Alterations in Blood-Brain Barrier Permeability to Large and Small Molecules and Leukocyte Accumulation after Traumatic Brain Injury: Effects of Post-Traumatic Hypothermia

Lotocki, George; Vaccari, Juan Pablo de Rivero; Perez, Enrique; Sanchez-Molano, Juliana; Furones-Alonso, Ofelia; Bramlett, Helen M.; Dietrich, W. Dalton

doi:10.1089/neu.2008.0802

Cited by 147 publications

(119 citation statements)

References 42 publications

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“…The importance of inflammasome as a key component of the innate immune response in brain injury has been recently emphasized and targeted for therapeutic interventions [36][37][38][39]. The inflammasome is a multiprotein complex responsible for the activation of caspase-1 and the processing of the inflammatory cytokines IL-1β and IL-18 [40]. In models of brain ischemia, evidence for inflammasome activation has been reported with elevations in inflammatory proteins such as ASC, and caspase-1.…”

Section: Discussionmentioning

confidence: 99%

Whole Body Vibration Therapy after Ischemia Reduces Brain Damage in Reproductively Senescent Female Rats

Raval¹,

Schatz²,

Bhattacharya³

et al. 2018

Preprint

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A risk of ischemic stroke increases exponentially after menopause. Even a mild-ischemic stroke can result in increased frailty. Frailty is a state of increased vulnerability to adverse outcomes, which subsequently increases risk of cerebrovascular events and severe cognitive decline, particularly after menopause.Several interventions to reduce frailty and subsequent risk of stroke and cognitive decline have been proposed in laboratory animals and patients. One of them is whole body vibration (WBV). WBV improves brain hemodynamics and lessens frailty-related functional and cognitive deterioration. The goal of current study is to test the efficacy of WBV in reducing post-ischemic stroke frailty and brain damage in reproductively senescent female rats. Reproductively senescent Sprague-Dawley female rats were exposed to transient middle cerebral artery occlusion (tMCAO) and randomly assigned to either WBV or control groups. Animals placed in the WBV group underwent 30 days of WBV (40 Hz) treatment performed twice daily for 15 min each session for 5 days each week. The motor functions of animals belonging to both groups were tested intermittently and at the end of treatment period. Brains were then harvested for inflammatory markers and histopathological analysis. The results demonstrate a significant reduction in inflammatory markers, infarct volume, and significant increases in brain-derived neurotrophic factor and improvement in functional activity after tMCAO in middle-aged female rats that were treated with WBV as compared to the control group. Our results may help faster translation of the WBV intervention for improved outcome after stroke, particularly among frail women.

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Section: Discussionmentioning

confidence: 99%

Whole Body Vibration Therapy after Ischemia Reduces Brain Damage in Reproductively Senescent Female Rats

Raval¹,

Schatz²,

Bhattacharya³

et al. 2018

Preprint

Self Cite

View full text Add to dashboard Cite

show abstract

“…To date, of the strategies employed, the use of hypothermia has received some attention. In animal experiments, posttraumatic hypothermia has been shown to exert multiple protective effects on various vascular abnormalities elicited by TBI ( Jiang et al, 1992;Lotocki et al, 2009;Ueda et al, 2003Ueda et al, , 2004Wei et al, 2009). However, other than in an initial report by Bedell and colleagues (2004) the potential beneficial effects of hypothermia on cerebral autoregulation have not been fully evaluated.…”

Section: Introductionmentioning

confidence: 99%

Effects of Hypothermia on Cerebral Autoregulatory Vascular Responses in Two Rodent Models of Traumatic Brain Injury

Fujita

Wei

Povlishock

2012

Journal of Neurotrauma

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Traumatic brain injury (TBI) can trigger disturbances of cerebral pressure autoregulation that can translate into the generation of secondary insults and increased morbidity/mortality. Few therapies have been developed to attenuate the damaging consequences of disturbed autoregulatory control, although some suggest that hypothermia may exert such protection. Here we reexamine this issue of traumatically induced autoregulatory disturbances and their modulation by hypothermic intervention, examining these phenomena in two different models of TBI. Adult rats were subjected to either impact acceleration injury (IAI) or lateral fluid percussion injury (LFPI) followed by the insertion of cranial windows to assess the pial arteriolar cerebral autoregulatory vascular response to the post-traumatic induction of sequential reductions of arterial blood pressure. The potential for continued pial vasodilation in response to declining blood pressure was directly measured post-injury and compared with that in injured groups subjected to 33°C of hypothermia of 1-2 h duration initiated 1 h postinjury. We observed that the TBI resulted in either impaired or abolished cerebral vascular dilation in response to the sequential declines in blood pressure. Following IAI there was a 50% reduction in the vasculature's ability to dilate in response to the induced hypotension. In contrast, following LFPI, the vascular response to hypotension was abolished both ipsilateral and contralateral to the LFPI. In animals sustaining IAI, the use of 1 h posttraumatic hypothermia preserved vascular dilation in response to declines in blood pressure in contrast to the LFPI in which the use of the same strategy afforded no improvement. However, with LFPI, the use of 2 h of hypothermia provided partial vascular protection. These results clearly illustrate that TBI can alter the cerebral autoregulatory vascular response to sequentially induced hypotensive insult, whereas the use of post-traumatic hypothermia provides benefit. Collectively, these studies also demonstrate that different animal models of TBI can evoke different biological responses to injury.

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“…Unlike the primary brain injury, it is a complex process that theoretically could be prevented and may be reversible. In secondary brain injury, there is a series of molecular, neurochemical, and cellular mechanism that may conduct to elevated intracranial pressure, BBB breakage, inflammation of the neural cell, cerebral edema, brain hypoxia, ischemia, and delayed neurodegeneration [21][22][23] . The MMPs represent one of the most prominent family associated with secondary brain injury.…”

Section: Discussionmentioning

confidence: 99%

Mangosteen Extract Reduces the Expression of Matrix Metalloproteinase -2 and -9 in Traumatic Brain Injury

Siahaan¹,

Lumintang²,

Dalimunthe³

2017

IJPTR

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: Traumatic brain injury (TBI) is one of the most significant cause for mortality and morbidity in young population. After the primary injury, there is secondary injury that will aggravate the injury and lead to cell death. Secondary injury can be prevented and reversible, providing opportunity for therapeutic intervention. Matrix metalloproteinases (MMPs) are endopeptidases that participates mainly in the dynamic modulation of the extracellular membrane. In some neurological diseases, MMPs will cause breakage of the blood brain barrier (BBB), hemorrhage, neuronal inflammation, and neuronal cell death. In this study, we used an experimental mouse model of TBI to examine the role of MMP-2 and MMP-9 and the therapeutic potential of mangosteen extract that contain natural MMP inhibitor. We observed that expression of MMP-2 and MMP-9 were reduced in treatment group. These findings suggested that mangosteen extract might be a potential therapeutic agent for TBI.

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Alterations in Blood-Brain Barrier Permeability to Large and Small Molecules and Leukocyte Accumulation after Traumatic Brain Injury: Effects of Post-Traumatic Hypothermia

Cited by 147 publications

References 42 publications

Whole Body Vibration Therapy after Ischemia Reduces Brain Damage in Reproductively Senescent Female Rats

Whole Body Vibration Therapy after Ischemia Reduces Brain Damage in Reproductively Senescent Female Rats

Effects of Hypothermia on Cerebral Autoregulatory Vascular Responses in Two Rodent Models of Traumatic Brain Injury

Mangosteen Extract Reduces the Expression of Matrix Metalloproteinase -2 and -9 in Traumatic Brain Injury

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