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PubMed1997

Combined differential lung ventilation and inhaled nitric oxide therapy in the management of unilateral pulmonary contusion.

Unilateral pulmonary contusion after blunt thoracic trauma can prove to be a devastating injury. Regional disturbances in blood flow and alveolar ventilation can significantly alter pulmonary function. We present a case report of unilateral pulmonary contusion that resulted in significant pulmonary dysfunction. This patient was successfully managed with multimodality therapy consisting of differential lung ventilation and inhaled nitric oxide. The effect of nitric oxide applied to the "normal" lung, the "injured" lung, and both lungs is described. The use of inhaled nitric oxide was associated with an increase in oxygenation when applied to the normal or both lungs. The use of nitric oxide in conjunction with differential lung ventilation appeared to offer benefit in this patient with severe unilateral pulmonary contusion.

Adult↗
PubMed2004

Cardiac troponin I as a predictor of arrhythmia and ventricular dysfunction in trauma patients with myocardial contusion.

BACKGROUND: Myocardial contusion during blunt chest trauma is common and may lead to potentially fatal cardiac complications. Therefore, it is useful to identify a serum marker reflecting the myocardial damage that can predict risk for cardiac complications. In this study, the authors determined the strength of the association between cardiac troponin I (cTnI) levels and the risk of arrhythmia or the development of left ventricular dysfunction in a cohort of patients with blunt chest trauma. METHODS AND RESULTS: In 187 multiply injured patients with blunt chest trauma, serial measurements of cTnI, total creatine kinase (CK), and isoenzyme of creatine kinase with muscle and brain subunits (CK-MB) were combined with sequential electrocardigraphic and echocardiographic recordings. The results showed that 63 patients (34%) had myocardial contusion, as defined by positive cTnI levels, of which 47 (25%) were symptomatic and 16 (9%) showed no abnormalities. The remaining 124 patients (66%) displaying negative CTnI levels were asymptomatic during the entire study. Severity of arrhythmia correlated directly with increase in cTnI levels. The levels of cTnI in the symptomatic group remained elevated significantly longer than the levels in the asymptomatic group. The depression of left ventricular ejection fraction was inversely correlated with the increase in cTn levels. The patients whose cTnI levels were below 1.05 microg/L at admission and during the first 6 hours afterward showed no cardiac abnormalities throughout the entire study period CONCLUSIONS: Levels of cTnI below 1.05 microg/L in asymptomatic patients at admission and within the first 6 hours after admission rule out myocardial injury, whereas positive cTn levels above 1.05 microg/L mandate further cardiologic workup for the detection and management of myocardial injury. Furthermore, the dynamics and peak levels of pathologic cTnI levels allow estimation of arrhythmia risk and left ventricular dysfunction in trauma patients with myocardial contusion.

Adolescent↗
PubMed2006

Macrophages and neurons are targets of retinoic acid signaling after spinal cord contusion injury.

The physiological reactions after spinal cord injury are accompanied by local synthesis of the transcriptional activator retinoic acid (RA). RA exerts its effects by binding to retinoic acid receptors (RAR) which heterodimerize with retinoid X receptors (RXR) and then act as ligand-activated transcription factors. To identify possible cellular targets of RA we investigated protein levels and cellular distribution of retinoid receptors in the rat spinal cord at 4, 7, 14 and 21 days after a contusion injury. In the nonlesioned spinal cord, immunoreactivity for RARalpha, RXRalpha, RXRbeta and RXRgamma was localized in the cytosol of neurons, that of RXRalpha and RXRbeta in astrocytes and that of RARalpha, RXRalpha and RXRgamma in some oligodendrocytes. After contusion injury RARalpha and all RXRs appeared in the cell nuclei of reactive microglia and macrophages. This nuclear staining began at 4 days, was most prominent at 7 and 14 days and had decreased at 21 days after injury. A similar nuclear translocation was also observed for the RARalpha, RXRalpha and RXRbeta staining in neurons situated around the border of the contusion. These observations suggest that RA participates as a signal for the physiological responses of microglia and neurons after CNS injury.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMedDate not supplied

The effect of anabolic steroids and corticosteroids on healing of muscle contusion injury.

The effect of an anabolic steroid (nandrolone decanoate, 20 mg/kg) and a corticosteroid (methylprednisolone acetate, 25 mg/kg) on healing muscle injured with a drop-mass technique in a reproducible muscle contusion injury model in the rat was studied. Healing was determined by measuring active contractile tension in each muscle and histologic analysis. At day 2, the corticosteroid group showed significant improvement in both twitch and tetanic strength relative to the controls. At day 7, this effect was reversed and the corticosteroid muscles were significantly weaker than the control muscles, but there was still no significant effect seen in the anabolic steroid group. At day 14, the corticosteroid muscles were totally degenerated, with disorganized muscle fiber architecture. The anabolic steroid muscles were significantly stronger in twitch, and a similar trend was seen in tetanus relative to control muscles. The results indicate that in an animal model corticosteroids may be beneficial in the short term, but they cause irreversible damage to healing muscle in the long term, including disordered fiber structure and a marked diminution in force-generating capacity. Anabolic steroids may aid in the healing of muscle contusion injury to speed the recovery of force-generating capacity. Although anabolic steroids are considered renegade drugs, they may have an ethical clinical application to aid healing in severe muscle contusion injury, and their use in the treatment of muscle injuries warrants further research.

Anabolic Agents↗
PubMed2000

Induction of Fos protein immunoreactivity by spinal cord contusion.

The objective of the present study was to identify neurons in the central nervous system that respond to spinal contusion injury in the rat by monitoring the expression of the nuclear protein encoded by the c-fos gene, an activity-dependent gene, in spinal cord and brainstem regions. Rats were anesthetized with urethane and the injury was produced by dropping a 5-g weight from 20.0 cm onto the exposed dura at the T10-L1 vertebral level (contusion group). The spinal cord was exposed but not lesioned in anesthetized control animals (laminectomy group); intact animals were also subjected to anesthesia (intact control). Behavioral alterations were analyzed by Tarlov/Bohlman scores, 2 h after the procedures and the animals were then perfused for immunocytochemistry. The patterns of Fos-like immunoreactivity (FLI) which were site-specific, reproducible and correlated with spinal laminae that respond predominantly to noxious stimulation or injury: laminae I-II (outer substantia gelatinosa) and X and the nucleus of the intermediolateral cell column. At the brain stem level FLI was detected in the reticular formation, area postrema and solitary tract nucleus of lesioned animals. No Fos staining was detected by immunocytochemistry in the intact control group. However, detection of FLI in the group submitted to anesthesia and surgical procedures, although less intense than in the lesion group, indicated that microtraumas may occur which are not detected by the Tarlov/Bohlman scores. There is both a local and remote effect of a distal contusion on the spinal cord of rats, implicating sensory neurons and centers related to autonomic control in the reaction to this kind of injury.

Animals↗
PubMed1995

Focal ischemia due to traumatic contusions documented by stable xenon-CT and ultrastructural studies.

A traumatic cerebral contusion causes a zone of perifocal neuronal necrosis, the cause of which is not known; the surgical management of these lesions remains controversial. To determine the pathophysiological mechanisms responsible for brain damage after contusions, the authors performed cerebral blood flow (CBF) mapping studies and related these to change in local cerebral blood volume (CBV) and ultrastructure. In 11 severely head injured patients with contusion, CBF and CBV were measured in pericontusional areas using stable xenon-computerized tomography (CT). These studies demonstrated a profound reduction in perilesional CBF (mean 17.5 +/- 4 ml/100 g/min), which was always accompanied by a zone of edema defined by CT density measurements. Mean CBV in these regions was 2.3 +/- 0.4 ml/100 g, a reduction to approximately one-half the value of 4.8 ml/100 g found in the nonedematous regions, and to approximately 35% of the value of 6.0 ml/100 g found in normal volunteers. Ultrastructural analysis of the pericontusional tissue, taken at surgery in four patients with high intracranial pressure showed glial swelling with narrowing of the microvascular lumina due to massive podocytic process swelling. Additionally, some suggestion of vascular occlusion due to erythrocyte and leukocyte stasis was seen. These data support the conclusion that microvascular compromise by compression and/or occlusion is a major event associated with profound perilesional hypoperfusion, which is a uniform finding within edematous pericontusional tissue.

Adolescent↗
PubMed1996

Blood-brain barrier breach following cortical contusion in the rat.

Adult Fisher 344 rats were subjected to a unilateral impact to the dorsal cortex above the hippocampus at 3.5 m/second, resulting in a 2-mm cortical depression. This caused severe cortical damage and neuronal loss in hippocampus subfields CA1, CA3, and hilus. Breakdown of the blood-brain barrier (BBB) was assessed by injecting the protein horseradish peroxidase (HRP) 5 minutes prior to or at various times after injury (5 minutes, 1, 3, 6, and 12 hours, 1, 2, 5, and 10 days). Animals were killed 1 hour after HRP injection and brain sections were reacted with diaminobenzidine to visualize extravascular accumulation of the protein. Maximum staining occurred in animals injected with HRP 5 minutes prior to or 5 minutes after cortical contusion. Staining at these time points was observed in the ipsilateral cortex of the impact area and areas adjacent to it, as well as in the ipsilateral hippocampus. Some modest staining occurred in the dorsal contralateral cortex near the superior sagittal sinus. Cortical HRP staining gradually decreased at increasing time intervals postinjury. By 10 days, no HRP staining was observed in any area of the brain. In the ipsilateral hippocampus, HRP staining was absent by 3 hours postinjury and remained so at the 6- and 12-hour time points. Surprisingly, HRP staining was again observed in the ipsilateral hippocampus 1 and 2 days after cortical contusion, indicating a biphasic opening of the BBB following head trauma and a possible second wave of secondary brain damage days after the contusion injury. These data indicate that regions not initially destroyed by cortical impact, but evidencing BBB breach, may be accessible to neurotrophic factors administered intravenously both immediately and days after brain trauma.

Animals↗
PubMed2004

Influence of apoptosis on neurological outcome following traumatic cerebral contusion.

OBJECT: Apoptosis has increasingly been implicated in the pathobiology of traumatic brain injury (TBI). The present study was undertaken to confirm the presence of apoptosis in the periischemic zone (PIZ) of traumatic cerebral contusions and to determine the role of apoptosis, if any, in neurological outcome. METHODS: Brain tissue harvested at Wentworth Hospital from the PIZ in 29 patients with traumatic supratentorial contusions was compared with brain tissue resected in patients with epilepsy. Immunohistochemical analyses were performed on the tissues to see if they contained the apoptosis-related proteins p53, bcl-2, bax, and caspase-3. The findings were then correlated to demographic, clinical, surgical, neuroimaging, and outcome data. In the PIZ significant increases of bax (18-fold; p < 0.005) and caspase-3 (20-fold; p < 0.005) were recorded, whereas bcl-2 was upregulated in only 14 patients (48.3%; 2.9-fold increase) compared with control tissue. Patients in the bcl-2-positive group exhibited improved outcomes at the 18-month follow-up examination despite an older mean age and lower mean admission Glasgow Coma Scale score (p < 0.03). Caspase-3 immunostaining was increased in those patients who died (Glasgow Outcome Scale [GOS] Score 1, 12 patients) when compared with those who experienced a good outcome (GOS Score 4 or 5, 17 patients) (p < 0.005). Regression analysis identified bcl-2-negative status (p < 0.04, odds ratio [OR] 5.5; 95% confidence interval [CI] 1.1-28.4) and caspase-3-positive status (p < 0.01, OR 1.4, 95% CI 1.1-1.8) as independent predictors of poor outcome. No immunostaining for p53 was recorded in the TBI specimens. CONCLUSIONS: The present findings confirm apoptosis in the PIZ of traumatic cerebral contusions and indicate that this form of cell death can influence neurological outcome following a TBI.

Adolescent↗
PubMed2005

Olfactory glia transplantation into cervical spinal cord contusion injuries.

OBJECT: The results of olfactory ensheathing cell (OEC) transplantation have raised great expectations as a potential treatment for spinal cord injury (SCI). Its capacity to promote functional neural repair, however, remains unclear. The authors studied axonal growth and locomotor recovery after C-7 contusion injury and OEC transplantation in adult rats. METHODS: Twenty-four male Wistar rats underwent a mild C-7 contusion injury that completely disrupted the dorsal corticospinal tract (DCST). In 14 rats OECs were transplanted into the lesion, and 10 were used as controls. At 3 months postcontusion, the kinematics of locomotion were assessed, and the CST was traced by injecting dextran tetramethylrhodamine bilaterally into the cerebral cortex. The animals were killed 2 weeks after tracer injection, and their spinal cords were studied immunohistochemically. Although the survival of transplanted cells varied, they were present in all cases. The authors observed neither OEC migration nor DCST axon regeneration in any of the cell transplant-treated rats. Corticospinal axons ended in retraction bulbs at the proximal edge of the lesion or, exceptionally, a few micrometers inside the transplant. The results of neurofilament immunohistochemical analysis provided evidence of neurites from systems other than the DCST growing into the transplant, but in some cases these neurites formed loops of pathological appearance. Contusion injury of C-7 caused chronic locomotor deficits that did not improve after OEC transplants. CONCLUSIONS: The findings in this study indicate that OEC transplants alone are not sufficient for neural repair and functional recovery after SCI. In addition, OECs can induce abnormal axonal growth, making further studies necessary before considering their clinical use.

Animals↗
PubMed2004

Development of a rat model of graded contusive spinal cord injury using a pneumatic impact device.

An animal model of spinal cord trauma is essential for understanding the injury mechanisms, cord regeneration, and to aid the development of new therapeutic modalities. This study focused on the development of a graded experimental contusion model for spinal cord injury (SCI) using a pneumatic impact device made in Korea. A contusive injury was made to the dorsal aspect of the cord. Three trauma groups were defined according to the impact velocity (IV). A control group (n=6), received laminectomy only. Group 1 (n=10), 2 (n=10), and 3 (n=10) had IVs of 1.5 m/sec, 2.0 m/sec, and 3.5 m/sec respectively. Functional assessments were made up to the 14th day after injury. The cord was removed at the 14th postinjury day and prepared for histopathologic examination. Significant behavioral and histopathological abnormalities were found in control and each trauma group. All trauma groups showed severe functional impairment immediately after injury but following different rates of functional recovery (Fig. 5). As the impact velocity and impulse increased, the depth of contusive lesion revealed to be profound the results show that the rat model reproduces spinal cord lesions consistently, has a distinctive value in assessing the effects of impact energy.

Animals↗
PubMed2000

Chemokine antagonist infusion attenuates cellular infiltration following spinal cord contusion injury in rat.

Spinal cord injury is accompanied by an initial inflammatory reaction followed by secondary injury that is caused, in part, by apoptosis. Recruitment of leukocytes from the blood compartment to the site of inflammation in the injured spinal cord has been attributed to locally generated chemotactic agents (cytokines and chemokines). In addition to upregulation in the message levels of a number of chemokines, we have found up-regulation in the message levels of several chemokine receptors following spinal cord contusion injury. To reduce the inflammatory response after spinal cord injury, we have blocked the interaction of chemokine receptors with their ligands using the vMIPII chemokine antagonist. Using a rat model of spinal cord contusion injury, we show that continuous infusion of the antagonist for up to 7 days results in a decrease in infiltrating hematogenous cells at the site of injury. Histological evaluation ofthe tissue showed fewer activated macrophages at the site of injury. Concomitantly, reduced neuronal loss and gliosis were observed in the antagonist infused spinal cord. In addition, increased expression of Bcl-2 gene, an endogenous inhibitor of apoptosis, was seen in the antagonist infused spinal cord at 7 days post injury. Morphologically, staining with the bisbenzamide dye Hoechst 33342 showed significantly more apoptotic bodies in the vehicle compared to antagonist infused spinal cord. Our data suggest that chemokine antagonist infusion post-injury results in limiting the inflammatory response following spinal cord contusion injury, thereby attenuating neuronal loss, possibly due to decreased apoptosis. These findings support the contention that disrupting chemokine interactions with their receptors may be an effective approach in reducing the secondary damage after spinal cord injury.

Animals↗
PubMed1999

[Headache as the consequence of brain concussion and contusion in closed head injuries in children].

The most frequent type of head injury in children is closed head trauma with brain concussion or contusion, and headache is the dominant complaint of early and late postinjury period. Because of scant number of studies on the problem of occurrence, characteristics and persistence of posttraumatic headache this study was undertaken in a group of 100 children (29 girls and 71 boys), aged 3-14 years old, 90 after brain concussion and 10 after contusion. Children with a history of injuries, central nervous system infections, with headaches before injury and chronic diseases were excluded. In 9 cases linear skull fracture was present after injury. The material was examined within one week after trauma, and then after 3, 6, and 12 months. After 3 months EEG was performed and repeated after 6 and 12 months in children with persistent headache or those without headache but with abnormal EEG results in the first examination. According to the additional diagnostic examinations, I excluded other causes of headache, besides head injury. In my observation 83% of children had headache after brain concussion and contusion. The majority--56%--had acute posttraumatic headache, but 27% of children complained of chronic headache, mainly tension type headache. Only 3% had migraine. In 21% of all group of 100 children, I noticed the headache persisting during the whole year of my observation. The important risk factor for the occurrence of posttraumatic headache were the age of child at the moment injury and the period of unconsciousness. The electroencephalographic recording still remains the important additional examination of posttraumatic consequences.

Acute Disease↗
PubMed2001

[Contusion eye traumas: etiology, clinical characteristics and final results].

PURPOSE: Examination of the aetiology, clinical characteristics and the final results for contusion traumas of the eyeball. MATERIAL AND METHODS: Retrospective examination of the clinical documentation for 247 patients (260 eyes of which 219 male and 41 female), treated in Emergency Eye Clinic during the period 1994-1996. The patients are separated in groups by their age. DISCUSSION AND RESULTS: Contusion traumas are more frequent in children and men aged up to 50 years old. The traumas are caused by different factors but these having housework and criminal character prevail. The eyeball is with not damaged entity in 225 eyes (86.54%) and with damaged entity in 35 eyes (13.46%). Injuries in both eyes are observed in 11 patients. The clinical characteristics show simultaneous injury of the front protection elements and the eyeball. More often all tissues and areas of the eye are damaged. Serious damages in the area of iris-lens diaphragm, vitreous and retina are observed. The final visual acuity in 178 eyes (68.48%) is between 20/40 and 20/20. CONCLUSION: The contusion traumas are more frequent in children and young men. The traumas caused by factors having housework and criminal character prevail. Usually all tissues and areas of the eye are damaged. The final visual acuity of the most of the eyes is between 20/40 and 20/20.

Adolescent↗
PubMed2001

[Study on the expression of fibronectin after cerebral contusion in rats for timing of injuries].

An experimental model of reproducible focal cerebral contusions in rats was made by a free-drop impacting right hemisphere. The expression of fibronectin and its mRNA after cerebral contusion were detected respectively by immunohistochemical staining and in situ hybridization. Results indicated that the expression of fibronectin and its mRNA increased after injury, and there existed a relationship between increased fibronectin and its mRNA and different intervals after brain injury. It is inferred that the expression of fibronectin and its mRNA can be used for timing of brain injuries and distinguishing antemortem and postmortem brain contusions.

Animals↗
PubMed2000

[A study of HSP70 and NF in brain contusion timing].

The changes of HSP70 and NF after brain contusion were studied by the immunohistochemistry method. HSP70 and NF were seen at 30 min after injury around the wound area, but faded away after 12-24 h. The result suggests that these two proteins could be used to estimate brain contusion time, to diagnose brain wound and to distinguish antemortem and postmortem brain contusion.

Animals↗
PubMed2000

[The changes of GFAP and PCNA after human brain contusion: an immunohistochemical study in forensic pathology].

In order to find out changes of GFAP and PCNA after human brain trauma, samples of 38 cases were studied by the immunnohistochemistry method combined with quantitative image analysis. The gray degree and area of PCNA positive cells increased to the maximum at the 4th day and then decreased gradually. GFAP positive cells began to increase significantly 12 hours after contusion, reached the maximum at the 4th day and stayed in high level until the 7th day. These results suggest that: (1) GFAP, PCNA show regular changes with survival time after brain contusion; (2) GFAP and PCNA can be used as time markers of brain contusion from 2-20 days.

Adult↗
PubMed2000

[Study on histology and the expression of Bax and Bcl-2 after cerebral contusion in rats].

To set up the experimental model of focal cerebral contusions in rats, and to study the histology and the expression of Bax and Bcl-2 after cerebral catusions. It was found that neurons and astrocytes around the wound area were changed morphologically and that polymorphonuclear leucocytes were present at 12-24 h after injury. A lot of foamy cells and astrocytes having a big dark nucleus appeared around the wound area on the 4th day after injury. On the 8-10th day, liquefaction necrosis was seen in areas of contusions. On the 12-14th day, the contusion focus healed up and became cystiform or glial node. Meantime, lots of astrocytes, capillary vessel and hemosiderin were observed. The expression of Bax and Bcl-2 increased after injury. There existed a relationship between increased Bax/Bcl-2 and different intervals after brain injury.

Animals↗
PubMed2003

[A study on the relationship between the expression of apoptosis-related gene and the injury time in earlier period following cerebral contusion].

OBJECTIVE: To investigate the relationship between the expressive variety of apoptosis-related gene Bcl-2, Fas and the brain injury time during earlier period after cerebral contusion. METHODS: The morphologia feature of brain tissue was observed under microscopy and immunohistochemistry, image analyze technique was applied to detected the expression of Bcl-2 and Fas. RESULTS: Typical apoptotic cells were seen 8 hours after cerebral contusion. The expression of apoptosis-related gene was noted after 30 minutes and keep increase subsequently. The expression of Bcl-2 reached maximum level at 4 hours after brain trauma and then declined. CONCLUSION: Detecting the expression of Bcl-2 and Fas would be of valuable in the distinguishment of promortem and postmortem injury, and the estimation of brain injury time during the earlier period after cerebral contusion.

Animals↗