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PubMed1995

The effect of the treatment of high-dose methylprednisolone on Na(+)-K(+)/Mg(+2) ATPase activity and lipid peroxidation and ultrastructural findings following cerebral contusion in rat.

BACKGROUND: Although use of corticosteroid in the management of head trauma has caused a great deal of controversy, corticosteroids have long been an adjunct in the management of severe closed head injury. The glucocorticoid steroid methylprednisolone (MP) has been proven to have significant antioxidant effect when administered in an antioxidant-high dose after central nervous system injury. METHODS: The sodium-potassium activated and magnesium dependent adenosine-5'-triphosphatase (Na(+)-K(+)/Mg(+2) ATPase EC.3.6.1.3.) activity, lipid peroxidation, and early ultrastructural findings were determined during the immediate posttraumatic period in rats. Mechanical brain injury was produced when a calibrated weight-drop device is allowed to fall on the skull's convexity over the right hemisphere, 1 to 2 mm lateral from the midline. In group I, rats were used to determine Na(+)-K(+)/Mg(+2) ATPase activity, the extent of lipid peroxidation, by measuring the level of malondialdehyde content and normal ultrastructural findings in two different brain areas (cerebral cortex and brain stem). In group II, physiologic saline was administered right after trauma in the same amount as methylprednisolone. In group III rats, methylprednisolone (30 mg/kg) was administered intravenously right after trauma. RESULTS: Na(+)-K(+)/Mg(+2) ATPase activity significantly decreased in the cerebral cortex and in brain stem within 2 hours after trauma (p < 0.05). There was significant difference in malondialdehyde content between groups II and III (p < 0.05). Methylprednisolone treatment reduced malondialdehyde content and induced the recovery of Na(+)-K(+)/Mg(+2) activity. CONCLUSIONS: These data suggest that inactivation of Na(+)-K(+)/Mg(+2) ATPase is closely correlated to changes of lipid peroxidation and the alteration of the ultrastructural findings in the early phases after head trauma. The glucocorticoid steroid methylprednisolone has been proven to have significant effect in activation of Na(+)-K(+)/Mg(+2) ATPase with significant reduction of malondialdehyde content.

Animals↗
PubMed2005

Co-expression of radial glial marker in macrophages/microglia in rat spinal cord contusion injury model.

Macrophages/microglia are implicated in spinal cord injury but their precise role in the process is not clear. Our previous studies have reported that radial glia (RG) possess properties of neural stem cells and remerged after central nervous system (CNS) injury which may play an important role in neural repair and regeneration. In the present study, we examined the expression of ED1 (a specific marker for activated macrophages/microglia) and RG in a spinal cord injury (SCI) model and detected the activation at 1, 4, 8, and 12 weeks in both dorsal funiculus and ventral white matter after SCI. For both ED1-positive cells and RG cells, there was a gradual increase in density and in number from 1 to 4 weeks followed by down-regulation up to 12 weeks after injury. The morphologies of macrophages and radial glia were different. However, some ED1-positive cells were also stained by RG marker. These results suggest that macrophages may have some lineage to radial glial cells.

Animals↗
PubMed2006

Injury severity determines Purkinje cell loss and microglial activation in the cerebellum after cortical contusion injury.

Clinical evidence suggests that the cerebellum is damaged after traumatic brain injury (TBI) and experimental studies have validated these observations. We have previously shown cerebellar vulnerability, as demonstrated by Purkinje cell loss and microglial activation, after fluid percussion brain injury. In this study, we examine the effect of graded controlled cortical impact (CCI) injury on the cerebellum in the context of physiologic and anatomical parameters that have been shown by others to be sensitive to injury severity. Adult male rats received mild, moderate, or severe CCI and were euthanized 7 days later. We first validated the severity of the initial injury using physiologic criteria, including apnea and blood pressure, during the immediate postinjury period. Increasing injury severity was associated with an increased incidence of apnea and higher mortality. Severe injury also induced transient hypertension followed by hypotension, while lower grade injuries produced an immediate and sustained hypotension. We next evaluated the pattern of subcortical neuronal loss in response to graded injuries. There was significant neuronal loss in the ipsilateral cortex, hippocampal CA2/CA3, and laterodorsal thalamus that was injury severity-dependent and that paralleled microglial activation. Similarly, there was a distinctive pattern of Purkinje cell loss and microglial activation in the cerebellar vermis that varied with injury severity. Together, these findings emphasize the vulnerability of the cerebellum to TBI. That a selective pattern of Purkinje cell loss occurs regardless of the type of injury suggests a generalized response that is a likely determinant of recovery and a target for therapeutic intervention.

Animals↗
PubMed2006

Increase in bFGF-responsive neural progenitor population following contusion injury of the adult rodent spinal cord.

The number of neural progenitor cells, especially nestin+ cells or BrdU-uptake cells is sparse in the normal adult rodent spinal cord. However, in the present study, we show that after spinal cord injury (SCI), many ordinarily quiescent cells were activated to become nestin+ and undergo mitosis (BrdU+) in the ependymal layer as well as in the parenchyma of the spinal cord. Nestin+ cells and BrdU+ cells were in most cases immunohistochemically GFAP+, some of which displayed radial glial cell morphology and partly participated in the border formation of the lesion. The culturing of injured rat spinal cord tissues generated more neurospheres earlier than did the culturing of intact tissues, and these neurosphere cells were multipotent and bFGF-responsive. Immunohistochemical analysis showed that there existed many bFGF+ cells after SCI, the number of which were almost 15 times greater than that in an intact spinal cord. Increased bFGF production after SCI might activate quiescent progenitor cells, and thus initiate their cell proliferation. Finally, SCI to the nestin-promoter green fluorescent protein (GFP) transgenic mice showed broad proliferation of progenitor cells that were induced in the injured spinal cord. The culturing of injured spinal cord tissues from these transgenic mice provides direct evidence that neurospheres can be generated by SCI-activated nestin+ cells. Thus, the activation of bFGF-responsive progenitor cells and the concomitant increase in the population of bFGF+ cells following SCI might be beneficial for spinal cord repair if these progenitor cells are properly manipulated.

Animals↗
PubMed2004

Allopregnanolone and progesterone decrease cell death and cognitive deficits after a contusion of the rat pre-frontal cortex.

We compared the effects of three different doses of allopregnanolone (4, 8 or 16 mg/kg), a metabolite of progesterone, to progesterone (16 mg/kg) in adult rats with controlled cortical impact to the pre-frontal cortex. Injections were given 1 h, 6 h and every day for 5 consecutive days after the injury. One day after injury, both progesterone-treated (16 mg/kg) and allopregnanolone (8 or 16 mg/kg)-treated rats showed less caspase-3 activity, and rats treated with allopregnanolone (16 mg/kg) showed less DNA fragmentation in the lesion area, indicating reduced apoptosis. Nineteen days after the injury, rats treated with progesterone and allopregnanolone (8 or 16 mg/kg) showed no difference in necrotic cavity size but had less cell loss in the medio-dorsal nucleus of the thalamus and less learning and memory impairments compared with the injured vehicle-treated rats. On that same day the injured rats treated with progesterone showed more weight gain compared with the injured rats treated with the vehicle. These results can be taken to show that progesterone and allopregnanolone have similar neuroprotective effects after traumatic brain injury, but allopregnanolone appears to be more potent than progesterone in facilitating CNS repair.

Animals↗
PubMed2004

[Contusive retinal detachment: a retrospective review of 48 patients].

PURPOSE: Analysis of the epidemiological, clinical and therapeutic characteristics of retinal detachment after ocular blunt trauma. MATERIAL AND METHODS: We retrospectively reviewed 48 patients with isolated retinal detachment after ocular blunt trauma, studying their epidemiological characteristics (age, sex and trauma circumstances), their clinic details and the surgical techniques used. RESULTS: The average age of our patients was 39.3 Years; most were male (75%). Assault and home accidents were the most common cause of ocular trauma (83.2%). Total retinal detachment was noted in 47.9%. Of the retinal breaks found, dialysis at the ora serrata was observed in 22%, atrophic holes in 33.9%, retinal breaks in 40.6% and giant tears in 4.2%. Most of the breaks were situated at the lower temporal quadrant. Forty one out of the 48 patients were operated on, with surgical treatment consisting in episcleral surgery in 38 cases and vitreoretinal surgery in three cases. Complete anatomical success was achieved in 92.7%. CONCLUSION: This survey shows that the prognosis of retinal detachment after ocular blunt trauma remains favorable given the young age and the absence of advanced vitreoretinal proliferation, but this should not affect the importance of prevention.

Accidents, Home↗
PubMed2004

Blunt thoracic trauma: flail chest, pulmonary contusion, and blast injury.

Blunt thoracic trauma can result in significant morbidity in injured patients. Both chest wall and the intrathoracic visceral injuries can lead to life-threatening complications if not anticipated and treated. Pain control, aggressive pulmonary toilet, and mechanical ventilation when necessary are the mainstays of supportive treatment. The elderly with blunt chest trauma are especially at risk for pulmonary deterioration in the several days postinjury and should be monitored carefully regardless of their initial presentation. Blunt thoracic trauma is also a marker for associated injuries, including severe head and abdominal injuries.

Accidents, Traffic↗
PubMed2003

Magnetic resonance imaging and pathological findings in a cat with brain contusions.

Necropsy was performed on a mongrel male cat of unknown age weighing 1.3 kg, which probably encountered a traffic accident. Gross pathological examination of the brain revealed reddish colour of the right cerebral hemisphere and haemorrhages on the surface of the right frontal lobe to temporal lobe. Histologically, there was diffuse vacuolation in the cortex of the right frontal lobe and extensive haemorrhages in the base of brain. These histopathological findings were consistent with areas of abnormal signals found on post-mortem magnetic resonance imaging (MRI). In this study, the MRI findings were identical to that reported in human cases of head trauma as well as histopathological changes.

Animals↗
PubMed2001

Myocardial contusion presented as acute myocardial infarction after chest trauma.

A 46-year-old male patient developed an acute myocardial infarction and congestive heart failure following blunt chest trauma. Electrocardiogram (ECG) revealed acute anterior myocardial infarction. Echocardiography showed akinesis of interventricular septum, dyskinesis in apical anterior wall, and severe impairment of left ventricular overall systolic function. Coronary angiography revealed normal coronary arteries. The patient followed a low-intensity physical medicine rehabilitation program. Follow-up was without new complications or deterioration of congestive heart failure. Five months later the patient presented with fulminant acute pulmonary edema and cardiogenic shock. Cardiopulmonary resuscitation was unsuccessful.

Coronary Angiography↗
PubMed2002

Increased protein oxidation and decreased creatine kinase BB expression and activity after spinal cord contusion injury.

Traumatic injury to the spinal cord triggers several secondary effects, including oxidative stress and compromised energy metabolism, which play a major role in biochemical and pathological changes in spinal cord tissue. Free radical generation and lipid peroxidation have been shown to be early events subsequent to spinal cord injury. In the present study, we demonstrated that protein oxidation increases in rat spinal cord tissue after experimental injury. As early as h after injury, the level of protein carbonyls at the injury epicenter was significantly higher than in control (169%, p < 0.05) and increased gradually over the next 4 weeks to 1260% of control level. Both caudal and rostral parts of the injured spinal cord demonstrated a mild increase of protein carbonyls by 4 weeks postinjury (135-138%, p < 0.05). Immunocytochemical analysis of protein carbonyls in the spinal cord cross-sections showed increased protein carbonyl immunoreactivity in the epicenter section compared to rostral and caudal sections of the same animal or control laminectomy animals. Increased protein carbonyl formation in damaged spinal cord tissue was associated with changes in activity and expression of an oxidative sensitive enzyme, creatine kinase BB, which plays an important role in the maintenance of ATP level in the CNS tissue. Damage to CK function in the CNS may severely aggravate the impairment of energy metabolism. The results of our study indicate that events associated with oxidative damage are triggered immediately after spinal cord trauma but continue to occur over the subsequent 4 weeks. These results suggest that antioxidant therapeutic strategies may be beneficial to lessen the consequences of the injury and potentially improve the restoration of neurological function.

Animals↗
PubMed2004

Post-trauma administration of caffeine plus ethanol reduces contusion volume and improves working memory in rats.

It has been demonstrated that ethanol exerts dose-dependent effects, both beneficial and detrimental, on the outcome of traumatic brain injury (TBI). Recently, it has been reported that co-administration of caffeine (10 mg/kg) and a low amount of alcohol (0.65 g/kg; caffeinol) reduces cortical infarct volume up to 80%, and improves motor coordination, following a rodent model of reversible common carotid/middle cerebral artery occlusion. However, the protective effects of caffeinol following other CNS insults, nor its influence on cognitive function, have been examined. Using a controlled cortical impact model of brain injury, the effect of caffeinol administration on TBI-associated motor and cognitive deficits was assessed. When given 15 min following injury, caffeinol reduced cortical tissue loss and improved working memory. However, no influence on motor skills, Morris water maze performance or associative learning and memory was observed. Delayed administration (6 h post-injury) of caffeinol containing a dose of ethanol (1 g/kg) previously demonstrated to improve motor performance eliminated the working memory benefit and cortical protection. These results indicate that early administration of caffeinol may be beneficial in lessening some of the deficits and cortical tissue loss associated with brain trauma.

Animals↗
PubMed2005

Telemetric monitoring of corpus spongiosum penis pressure in conscious rats for assessment of micturition and sexual function following spinal cord contusion injury.

Disruption of bladder function and sexual reflexes are major complications following spinal cord injury (SCI). We examined the use of telemetric monitoring of corpus spongiosum penis (CSP) pressures for assessment of micturition and erectile events following SCI in rats. Pressure catheters were implanted in the bulb of the CSP of seven male Long-Evans hooded rats, subjected to a standardized weight drop SCI (10 g x 12.5 mm) at T10. CSP pressures were analyzed for spontaneously occurring micturition and erectile events, and during ex copula reflex erection tests until 25 days after SCI. Urine volume was determined until 21 days after SCI. Results show initial loss of bladder function after SCI with gradual return of reflex micturition. When compared to baseline (BL), micturition pressure characteristics after SCI included prolonged duration, increased area under the curve (AUC), increased mean pressures, increased number of pressure peaks, and increased peak frequency. At 21 days after SCI, the urine volume per micturition was significantly increased. The number of full erectile events decreased significantly following SCI. Pressure wave analyses demonstrated increased AUC, increased maximum pressures, increased suprasystolic peak duration, increased AUC of the suprasystolic peaks, and increased maximum pressures of the suprasystolic peaks during recovery. The number of partial erectile events decreased significantly following SCI. Ex copula reflex erection testing demonstrated significantly decreased latency. The study demonstrates that telemetric monitoring of CSP pressures in conscious rats is a valuable and reliable method for assessing recovery of autonomic function following SCI.

Animals↗