The effect of age on outcome following traumatic brain injury in rats

1991 ◽  
Vol 75 (6) ◽  
pp. 916-921 ◽  
Author(s):  
Robert J. Hamm ◽  
Larry W. Jenkins ◽  
Bruce G. Lyeth ◽  
Daphne M. White-Gbadebo ◽  
Ronald L. Hayes
Keyword(s):  
Traumatic Brain Injury ◽  
Heart Rate ◽  
Brain Injury ◽  
Young Adult ◽  
Mortality Rate ◽  
Neurological Deficits ◽  
Acute Hypertension ◽  
Fluid Percussion ◽  
Age Related ◽  
Related Increase

✓ Age of the patient is one of the most important predictors of outcome following human traumatic brain injury. This study employs the fluid-percussion model to investigate the effects of aging on outcome following traumatic brain injury in rats. The results revealed that there was an age-associated increase in mortality rate following both low (1.7 to 1.8 atm) and moderate (2.00 to 2.25 atm) levels of traumatic brain injury. Age-related changes in systemic physiological, neurological, and histopathological indexes of brain injury were also examined following a low level of traumatic brain injury. Traumatic brain injury produced equivalent acute hypertension and increased plasma glucose levels in both young adult and aging rats. Injury produced an acute increase in heart rate in the young adult rat group, while the heart rate decreased in the aged rats. At low levels of brain injury, no significant gross histopathological alterations were produced in either age group. Neurological outcome was assessed by measuring the duration of suppression of a number of nonpostural and postural reflexes and more complex somatomotor functions (righting, escape, head support). Except for head support, there was a significant age-related increase in the duration of the suppression of these reflexes following brain injury. These data demonstrate that aging is associated with an increased mortality rate and greater acute neurological deficits following traumatic brain injury. These data also demonstrate the usefulness of the fluid-percussion model for studying the mechanisms responsible for the age-related increase in vulnerability to brain injury.

Abstract W P260: Role of the Prostaglandin E2 EP1 Receptor in Traumatic Brain Injury

Stroke ◽  
2015 ◽  
Vol 46 (suppl_1) ◽  
Author(s):  
Alexander V Glushakov ◽  
Jawad A Fazal ◽  
Shuh Narumiya ◽  
Sylvain Dore
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Young Adult ◽  
Brain Injuries ◽  
Neurological Deficits ◽  
Cortical Lesions ◽  
Brain Pathology ◽  
Adult Mice ◽  
Ep1 Receptor

Introduction: Brain injuries promote upregulation of so-called proinflammatory prostaglandin E2 leading to overactivation of a class of its cognate G-protein coupled receptors, notably EP1, which is considered as a promising target for treatment of ischemic stroke and, possibly, other neurological disorders involving excitotoxicity. However, our recent data suggest that of EP1 receptor in intracerebral hemorrhage may play a protective role. The goal of this study was to investigate a translational potential of EP1 receptor for treatment of traumatic brain injury (TBI). Methods: The acute brain injury was induced using controlled cortical impact (CCI) in wildtype (WT) and genetic EP1 receptor knockout mice (EP1-/-). Neurological deficit scores (NDS) and anatomical brain pathology were accessed at 48h after injury. Results: CCI resulted in significant cortical lesions, localized hippocampal edema and neurological deficits compared to animals from sham group underwent craniotomy only. The NDS after CCI were significantly higher in older mice (7-11mo) compared to young adult animals (2-4mo) in both WT and EP1-/- groups. Treatment with a selective antagonist SC-51089 with repeated doses of 20-100μg/kg after CCI had no significant effects on cortical lesions, hippocampal edema and NDS in young adult mice of both WT and EP1-/- genotypes. Post-treatment with 17-pt-PGE2 (300μg/kg) had no significant effects on anatomical brain pathology in young adult mice, but improved NDS at 24h in WT but not in EP1-/- mice. Immunohistochemistry revealed significant increases in GFAP and Iba1 immunoreactivity in selected brain regions surrounding injury suggesting astrogliosis and microglia activation. EP1 receptor knockout had no effects on GFAP and Iba1 expression in young adult mice, whereas lead to a significant attenuation of GFAP immunoreactivity in older mice. Conclusions: This study provides, for the first time, a clarification on the role of EP1 receptor in a preclinical model of contusive TBI. The results suggest that EP1 receptor might be involved in complex pathways differentially associated with neurological deficits. In addition, this study provides further clarification on clinical use of EP1 receptor ligands for treatment of acute brain injuries.

Possible protective effect of endogenous opioids in traumatic brain injury

1990 ◽  
Vol 72 (2) ◽  
pp. 252-261 ◽  
Author(s):  
Ronald L. Hayes ◽  
Bruce G. Lyeth ◽  
Larry W. Jenkins ◽  
Richard Zimmerman ◽  
Tracy K. McIntosh ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Body Weight ◽  
Brain Injury ◽  
Endogenous Opioids ◽  
Neurological Deficits ◽  
Content Type ◽  
Fluid Percussion ◽  
Fluid Percussion Injury ◽  
Drug Treatments

✓ Naloxone (0.1, 1.0, or 20.0 mg/kg), morphine (1.0 or 10.0 mg/kg), or saline was administered systemically intraperitoneally to rats 15 minutes prior to moderate fluid-percussion brain injury. The effects of the drugs were measured on systemic physiological, neurological, and body-weight responses to injury. The animals were trained prior to injury and were assessed for 10 days after injury on body-weight responses and neurological endpoints. Low doses of naloxone (0.1 or 1.0 mg/kg) significantly exacerbated neurological deficits associated with injury. Morphine (10.0 mg/kg) significantly reduced neurological deficits associated with injury. The drugs had no effect on neurological measures or body weight in sham-injured animals. Drug treatments did not significantly alter systemic physiological responses to injury. Data from these experiments suggest the involvement of endogenous opioids in at least some components of neurological deficits following traumatic brain injury and suggest the possibility that at least some classes of endogenous opioids may protect against long-term neurological deficits produced by fluid-percussion injury to the rat.

scholarly journals THE EFFECT OF A TRAUMATIC BRAIN INJURY ON CHANGES IN THE HEART RATE OF RATS SUBJECT TO VARIOUS MODES OF MOTOR ACTIVITY

2021 ◽  
Vol 10 (4) ◽  
pp. 3310-3315
Author(s):  
Bulat Ildarovich Vakhitov
Keyword(s):  
Traumatic Brain Injury ◽  
Heart Rate ◽  
Brain Injury ◽  
Motor Activity ◽  
Heart Rate Response ◽  
Age Groups ◽  
Preschool Age ◽  
Pronounced Increase ◽  
Age Related ◽  
First Time

For the first time, studies have been conducted to study the reaction of animal heart rate to various modes of motor activity after a traumatic brain injury. It was revealed that on the first day after modeling an open head injury in rats of all age groups, a pronounced increase in heart rate was observed. In this case, the smallest heart rate response to brain injury is observed in animals of immature age. It was found that the implementation of systematic dynamic exercises by animals of mature and preschool age after modeling a craniocerebral injury contributes to a significant decrease in heart rate. A more pronounced formation of training bradycardia is observed in immature animals. It was revealed that limiting motor activity and performing isometric exercises after a traumatic brain injury maintain heart rate at an increased level in all age groups of animals and significantly inhibits the natural, age-related decrease in heart rate in immature animals.

AGE-RELATED INCREASE IN PROTEIN KINASE B (AKT) AFTER PEDIATRIC TRAUMATIC BRAIN INJURY

2002 ◽  
Vol 30 (Supplement) ◽  
pp. A7
Author(s):  
Yi-Chen Lai ◽  
P M Kochanek ◽  
P M Shore ◽  
K Janesko ◽  
H Bayir ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Protein Kinase ◽  
Protein Kinase B ◽  
Pediatric Traumatic Brain Injury ◽  
Age Related ◽  
Related Increase

scholarly journals Rhein Protects Against Neurological Deficits After Traumatic Brain Injury in Mice via Inhibiting Neuronal Pyroptosis

2020 ◽  
Vol 11 ◽  
Author(s):  
Fangfang Bi ◽  
Huaifen Ma ◽  
Chen Ji ◽  
Cuicui Chang ◽  
Wenbo Liu ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neurological Deficits

scholarly journals Traumatic Brain Injury and the Importance of Neurosurgical Care: 10-year Retrospective Study on Cadavers

Folia Medica ◽  
2020 ◽  
Vol 62 (1) ◽  
pp. 105-111 ◽  
Author(s):  
Alexandrina Nikova ◽  
Ivaylo Dimitrov ◽  
Theodossios Birbilis ◽  
Lora Zaharieva
Keyword(s):  
Health Care ◽  
Traumatic Brain Injury ◽  
Retrospective Study ◽  
Brain Injury ◽  
Mortality Rate ◽  
Brain Injuries ◽  
Common Type ◽  
Quick Response ◽  
Male Predominance ◽  
Transport Accidents

Objective: Traumatic brain injury (TBI) due to transport accidents is a serious cause of death and disability. In every case, however, quick response and a proper health care are required.   Materials and methods: We collected 10-year data retrospectively from the laboratory of forensic science and toxicology in Montana, Bulgaria with the intention to show the importance of neurosurgical care in the traumatology and its connection to mortality rate.   Results: 124 cadavers were included with significant male predominance. The data analysis shows that the mortality rate at the hospitals without neurosurgical facilities and the mortality at the scene of the accident is the same for traffic brain injuries. Furthermore, we found that the age has no correlation with the mortality rate.   Conclusion: Road injuries are the most common type of brain injury. We believe that the outcome of these TBIs depends on the availability of a neurosurgical unit.

Sign in / Sign up

Export Citation Format

Share Document