Effects of hypothermia on thrombin-induced brain edema formation

Kawai, Nobuyuki; Kawanishi, Masahiko; Okauchi, Masanobu; Nagao, Seigo

doi:10.1016/s0006-8993(01)02026-1

Cited by 58 publications

(36 citation statements)

References 29 publications

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“…In this regard, we have previously shown that edema formation is delayed after striatal excitotoxicity in the aged rat brain [23], which may possibly be related to a reduction in BBB permeability [58], and is certainly related to the reduced neutrophil infiltration reported in this study. Neutrophils have been implicated in the generation of vasogenic cerebral edema and may play a role in BBB breakdown [59].…”

Section: Aged-induced Changes In Neutrophil Densitysupporting

confidence: 57%

Decreased myeloperoxidase expressing cells in the aged rat brain after excitotoxic damage

Campuzano¹,

Castillo-Ruiz²,

Acarín³

et al. 2011

Experimental Gerontology

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Brain aging is associated to several morphological and functional alterations that influence the evolution and outcome of CNS damage. Acute brain injury such as an excitotoxic insult induces initial tissue damage followed by associated inflammation and oxidative stress, partly attributed to neutrophil recruitment and the expression of oxidative enzymes such as myeloperoxidase (MPO), among others. However, to date, very few studies have focused on how age can influence neutrophil infiltration after acute brain damage. Therefore, to evaluate the age-dependent pattern of neutrophil cell infiltration following an excitotoxic injury, intrastriatal injection of Nmethyl-D-aspartate was performed in young and aged male Wistar rats. Animals were sacrificed at different times between 12 hours post-lesion (hpl) to 14 days post-lesion (dpl). Cryostat sections were processed for myeloperoxidase (MPO) immunohistochemistry, and double labeling for either neuronal cells (NeuN), astrocytes (GFAP), perivascular macrophages (ED-2), or microglia/macrophages (tomato lectin histochemistry). Our observations showed that MPO+ cells were observed in the injured striatum from 12 hpl (when maximum values were found) until 7 dpl, when cell density was strongly diminished. However, at all survival times analyzed, the overall density of MPO+ cells was lower in the aged versus the adult injured striatum. MPO+ cells were mainly identified as neutrophils (especially at 12 hpl and 1 dpl), but it should be noted that MPO+ neurons and microglia/macrophages were also found. MPO+ neurons were most commonly observed at 12 hpl and reduced in the aged. MPO+ microglia/macrophages were the main population expressing MPO from 3 dpl, when density was also reduced in aged subjects.These results point to neutrophil infiltration as another important factor contributing to the different response of the adult and aged brain to damage, highlighting the need of using aged animals for the study of acute agerelated brain insults.

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Section: Aged-induced Changes In Neutrophil Densitysupporting

confidence: 57%

Decreased myeloperoxidase expressing cells in the aged rat brain after excitotoxic damage

Campuzano¹,

Castillo-Ruiz²,

Acarín³

et al. 2011

Experimental Gerontology

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“…Ruan et al (2008) suggested that activated microglia could release neurotoxic substances and inflammatory factors to cause inflammatory injury to brain tissue. Kawai et al (2001) showed that the directional injection of thrombin into the rat brain could generate apparent encephaledema, cause inflammation, and induce apoptosis.…”

Section: Introductionmentioning

confidence: 99%

Effects of thrombin on the secondary cerebral injury of perihematomal tissues of rats after intracerebral hemorrhage

Liu¹,

Shi²,

Zhou³

2014

Genet. Mol. Res.

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ABSTRACT. This study aimed to investigate the effects of thrombin released in hematoma after intracerebral hemorrhage (ICH) on the cerebral injury of perihematomal tissues and to evaluate the protection effect of hirudin on the cerebral injury after ICH. We used the autologous uncoagulated blood injection method to prepare the ICH rat model, and all rats were randomly divided into a normal group, an ICH group, or a hirudin group. At different time points, rat heads were cut to harvest brain sections. Immunohistochemical staining, histochemical staining, and hematoxylin and eosin staining were conducted for CD34, microglia, and neutrocytes. CD34-positive microvessels were most abundant in brain tissues of the sham-operation group. At 12 h after ICH, CD34 expression reduced and reached the minimum level at 72 h (P < 0.01). At 6 h after ICH, microglia expression was visible and reached a peak at 48 h (P < 0.01). At 12 h after ICH, neutrocyte infiltration was visible and the number was greatest at 48 h (P < 0.01). The early application of hirudin after ICH could significantly reduce microglia and neutrocyte expression and could significantly slow down the CD34 decrease trend (P < 0.01). However, hirudin application in the edematization stage after ICH did not significantly increase CD34-positive microvessel abundance (P > 0.05). A thrombin-mediated inflammatory reaction is involved in the cerebral injury after ICH, and the early application of hirudin has a protective effect.

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“…This edema -termed perihemorrhagic edema -has been associated with poor outcomes (22,23,25). Data from animal models of ICH suggest that hypothermia can improve these injurious processes, but not outcomes (27)(28)(29)(30)(31)(32)(33).…”

Section: Therapeutic Hypothermia For Intracerebral Hemmorhagementioning

confidence: 99%

Hypothermia for Intracerebral Hemorrhage, Subarachnoid Hemorrhage & Spinal Cord Injury

Tannehill¹

2013

Therapeutic Hypothermia in Brain Injury

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Effects of hypothermia on thrombin-induced brain edema formation

Cited by 58 publications

References 29 publications

Decreased myeloperoxidase expressing cells in the aged rat brain after excitotoxic damage

Decreased myeloperoxidase expressing cells in the aged rat brain after excitotoxic damage

Effects of thrombin on the secondary cerebral injury of perihematomal tissues of rats after intracerebral hemorrhage

Hypothermia for Intracerebral Hemorrhage, Subarachnoid Hemorrhage & Spinal Cord Injury

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