Oxaloacetate-treatment caused a significant reduction of brain water content after closed head trauma

Abstract The present study was designed to test the effectiveness of furosemide in reducing cerebral edema due to closed head trauma. A Remington Humane Stunner was used to deliver blows to the heads of anesthetized cats. Impacted animals were divided into three groups: (a) trauma, no drug, and ad lib. fluid intake after head injury; (b) trauma, no drug, and standardized fluid intake (0.9% NaCl; 10 ml/Ib/day); and (c) trauma, furosemide (3 mg/lb/day), and standardized fluid intake. For the treated cats, we began furosemide therapy 1 hour after head injury and used three intramuscular injections/day. The animals were killed 48 hours after head trauma. From animals with unilateral contusion, we took bilateral white matter samples from five points along the centrum semiovale and tested for edema using density determinations with an organic density gradient. Serum electrolytes, blood urea nitrogen, and weight were determined before the cats were impacted and before they were killed. All impacted animals demonstrated weight loss. Density data showed a normal water content for white matter in the uncontused hemispheres of all impacted cats. Contused hemispheres showed a significant decrease in density (increase in brain water content) for both treated and untreated cats. In the furosemidetreated animals, however, the brain edema was significantly less than that found in the untreated groups. Analysis of data from individual brain sections of furosemide-treated animals suggested a reduction in the spread of edema fluid 48 hours after head injury.

Download Full-text

Effects of Pharmacological Dose of Dexamethasone Given Postnatally on Blood-Brain Barrier Permeability and Brain Water Content

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.2002.282.2.r632 ◽

2002 ◽

Vol 282 (2) ◽

pp. R632-R633

Author(s):

P. Temesvári k. Lazics f. Domoki f. Bari

Keyword(s):

Water Content ◽

Blood Brain Barrier ◽

Brain Barrier ◽

Brain Water Content ◽

Barrier Permeability ◽

Blood Brain Barrier Permeability ◽

Blood Brain ◽

Brain Barrier Permeability ◽

Brain Water

Download Full-text

Ulinastatin alleviates traumatic brain injury by reducing endothelin-1

Translational Neuroscience ◽

10.1515/tnsci-2021-0001 ◽

2020 ◽

Vol 12 (1) ◽

pp. 001-008

Author(s):

Ting Liu ◽

Xing-Zhi Liao ◽

Mai-Tao Zhou

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Western Blot ◽

Water Content ◽

Brain Edema ◽

Rat Model ◽

Neurosurgical Procedures ◽

Brain Water Content ◽

The Brain ◽

Brain Water

Abstract Background Brain edema is one of the major causes of fatality and disability associated with injury and neurosurgical procedures. The goal of this study was to evaluate the effect of ulinastatin (UTI), a protease inhibitor, on astrocytes in a rat model of traumatic brain injury (TBI). Methodology A rat model of TBI was established. Animals were randomly divided into 2 groups – one group was treated with normal saline and the second group was treated with UTI (50,000 U/kg). The brain water content and permeability of the blood–brain barrier were assessed in the two groups along with a sham group (no TBI). Expression of the glial fibrillary acidic protein, endthelin-1 (ET-1), vascular endothelial growth factor (VEGF), and matrix metalloproteinase 9 (MMP-9) were measured by immunohistochemistry and western blot. Effect of UTI on ERK and PI3K/AKT signaling pathways was measured by western blot. Results UTI significantly decreased the brain water content and extravasation of the Evans blue dye. This attenuation was associated with decreased activation of the astrocytes and ET-1. UTI treatment decreased ERK and Akt activation and inhibited the expression of pro-inflammatory VEGF and MMP-9. Conclusion UTI can alleviate brain edema resulting from TBI by inhibiting astrocyte activation and ET-1 production.

Download Full-text

FGF10 Attenuates Experimental Traumatic Brain Injury through TLR4/MyD88/NF-κB Pathway

Cells Tissues Organs ◽

10.1159/000511381 ◽

2021 ◽

pp. 1-9

Author(s):

Qinhan Hou ◽

Hongmou Chen ◽

Quan Liu ◽

Xianlei Yan

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Protein Expression ◽

Water Content ◽

Neurological Deficit ◽

Neuronal Apoptosis ◽

Neuronal Damage ◽

Intraventricular Injection ◽

Brain Water Content ◽

Brain Water

Traumatic brain injury (TBI) can induce neuronal apoptosis and neuroinflammation, resulting in substantial neuronal damage and behavioral disorders. Fibroblast growth factors (FGFs) have been shown to be critical mediators in tissue repair. However, the role of FGF10 in experimental TBI remains unknown. In this study, mice with TBI were established via weight-loss model and validated by increase of modified neurological severity scores (mNSS) and brain water content. Secondly, FGF10 levels were elevated in mice after TBI, whereas intraventricular injection of Ad-FGF10 decreased mNSS score and brain water content, indicating the remittance of neurological deficit and cerebral edema in TBI mice. In addition, neuronal damage could also be ameliorated by stereotactic injection of Ad-FGF10. Overexpression of FGF10 increased protein expression of Bcl-2, while it decreased Bax and cleaved caspase-3/PARP, and improved neuronal apoptosis in TBI mice. In addition, Ad-FGF10 relieved neuroinflammation induced by TBI and significantly reduced the level of interleukin 1β/6, tumor necrosis factor α, and monocyte chemoattractant protein-1. Moreover, Ad-FGF10 injection decreased the protein expression level of Toll-like receptor 4 (TLR4), MyD88, and phosphorylation of NF-κB (p-NF-κB), suggesting the inactivation of the TLR4/MyD88/NF-κB pathway. In conclusion, overexpression of FGF10 could ameliorate neurological deficit, neuronal apoptosis, and neuroinflammation through inhibition of the TLR4/MyD88/NF-κB pathway, providing a potential therapeutic strategy for brain injury in the future.

Download Full-text

Quantitation of Photochemically Induced Focal Cerebral Ischemia in the Rat

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.1988.11 ◽

1988 ◽

Vol 8 (1) ◽

pp. 89-95 ◽

Cited By ~ 77

Author(s):

John J. Grome ◽

Gerlinde Gojowczyk ◽

Wolfgang Hofmann ◽

David I. Graham

Keyword(s):

Cerebral Ischemia ◽

Water Content ◽

Rose Bengal ◽

Tissue Damage ◽

Focal Cerebral Ischemia ◽

Ischemic Damage ◽

Brain Water Content ◽

Ischemic Insult ◽

Ischemic Lesion ◽

Brain Water

This study was carried out with a recently developed model of focal cerebral ischemia in the rat based on the photochemical induction of thrombotic stroke using the dye Rose Bengal. We examined the change in the volume of the lesion and brain water content, in separate groups of rats, at different times (1, 4, 24, 72, and 168 h) after the induction of the ischemic lesion. The volume of ischemic damage increased rapidly between 1 and 24 h after the ischemic insult and decreased between 24 and 168 h. The lesion at 168 h was significantly larger than that following 1 h of ischemia and similar to that obtained at 4 h, suggesting that the maximum extent of tissue damage (without the involvement of significant edema) was reached within the first 4 h in this model. The enlargement of the lesion after 4 h correlated closely with changes in brain water content.

Download Full-text