density protein-95, and synapse associated protein-97). Following TBI, TBARS were significantly increased in both the injured cortex and ipsilateral hippocampus. Regardless of the dose and delay in treatment, PYC treatment significantly lowered TBARS. PYC treatment significantly protected both the cortex and hippocampus from injury-related declines in pre-and postsynaptic proteins. These results demonstrate that a single i.v. treatment of PYC is neuroprotective after TBI with a therapeutic window of at least 4 h post trauma. The natural bioflavonoid PYC may provide a possible therapeutic intervention in neurotrauma.

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Diffuse prolonged depression of cerebral oxidative metabolism following concussive brain injury in the rat: a cytochrome oxidase histochemistry study

Cited by 223 publications

References 57 publications

Cerebral Blood Flow and Autoregulation After Pediatric Traumatic Brain Injury

Cerebral Blood Flow and Autoregulation After Pediatric Traumatic Brain Injury

Mild head injury increasing the brain's vulnerability to a second concussive impact

Dose- and Time-Dependent Neuroprotective Effects of Pycnogenol^® following Traumatic Brain Injury

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Diffuse prolonged depression of cerebral oxidative metabolism following concussive brain injury in the rat: a cytochrome oxidase histochemistry study

Cited by 223 publications

References 57 publications

Cerebral Blood Flow and Autoregulation After Pediatric Traumatic Brain Injury

Cerebral Blood Flow and Autoregulation After Pediatric Traumatic Brain Injury

Mild head injury increasing the brain's vulnerability to a second concussive impact

Dose- and Time-Dependent Neuroprotective Effects of Pycnogenol® following Traumatic Brain Injury

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Product

Resources

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Dose- and Time-Dependent Neuroprotective Effects of Pycnogenol^® following Traumatic Brain Injury