Brain Injuries ; etiology ; prevention & control ; Humans ; Hyperbilirubinemia ; complications ; prevention & control

OBJECTIVETo investigate the influence of therapeutic bloodletting at Jing-well points and hypothermia on acute cerebral edema after traumatic brain injury (TBI) in rats.

METHODSSeventy-five SD rats were randomly divided into sham-operation group (Sham), TBI group (TBI), bloodletting group (BL), mild-induced hypothermia group (MIH), and bloodletting plus MIH group (BL + MIH) (n = 15). The model of TBI was established by electric controlled cortical impactor (eCCI). The rats of BL group were bloodletting at Jing-well points immediately after injury, twice daily. While the MIH group was settled on a hypothermia blanket promptly after TBI for 6 hours, so that the temperature dropped to 32 degrees. Each of measurement was performed after 48 hours. Magnetic resonance imaging (MRI) was used to evaluate the dynamic impairment of cerebral edema after TBI (n = 3). In addition, mNSS score, measurements of wet and dry brain weight, and Evans Blue assay were performed to investigate the neurologic deficit, cerebral water content (n = 8), and blood-brain barrier permeability (BBB), (n = 4), respectively.

RESULTSMRI analysis showed that the cerebral edema, hematoma and midline shifting of rats in TBI group was more serious than other treatment group. Meanwhile compared with TBI group, the mNSS scores of every treatment group were meaningfully lower (all P < 0.05). Furthermore, treatment with BL+ MIH group was superior to the separated BL and MIH group (all P < 0.01). In addition, brain water content of each intervention group reduced to varying degrees (all P < 0.05), especially that of MIH group and BL + MIH group (P <0.01). BBB permeability of each treatment group was also significantly improved (all P < 0.01), and the improvement in MIH group and BL + MIH group was much better than the BL alone group (P < 0.05, P < 0.01).

CONCLUSIONOur major finding is that bloodletting at Jing-well points and MIH can reduce cerebral edema and BBB dysfunction and exert neuroprotective effects after TBI. The results suggest that the combination of BL and MIH is more effective than other treatment being used alone.

Animals ; Blood-Brain Barrier ; Bloodletting ; Brain ; pathology ; Brain Edema ; prevention & control ; Brain Injuries ; therapy ; Hypothermia, Induced ; Rats ; Rats, Sprague-Dawley

AIMTo investigate the effects of the duration of cerebral ischemic preconditioning(CIP) and interval between CIP and the subsequent ischemic insult on the protection of CIP against delayed neuronal death (DND) in the CA1 hippocampus normally induced by brain ischemic insult.

METHODSFour-vessel occlusion cerebral ischemic model of rats (54) was used. The brain of the rats was sectioned and stained with thionin to show DND in the CA1 hippocampus.

RESULTSNo DND was found in the hippocampus of the rats subjected to sham operation and CIP, in which 3 min cerebral ischemic preconditioning was performed. Obvious destruction of the CA1 hippocampus was found in brain ischemic insult group, in which histological (HG) was 2-3 in 6 min and 10 min ischemia subgroups and grade 3 in 15 min ischemia subgroup. In CIP + brain ischemic insult group, no obvious neuronal damage was found in 3 min-3d-6 min (CIP for 3 min was followed by a brain ischemic insult for 6 min at an interval of 3 d, the same as the following) and 3 min-3 d-10 min groups, indicating that CIP effectively protected neurons of the CA1 hippocampus against DND normally induced by ischemic insult for 6 or 10 min. However, in 3 min-1 d-10 min and 3 min-3 d-15 min groups, the protective effect of CIP was lower than that in the 3 min-3 d-10 min group. The quantitative analysis of the protective effect of CIP on the CA1 hippocampal neurons showed that there was no significant difference in protecting number and protecting index between 3 min-3 d-6 min and 3 min-3 d-10 min groups (P > 0.05). However, the growth index in 3 min-3 d-10 min group was obvious larger than that in 3 min-3 d-6 min (P < 0.05).

CONCLUSIONAlthough the protective effects of CIP in 3 min-3 d-6 min and 3 min-3 d-10 min groups were similar, the protective effect of CIP in 3 min-3 d-10 min group was sensitively found. Maximal protective potential of CIP could be induced when using the time parameters of 3 min-3 d-10 min to establish the model of global cerebral ischemic tolerance.

Animals ; Brain Injuries ; pathology ; prevention & control ; Brain Ischemia ; pathology ; prevention & control ; Cell Death ; Hippocampus ; pathology ; Ischemic Preconditioning ; Male ; Neurons ; pathology ; Rats ; Rats, Wistar ; Time Factors

Mesenchymal stem cell (MSC) transplantation is considered one of the most promising therapeutic strategies for the repair of brain injuries and plays an important role in various links of nerve repair. Recent studies have shown that MSC-derived exosomes may dominate the repair of brain injuries and help to promote angiogenesis, regulate immunity, inhibit apoptosis, and repair the nerves, and therefore, they have a great potential in the treatment of brain injuries in neonates. With reference to these studies, this article reviews the mechanism of action of exosomes in the repair of brain injuries and related prospects and challenges, in order to provide new directions for the treatment of brain injuries in neonates with stem cells.
Apoptosis ; Brain Injuries ; therapy ; Exosomes ; physiology ; Humans ; Inflammation ; prevention & control ; Mesenchymal Stem Cell Transplantation ; Neovascularization, Physiologic ; T-Lymphocytes ; immunology

OBJECTIVEHypokalemia is a frequent complication observed after traumatic brain injury (TBI). We evaluated the effect of spironolactone on preventing hypokalemia following moderate to severe TBI.

METHODSPatients with moderate to severe TBI, whose Glasgow Coma Scale (GCS) scores of 9-12 and less than 9, respectively, were equally randomized into intervention and control groups, matching with severity of trauma and baseline serum level of potassium. For the intervention group, we administrated spironolactone (1 mg/kg per day) on the second day of admission or the first day of gavage tolerance and continued it for seven days. No additional intervention was done for controls. Hypokalemia (mild: 3-3.5 mg/L, moderate: 2.5-3 mg/L, and severe: less than 2.5 mg/L serum K+) and other electrolyte abnormalities were compared between the two groups at the end of the intervention.

RESULTSSixty-eight patients (58 males and 10 females) were included with mean age equal to (33.1+/-11.8) years, and GCS equal to 7.6+/-2.8. The two groups were similar in baseline characteristics. Patients who received spironolactone were significantly less likely to experience mild, moderate, or severe hypokalemia (8.8%, 2.9%, and 0) compared with controls (29.4%, 11.7%, and 2.9%, respectively, P less than 0.05). No significant difference was observed between the two groups in the occurrence of other electrolyte abnormalities, hyperglycemia or oliguria.

CONCLUSIONSpironolactone within the first week of head injury could prevent the occurrence of late hypokalemia with no severe side effects.

Adult ; Brain Injuries ; complications ; Female ; Humans ; Hypokalemia ; prevention & control ; Male ; Middle Aged ; Spironolactone ; adverse effects ; therapeutic use

Glial scar formed by central nervous system (CNS) injury is the main inhibitory barrier of nerve regeneration. How to promote axonal regeneration after injury,how to accelerate neural network reconstruction and how to improve brain function recovery have become a hot problem to be solved in the field of neuroscience. This article focuses on the recent advances of therapeutic strategies for axonal regeneration.
Animals ; Astrocytes ; pathology ; Brain Injuries ; pathology ; physiopathology ; Cicatrix ; prevention & control ; Humans ; Nerve Regeneration ; Neuroglia ; pathology ; Neuronal Plasticity ; physiology ; Neurons ; physiology ; Proteoglycans ; metabolism ; Spinal Cord Injuries ; pathology ; physiopathology

OBJECTIVETo investigate the early effect of thyrotropin-releasing hormone (TRH) on cerebral free radical reactions after acute brain injury in rabbits.

METHODS30 healthy white rabbits were randomly divided into three groups: Group A (n=10), Group B (n=12) and Group C (n=8). The rabbits in Group A and Group B were injured by direct hit. At 0.5-4 hours after injury, the rabbits in Group A were injected with TRH (8 mg/kg body weight) through a vein and the rabbits in Group B were injected with normal saline of equal volume. The rabbits in Group C served as the normal control. Then all the rabbits were killed and brain tissues were obtained. The content of lipoperoxide (LPO), the activity of superoxide dismutase (SOD) and the water content of the brain tissues were measured.

RESULTSThe contents of LPO and water in brain tissues in Group A were lower and the activity of SOD was higher than those of Group B (P<0.05). After injury, intracranial pressure (ICP) rose rapidly and continuously with time passing by. When TRH was given to the animals in Group A, the rising speed of ICP slowed down significantly.

CONCLUSIONSTRH can decrease the cerebral free radical reactions and cerebral edema after acute brain injury in rats.

Animals ; Brain Edema ; etiology ; prevention & control ; Brain Injuries ; complications ; metabolism ; Female ; Free Radicals ; metabolism ; Intracranial Pressure ; Lipid Peroxidation ; Male ; Rabbits ; Superoxide Dismutase ; metabolism ; Thyrotropin-Releasing Hormone ; pharmacology

Our study was designed to determine whether methylprednisolone exerts a beneficial effect after experimental moderate diffuse brain injury and whether this possible beneficial effect is affected by the dosage, the timing of administration, and the methods of treatment. A total of 200 anesthetized adult rats were injured utilizing a weight-drop device through a Plexiglas guide tube. These rats were divided into eight groups: Group 1 (n=35) was assigned to receive no methylprednisolone after impact (control group), Group 2 (n=25) received an initial intraperitoneal administration of methylprednisolone with a dose of 5 mg/kg at 1hour after cranial impact, followed by administration with a maintenance dose of 5 mg/kg/4 hours. Group 3 (n=25), group 5 (n=25), and group 7 (n=20) received an initial 30 mg/kg at 1 hour, 4 hours, and 8 hours, respectively without a maintenance dose. Group 4 (n=25), group 6 (n=25), and group 8 (n=20) received an initial 30 mg/kg at 1 hour, 4 hours, and 8 hours after impact, with a maintenance dose of 15 mg/kg/4 hours. Measured water content of brain tissue expressed the amount of water as the difference between fresh and dry weight. At 48 hours after impact, the water content in group 4 and 6 were significantly lower than group 1. Mean SD was 61.4 0.37% in group 4 (p<0.03), 61.5 0.34% in group 6 (p<0.001), and 63.6 0.48% in group 1. Compared to group 1, the difference was not statistically significant in group 2 (p>0.1), group 3 (p>0.5), group 5 (p>0.6), group 7 (p>0.1), and group 8 (p>0.5). Groups treated with mega dose before 4hours after head injury, including maintenance dose, showed beneficial effects. Our study suggests that the efficacy of methylprednisolone in head injury was related to the dosage, the timing of administration, and method of treatment.
Animal ; Brain Edema/prevention | control* ; Brain Injuries/drug therapy* ; Dose-Response Relationship, Drug ; Injections, Intraperitoneal ; Methylprednisolone/therapeutic use* ; Neuroprotective Agents/therapeutic use* ; Rats ; Rats, Sprague-Dawley

OBJECTIVE: To detect the impact of artificial cerebrospinal fluid lavage time on the edema of traumatic brain injury. METHODS: A total of 240 SD rats were randomly divided into a sham group, a traumatic brain injury model group, 3 artificial cerebrospinal fluid lavage groups (3 h, 6 h and 9 h). Each group was divided into 4 sub-groups by time of sacrifice namely 12 h, 1 d, 3 d and 7 d postoperatively. We detected the content of brain water, sodium, and potassium, and the VEGF expression to confirm whether the duration of lavage could reduce the traumatic brain edema. RESULTS: Compared with the sham group and the traumatic brain injury model group, brain water content and sodium content were decreased, while the potassium content and the VEGF levels were increased in the artificial cerebrospinal fluid lavage groups. Significant difference was found at 12 h, 1 d, and 3 d after the injury (P<0.05). With the increase of artificial cerebrospinal fluid lavage time, the difference was more obvious. CONCLUSION Artificial cerebrospinal fluid lavage can reduce the brain edema after traumatic brain injury. The longer the lavage, the more obvious the effect.
Animals ; Brain Edema ; etiology ; prevention & control ; Brain Injuries ; complications ; Cerebrospinal Fluid ; Male ; Osmosis ; Pharmaceutical Solutions ; therapeutic use ; Rats ; Rats, Sprague-Dawley ; Therapeutic Irrigation ; methods

With the increasing incidence of blast injury, the research on its mechanisms and protective measures draws more and more attention. Blast injury has many characteristics different from general war injuries or trauma. For example, soldiers often have various degrees of visceral injury without significant surface damage, combined injuries and arterial air embolism. Researchers in China began to investigate blast injury later than the United States and Sweden, but the development is so fast that lots of achievements have been gained, including the development of biological shock tube, the mechanisms and characteristics of blast injury in various organs, as well as protective measures under special environments. This article reviews the past and current situation of blast injury research in China.
Animals ; Blast Injuries ; diagnosis ; etiology ; prevention & control ; therapy ; Brain Injuries, Traumatic ; etiology ; China ; Disease Models, Animal ; Ear ; injuries ; Eye Injuries ; etiology ; High-Energy Shock Waves ; Humans ; Lung Injury ; etiology ; Research