The Time Course of Vasogenic Oedema After Focal Human Head Injury — Evidence from SPECT Mapping of Blood Brain Barrier Defects

1990 ◽  
pp. 286-288 ◽  
Author(s):  
R. Bullock ◽  
P. Statham ◽  
J. Patterson ◽  
D. Wyper ◽  
D. Hadley ◽  
...  
Keyword(s):  
Head Injury ◽  
Blood Brain Barrier ◽  
Time Course ◽  
Human Head ◽  
Brain Barrier ◽  
Vasogenic Oedema ◽  
Blood Brain

scholarly journals Immunolocalization of Heat Shock Protein after Fluid Percussive Brain Injury and Relationship to Breakdown of the Blood-Brain Barrier

1993 ◽  
Vol 13 (1) ◽  
pp. 116-124 ◽  
Author(s):  
Hirokazu Tanno ◽  
Russ P. Nockels ◽  
Lawrence H. Pitts ◽  
Linda J. Noble
Keyword(s):  
Brain Injury ◽  
Head Injury ◽  
Blood Vessels ◽  
Blood Brain Barrier ◽  
Time Course ◽  
Cortical Layer ◽  
Brain Barrier ◽  
Impact Site ◽  
Blood Brain ◽  
The Impact

We have previously developed a model of mild, lateral fluid percussive head injury in the rat and demonstrated that although this injury produced minimal hemorrhage, breakdown of the blood–brain barrier was a prominent feature. The relationship between posttraumatic blood–brain barrier disruption and cellular injury is unclear. In the present study we examined the distribution and time course of expression of the stress protein HSP72 after brain injury and compared these findings with the known pattern of breakdown of the blood–brain barrier after a similar injury. Rats were subjected to a lateral fluid percussive brain injury (4.8–5.2 atm, 20 ms) and killed at 1, 3, and 6 h and 1,3, and 7 days after injury. HSP72-like immunoreactivity was evaluated in sections of brain at the light-microscopic level. The earliest expression of HSP72 occurred at 3 h postinjury and was restricted to neurons and glia in the cortex surrounding a necrotic area at the impact site. By 6 h, light immunostaining was also noted in the pia-arachnoid adjacent to the impact site and in certain blood vessels that coursed through the area of necrosis. Maximal immunostaining was observed by 24 h postinjury, and was primarily associated with the cortex immediately adjacent to the region of necrosis at the impact site. This region consisted of darkly immunostained neurons, glia, and blood vessels. Immunostaining within the region of necrosis was restricted to blood vessels. HSP72-like immunoreactivity was also noted in a limited number of neurons and glia in other brain regions, including the parasagittal cortex, deep cortical layer VI, and CA3 in the posterior hippocampus. Immunoreactive cells in these areas were not apparent until 24 h postinjury. By 7 days postinjury, HSP72-like immunoreactivity was minimal or absent in these injured brains and notable cell loss was apparent only in the impact site. This study demonstrates an early and pronounced expression of HSP72 at the impact site and a more delayed and less prominent expression of this protein in other regions of the brain. These findings parallel the temporal and regional pattern of breakdown of the blood–brain barrier after a similar head injury.

Time Course and Size of Blood–Brain Barrier Opening in a Mouse Model of Blast-Induced Traumatic Brain Injury

2016 ◽  
Vol 33 (13) ◽  
pp. 1202-1211 ◽  
Author(s):  
Christopher D. Hue ◽  
Frances S. Cho ◽  
Siqi Cao ◽  
Russell E. Nicholls ◽  
Edward W. Vogel III ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mouse Model ◽  
Blood Brain Barrier ◽  
Time Course ◽  
Brain Barrier ◽  
Blood Brain ◽  
Barrier Opening ◽  
Blood Brain Barrier Opening

scholarly journals Unravelling the mechanisms of blood–brain barrier dysfunction in repetitive mild head injury

Brain ◽  
2020 ◽  
Vol 143 (6) ◽  
pp. 1625-1628
Author(s):  
Jeffrey B Ware ◽  
Danielle K Sandsmark ◽  
Ramon Diaz-Arrastia
Keyword(s):  
Head Injury ◽  
Blood Brain Barrier ◽  
American Football ◽  
Brain Barrier ◽  
Football Players ◽  
Mild Head Injury ◽  
Barrier Dysfunction ◽  
Blood Brain

This scientific commentary refers to ‘Slow blood-to-brain transport underlies enduring barrier dysfunction in American football players’, by Veksler et al. (doi:10.1093/brain/awaa140).

The endocannabinoid 2-AG protects the blood–brain barrier after closed head injury and inhibits mRNA expression of proinflammatory cytokines

2006 ◽  
Vol 22 (2) ◽  
pp. 257-264 ◽  
Author(s):  
David Panikashvili ◽  
Na'ama A. Shein ◽  
Raphael Mechoulam ◽  
Victoria Trembovler ◽  
Ron Kohen ◽  
...  
Keyword(s):  
Head Injury ◽  
Mrna Expression ◽  
Blood Brain Barrier ◽  
Proinflammatory Cytokines ◽  
Closed Head Injury ◽  
Brain Barrier ◽  
Blood Brain ◽  
Closed Head

Effects of insulin on hexose transport across blood-brain barrier in normoglycemia

1987 ◽  
Vol 252 (3) ◽  
pp. E299-E303 ◽  
Author(s):  
H. Namba ◽  
G. Lucignani ◽  
A. Nehlig ◽  
C. Patlak ◽  
K. Pettigrew ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Rate Constants ◽  
Time Course ◽  
Brain Barrier ◽  
Tissue Concentrations ◽  
Arterial Blood ◽  
Blood Brain ◽  
Measured Time ◽  
Time Courses ◽  
Arterial Plasma

The effects of insulin on 3-O-[14C]methylglucose transport across the blood-brain barrier (BBB) were studied in conscious rats under steady-state normoglycemic conditions. The [14C]methylglucose was infused intravenously at a constant rate, and animals were killed at various times between 5 and 30 min after the initiation of the infusion. The time course of the arterial plasma concentration of [14C]methylglucose was determined in timed arterial blood samples taken during the infusion. Local cerebral tissue concentrations of [14C]methylglucose at the time of killing were determined by quantitative autoradiography of brain sections. The rate constants for inward and outward transport of [14C]methylglucose across the BBB, K1, and k2, respectively, were estimated by a least-squares, best-fit of a kinetic equation to the measured time courses of plasma and tissue concentrations. K1 and k2 were reduced by an average of 24 and 31%, respectively, in gray matter and 7 and 16% in white matter from values estimated similarly in normal insulinemic control rats. The equilibrium distribution ratio, K1/k2, for [14C]methylglucose in brain increased by approximately 10–11% in the hyperinsulinemic animals. Because 3-O-[14C]methylglucose shares the same carrier that transports glucose and other hexoses across the BBB, these results suggest that hyperinsulinemia decreases the rate constants for transport but increases the distribution space for hexoses in brain. These effects are, however, quite small and are probably minor or negligible when compared with the major effects of insulin in other tissues.

scholarly journals Cyclophilin a signaling induces pericyte-associated blood-brain barrier disruption after subarachnoid hemorrhage

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Pengyu Pan ◽  
Hengli Zhao ◽  
Xuan Zhang ◽  
Qiang Li ◽  
Jie Qu ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Blood Brain Barrier ◽  
Time Course ◽  
Brain Barrier ◽  
Blood Brain Barrier Disruption ◽  
Blood Brain ◽  
Junction Protein ◽  
Brain Barrier Disruption ◽  
Harmful Effects ◽  
Cypa Expression

Abstract Objective The potential roles and mechanisms of pericytes in maintaining blood–brain barrier (BBB) integrity, which would be helpful for the development of therapeutic strategies for subarachnoid hemorrhage (SAH), remain unclear. We sought to provide evidence on the potential role of pericytes in BBB disruption and possible involvement and mechanism of CypA signaling in both cultured pericytes and SAH models. Methods Three hundred fifty-three adult male C57B6J mice weighing 22 to 30 g, 29 CypA−/− mice, 30 CypA+/+ (flox/flox) mice, and 30 male neonatal C57B6J mice were used to investigate the time course of CypA expression in pericytes after SAH, the intrinsic function and mechanism of CypA in pericytes, and whether the known receptor CD147 mediates these effects. Results Our data demonstrated both intracellular CypA and CypA secretion increased after SAH and could activate CD147 receptor and downstream NF-κB pathway to induce MMP9 expression and proteolytic functions for degradation of endothelium tight junction proteins and basal membranes. CypA served as autocrine or paracrine ligand for its receptor, CD147. Although CypA could be endocytosed by pericytes, specific endocytosis inhibitor chlorpromazine did not have any effect on MMP9 activation. However, specific knockdown of CD147 could reverse the harmful effects of CypA expression in pericytes on the BBB integrity after SAH. Conclusions This study demonstrated for the first time that CypA mediated the harmful effects of pericytes on BBB disruption after SAH, which potentially mediated by CD147/NF-κB/MMP9 signal, and junction protein degradation in the brain. By targeting CypA and pericytes, this study may provide new insights on the management of SAH patients.

In vivo assessment of the window of barrier opening after osmotic blood—brain barrier disruption in humans

2000 ◽  
Vol 92 (4) ◽  
pp. 599-605 ◽  
Author(s):  
Tali Siegal ◽  
Rina Rubinstein ◽  
Felix Bokstein ◽  
Allan Schwartz ◽  
Alexander Lossos ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Time Course ◽  
Photon Emission ◽  
Brain Barrier ◽  
Therapeutic Window ◽  
Content Type ◽  
Blood Brain ◽  
The Mean ◽  
Fine Print

Object. Osmotic blood—brain barrier (BBB) disruption induced by intraarterial infusion of mannitol is used in conjunction with chemotherapy to treat human brain tumors. The time course to barrier closure, or the so-called therapeutic window, has been examined in animals but little information is available in humans. The authors, therefore assessed the time course to barrier closure after osmotic BBB disruption in humans.Methods. Disruption of the BBB was demonstrated using 99mTc-glucoheptonate (TcGH) single-photon emission computerized tomography (SPECT) scanning in 12 patients who were treated monthly with combination chemotherapy in conjunction with BBB disruption. The primary diagnosis was primary central nervous system lymphoma in seven patients and primitive neuroectodermal tumors in five. The TcGH (20 mCi) was injected at 1- to 480-minute intervals after osmotic BBB disruption, and patients underwent SPECT scanning after 4 hours. A total of 38 studies was performed. Good-to-excellent BBB disruption was obtained in 29 procedures and poor-to-moderate disruption was seen in the other nine studies.The TcGH indices correlated with the degree of BBB disruption as measured postprocedure on contrast-enhanced CT scans (r = 0.852). Mean baseline TcGH indices were 1.02 ± 0.07. For the group of patients with good-to-excellent disruptions the mean indices at 1 minute postdisruption measured 2.19 ± 0.18. After 40 minutes no significant change was noted (mean index 2.13 ± 0.2). Then the indices declined more steeply and at 120 minutes after the disruption the index was 1.36 ± 0.02. A very slow decline was noted between 120 and 240 minutes after mannitol infusion. At 240 minutes the barrier was still open for all good-to-excellent disruptions (index 1.33 ± 0.08) but at 480 minutes the mean indices had returned to the baseline level.Conclusions. Results of these in vivo human studies indicate that the time course to closure of the disrupted BBB for low-molecular-weight complexes is longer than previously estimated. The barrier is widely open during the first 40 minutes after osmotic BBB disruption and returns to baseline levels only after 6 to 8 hours following the induction of good or excellent disruption. These findings have important clinical implications for the design of therapeutic protocols.

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