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Stroke Induced Hydrocephalus
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ironjustice
Dec 5, 2012, 2:08:37 PM12/5/12
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Subarachnoid Hemorrhage-Induced Hydrocephalus in Rats
Shuichi Okubo, MD, Jennifer Strahle, MD, Richard F. Keep, PhD, Ya Hua,
MD and Guohua Xi, MD
Department of Neurosurgery, University of Michigan, Ann Arbor, MI.
Correspondence to Guohua Xi, MD, R5018 BSBR, University of Michigan,
109 Zina Pitcher Place, Ann Arbor, MI 48109-2200. E-mail
guoh...@umich.edu
Abstract
Background and Purpose
Hydrocephalus is an important complication of subarachnoid hemorrhage
(SAH). We investigated the occurrence of acute hydrocephalus in a rat
SAH model.
Methods
SAH was induced by endovascular perforation in adult male Sprague-
Dawley rats (n=36). Sham rats (n=8) underwent the same procedure
without perforation. MRI was performed 24 hours after SAH and the
volume of the ventricular system and extent of T2* hypointensity
lesions were measured. We defined hydrocephalus as ventricular volume
> +3 SDs above the mean in sham animals. SAH grade was determined and
brains were used for histology, immunohistochemistry, Perls staining,
and Western blot analysis. Ventricular wall damage was defined as
percentage of ependymal surface disruption.
Results
All surviving rats (n=27) after SAH had ventricular enlargement
(33.6±4.7 versus 13.5±1.4 mm3 in sham animals, P<0.01). Ventricular
volume correlated with SAH severity (r=0.48; P<0.05). Out of 27 SAH
rats, 12 demonstrated hydrocephalus and all had intraventricular blood
accumulation. Rats with hydrocephalus had more severe ventricular wall
damage (7.4±1.2%) than the sham animals (0.6±0.2%; P<0.01) and rats
without hydrocephalus (1.1±0.2%; P<0.01). Periventricular iron
deposition was observed and heme oxygenase-1 and Iba-1 expression were
markedly increased in hydrocephalus rats.
Conclusions
SAH causes ventricular enlargement in a rat endovascular perforation
model, with hydrocephalus occurring in 44% of animals at 24 hours.
Rats with hydrocephalus had more severe SAH, intraventricular
hemorrhage, and greater ventricular wall damage.
Key Words:acute hydrocephalusironratssubarachnoid Received April 23,
2012.
Revision received September 28, 2012.
Accepted October 24, 2012.
© 2012 American Heart Association, Inc.
--------
"Reduced brain lesion volume and edema and improved neurologic
function"
Efficacy of the lipid-soluble iron chelator 2,2'-dipyridyl against
hemorrhagic brain injury.
Neurobiol Dis. 2011 Sep 10.
Wu H, Wu T, Li M, Wang J.
Department of Anesthesiology/Critical Care Medicine, Johns Hopkins
University, School of Medicine, Baltimore, MD, USA;
Department of Pathology, First Clinical Hospital, Harbin Medical
University, Harbin 150001, China.
Abstract
Previous studies have indicated that 2,2'-dipyridyl, a lipid-soluble
ferrous iron chelator, can reduce brain injury after cerebral
ischemia
and reduce cerebral vasospasm after subarachnoid hemorrhage.
In this study, we examined the efficacy of 2,2'-dipyridyl after
intracerebral hemorrhage (ICH) in 12-month-old mice.
ICH was modeled by intrastriatal injection of collagenase or
autologous whole blood. 2,2'-Dipyridyl or vehicle was administered
intraperitoneally 2h before ICH (pretreatment) or 6h after ICH (post-
treatment) and then once daily for up to 3days.
Mice in the pretreatment group were sacrificed 1 or 3days after ICH
and examined for iron deposition, neuronal death, oxidative stress,
microglial/astrocyte activation, neutrophil infiltration, and white
matter damage.
Mice in the post-treatment group were examined for brain lesion
volume
and edema on day 3 and for neurologic deficits on days 1, 3, and 28
after ICH.
Pretreatment with 2,2'-dipyridyl decreased iron accumulation and
neuronal death, attenuated production of reactive oxygen species,
reduced microglial activation without affecting astrocytes or
neutrophil infiltration, and attenuated white matter damage.
Post-treatment reduced brain lesion volume and edema and improved
neurologic function.
These results indicate that the lipid-soluble ferrous iron chelator
2,2'-dipyridyl can reduce brain injury and improve functional outcome
after ICH.
Copyright © 2011. Published by Elsevier Inc.
PMID:21930208
------------------------
Alpha Lipoic Acid Alleviates Oxidative Stress and Preserves
Blood Brain Permeability in Rats with Subarachnoid Hemorrhage
Ersahin M, Toklu HZ, et al,
Neurochem Res, 2009 Oct 13;
Department of Neurosurgery,
Haydarpasa Numune Education and Research Hospital,
Istanbul, Turkey.
Summary:
In a study involving Wistar albino rats induced with subarachnoid
hemorrhage (SAH), treatment with alpha-lipoic acid (ALA, 100 mg/kg,
po)
was found to reverse the adverse neurological effects brought about
by
the SAH.
Specifically, SAH-induced increases in reactive oxygen species, DNA
fragmentation ratios, malondialdehyde levels, and myeloperoxidase
activity, and decreases in brain glutathione content and Na(+), K(+)-
ATP-ase activity were reversed as a result of ALA administration.
In addition, ALA reversed SAH-induced histopathological alterations,
and improved increased brain edema, impaired blood-brain barrier
permeability, and neurological scores.
The authors conclude, “The results demonstrate that ALA exerts
neuroprotective effects via the enhancement of endogenous antioxidant
enzyme activity, the inhibition of neutrophil accumulation and free
radical generation, suggesting a therapeutic potential in reducing
secondary injury after SAH in patients.”
SUBARACHNOID HEMORRHAGE, OXIDATIVE STRESS - Alpha Lipoic Acid, ALA
Reference: “Alpha Lipoic Acid Alleviates Oxidative Stress and
Preserves Blood Brain Permeability in Rats with Subarachnoid
Hemorrhage,”
------------------
Dietary supplementation with (R)-alpha-lipoic acid reverses the
age-related accumulation of iron and depletion of antioxidants in the
rat cerebral cortex.
Suh JH, Moreau R, Heath SH, Hagen TM.
Department Biochemistry and Biophysics, Linus Pauling Institute,
Oregon State University, Corvallis, Oregon 97331, USA.
Accumulation of divalent metal ions (e.g. iron and copper) has been
proposed to contribute to heightened oxidative stress evident in
aging and neurodegenerative disorders.
To understand the extent of iron accumulation and its effect on
antioxidant status, we monitored iron content in the cerebral cortex
of F344 rats by inductively coupled plasma atomic emission
spectrometry (ICP-AES) and found that the cerebral iron levels in
24-28-month-old rats were increased by 80% (p<0.01) relative to
3-month-old rats.
Iron accumulation correlated with a decline in glutathione (GSH) and
the GSH/GSSG ratio, indicating that iron accumulation altered
antioxidant capacity and thiol redox state in aged animals.
Because (R)-alpha-Lipoic acid (LA) is a potent chelator of divalent
metal ions in vitro and also regenerates other antioxidants, we
monitored whether feeding LA (0.2% [w/w]; 2 weeks) could lower
cortical
iron and improve antioxidant status.
Results show that cerebral iron levels in old LA-fed animals were
lower when compared to controls and were similar to levels seen in
young rats.
Antioxidant status and thiol redox state also improved markedly in
old LA-fed rats versus controls.
These results thus show that LA supplementation may be a means to
modulate
the age-related accumulation of cortical iron content, thereby
lowering oxidative stress associated with aging.
PMID: 15829111
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://tinyurl.com/634q5a
Man Is A Herbivore!
http://tinyurl.com/4rq595
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk
Shuichi Okubo, MD, Jennifer Strahle, MD, Richard F. Keep, PhD, Ya Hua,
MD and Guohua Xi, MD
Department of Neurosurgery, University of Michigan, Ann Arbor, MI.
Correspondence to Guohua Xi, MD, R5018 BSBR, University of Michigan,
109 Zina Pitcher Place, Ann Arbor, MI 48109-2200. E-mail
guoh...@umich.edu
Abstract
Background and Purpose
Hydrocephalus is an important complication of subarachnoid hemorrhage
(SAH). We investigated the occurrence of acute hydrocephalus in a rat
SAH model.
Methods
SAH was induced by endovascular perforation in adult male Sprague-
Dawley rats (n=36). Sham rats (n=8) underwent the same procedure
without perforation. MRI was performed 24 hours after SAH and the
volume of the ventricular system and extent of T2* hypointensity
lesions were measured. We defined hydrocephalus as ventricular volume
> +3 SDs above the mean in sham animals. SAH grade was determined and
brains were used for histology, immunohistochemistry, Perls staining,
and Western blot analysis. Ventricular wall damage was defined as
percentage of ependymal surface disruption.
Results
All surviving rats (n=27) after SAH had ventricular enlargement
(33.6±4.7 versus 13.5±1.4 mm3 in sham animals, P<0.01). Ventricular
volume correlated with SAH severity (r=0.48; P<0.05). Out of 27 SAH
rats, 12 demonstrated hydrocephalus and all had intraventricular blood
accumulation. Rats with hydrocephalus had more severe ventricular wall
damage (7.4±1.2%) than the sham animals (0.6±0.2%; P<0.01) and rats
without hydrocephalus (1.1±0.2%; P<0.01). Periventricular iron
deposition was observed and heme oxygenase-1 and Iba-1 expression were
markedly increased in hydrocephalus rats.
Conclusions
SAH causes ventricular enlargement in a rat endovascular perforation
model, with hydrocephalus occurring in 44% of animals at 24 hours.
Rats with hydrocephalus had more severe SAH, intraventricular
hemorrhage, and greater ventricular wall damage.
Key Words:acute hydrocephalusironratssubarachnoid Received April 23,
2012.
Revision received September 28, 2012.
Accepted October 24, 2012.
© 2012 American Heart Association, Inc.
--------
"Reduced brain lesion volume and edema and improved neurologic
function"
Efficacy of the lipid-soluble iron chelator 2,2'-dipyridyl against
hemorrhagic brain injury.
Neurobiol Dis. 2011 Sep 10.
Wu H, Wu T, Li M, Wang J.
Department of Anesthesiology/Critical Care Medicine, Johns Hopkins
University, School of Medicine, Baltimore, MD, USA;
Department of Pathology, First Clinical Hospital, Harbin Medical
University, Harbin 150001, China.
Abstract
Previous studies have indicated that 2,2'-dipyridyl, a lipid-soluble
ferrous iron chelator, can reduce brain injury after cerebral
ischemia
and reduce cerebral vasospasm after subarachnoid hemorrhage.
In this study, we examined the efficacy of 2,2'-dipyridyl after
intracerebral hemorrhage (ICH) in 12-month-old mice.
ICH was modeled by intrastriatal injection of collagenase or
autologous whole blood. 2,2'-Dipyridyl or vehicle was administered
intraperitoneally 2h before ICH (pretreatment) or 6h after ICH (post-
treatment) and then once daily for up to 3days.
Mice in the pretreatment group were sacrificed 1 or 3days after ICH
and examined for iron deposition, neuronal death, oxidative stress,
microglial/astrocyte activation, neutrophil infiltration, and white
matter damage.
Mice in the post-treatment group were examined for brain lesion
volume
and edema on day 3 and for neurologic deficits on days 1, 3, and 28
after ICH.
Pretreatment with 2,2'-dipyridyl decreased iron accumulation and
neuronal death, attenuated production of reactive oxygen species,
reduced microglial activation without affecting astrocytes or
neutrophil infiltration, and attenuated white matter damage.
Post-treatment reduced brain lesion volume and edema and improved
neurologic function.
These results indicate that the lipid-soluble ferrous iron chelator
2,2'-dipyridyl can reduce brain injury and improve functional outcome
after ICH.
Copyright © 2011. Published by Elsevier Inc.
PMID:21930208
------------------------
Alpha Lipoic Acid Alleviates Oxidative Stress and Preserves
Blood Brain Permeability in Rats with Subarachnoid Hemorrhage
Ersahin M, Toklu HZ, et al,
Neurochem Res, 2009 Oct 13;
Department of Neurosurgery,
Haydarpasa Numune Education and Research Hospital,
Istanbul, Turkey.
Summary:
In a study involving Wistar albino rats induced with subarachnoid
hemorrhage (SAH), treatment with alpha-lipoic acid (ALA, 100 mg/kg,
po)
was found to reverse the adverse neurological effects brought about
by
the SAH.
Specifically, SAH-induced increases in reactive oxygen species, DNA
fragmentation ratios, malondialdehyde levels, and myeloperoxidase
activity, and decreases in brain glutathione content and Na(+), K(+)-
ATP-ase activity were reversed as a result of ALA administration.
In addition, ALA reversed SAH-induced histopathological alterations,
and improved increased brain edema, impaired blood-brain barrier
permeability, and neurological scores.
The authors conclude, “The results demonstrate that ALA exerts
neuroprotective effects via the enhancement of endogenous antioxidant
enzyme activity, the inhibition of neutrophil accumulation and free
radical generation, suggesting a therapeutic potential in reducing
secondary injury after SAH in patients.”
SUBARACHNOID HEMORRHAGE, OXIDATIVE STRESS - Alpha Lipoic Acid, ALA
Reference: “Alpha Lipoic Acid Alleviates Oxidative Stress and
Preserves Blood Brain Permeability in Rats with Subarachnoid
Hemorrhage,”
------------------
Dietary supplementation with (R)-alpha-lipoic acid reverses the
age-related accumulation of iron and depletion of antioxidants in the
rat cerebral cortex.
Suh JH, Moreau R, Heath SH, Hagen TM.
Department Biochemistry and Biophysics, Linus Pauling Institute,
Oregon State University, Corvallis, Oregon 97331, USA.
Accumulation of divalent metal ions (e.g. iron and copper) has been
proposed to contribute to heightened oxidative stress evident in
aging and neurodegenerative disorders.
To understand the extent of iron accumulation and its effect on
antioxidant status, we monitored iron content in the cerebral cortex
of F344 rats by inductively coupled plasma atomic emission
spectrometry (ICP-AES) and found that the cerebral iron levels in
24-28-month-old rats were increased by 80% (p<0.01) relative to
3-month-old rats.
Iron accumulation correlated with a decline in glutathione (GSH) and
the GSH/GSSG ratio, indicating that iron accumulation altered
antioxidant capacity and thiol redox state in aged animals.
Because (R)-alpha-Lipoic acid (LA) is a potent chelator of divalent
metal ions in vitro and also regenerates other antioxidants, we
monitored whether feeding LA (0.2% [w/w]; 2 weeks) could lower
cortical
iron and improve antioxidant status.
Results show that cerebral iron levels in old LA-fed animals were
lower when compared to controls and were similar to levels seen in
young rats.
Antioxidant status and thiol redox state also improved markedly in
old LA-fed rats versus controls.
These results thus show that LA supplementation may be a means to
modulate
the age-related accumulation of cortical iron content, thereby
lowering oxidative stress associated with aging.
PMID: 15829111
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://tinyurl.com/634q5a
Man Is A Herbivore!
http://tinyurl.com/4rq595
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk
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