The effects of decompressive craniectomy on cerebral blood flow volume and brain metabolism in different aged patients with severe traumatic brain injury

Objective To explore effects of decompressive craniectomy on cerebral blood flow volume and brain metabolism in different aged patients with severe traumatic brain injury. Methods 71 cases were divided into three groups according age: group A( 【 30 years) ,group B ( 30 ～ 50 years) 。

Pulsed arterial spin labeling effectively and dynamically observes changes in cerebral blood flow after mild traumatic brain injury

Cerebral blood flow is strongly associated with brain function, and is the main symptom and diagnostic basis for a variety of encephalopathies. However, changes in cerebral blood flow after mild traumatic brain injury remain poorly understood. This study sought to observe changes in cerebral blood flow in different regions after mild traumatic brain injury using pulsed arterial spin labeling. Our results demonstrate maximal cerebral blood flow in gray matter and minimal in the white matter of patients with mild traumatic brain injury. At the acute and subacute stages, cerebral blood flow was reduced in the occipital lobe, parietal lobe, central region, subcutaneous region, and frontal lobe. Cerebral blood flow was restored at the chronic stage. At the acute, subacute, and chronic stages, changes in cerebral blood flow were not apparent in the insula. Cerebral blood flow in the temporal lobe and limbic lobe diminished at the acute and subacute stages, but was restored at the chronic stage. These findings suggest that pulsed arterial spin labeling can precisely measure cerebral blood flow in various brain regions, and may play a reference role in evaluating a patient＇s condition and judging prognosis after traumatic brain injury.

Characteristics of traumatic brain injury models:from macroscopic blood flow changes to microscopic mitochondrial changes

Controlled cortical impingement is a widely accepted method to induce traumatic brain injury to establish a traumatic brain injury animal model.A strike depth of 1 mm at a certain speed is recommended for a moderate brain injury and a depth of>2 mm is used to induce severe brain injury.However,the different effects and underlying mechanisms of these two model types have not been proven.This study investigated the changes in cerebral blood flow,differences in the degree of cortical damage,and differences in motor function under different injury parameters of 1 and 2 mm at injury speeds of 3,4,and 5 m/s.We also explored the functional changes and mitochondrial damage between the 1 and 2 mm groups in the acute(7 days)and chronic phases(30 days).The results showed that the cerebral blood flow in the injured area of the 1 mm group was significantly increased,and swelling and bulging of brain tissue,increased vascular permeability,and large-scale exudation occurred.In the 2 mm group,the main pathological changes were decreased cerebral blood flow,brain tissue loss,and cerebral vasospasm occlusion in the injured area.Substantial motor and cognitive impairments were found on day 7 after injury in the 2 mm group;at 30 days after injury,the motor function of the 2 mm group mice recovered significantly while cognitive impairment persisted.Transcriptome sequencing showed that compared with the 1 mm group,the 2 mm group expressed more ferroptosis-related genes.Morphological changes of mitochondria in the two groups on days 7 and 30 using transmission electron microscopy revealed that on day 7,the mitochondria in both groups shrank and the vacuoles became larger;on day 30,the mitochondria in the 1 mm group became larger,and the vacuoles in the 2 mm group remained enlarged.By analyzing the proportion of mitochondrial subgroups in different groups,we found that the model mice had different patterns of mitochondrial composition at different time periods,suggesting that the difference in the degree of damage among traumatic brain injury groups may reflect the mitochondrial changes.Taken together,differences in mitochondrial morphology and function between the 1 and 2 mm groups provide a new direction for the accurate classification of traumatic brain injury.Our results provide reliable data support and evaluation methods for promoting the establishment of standard mouse controlled cortical impingement model guidelines.

Reduction of epinephrine in the lumbar spinal cord following repetitive blast-induced traumatic brain injury in rats

Traumatic brain inju ry-induced unfavorable outcomes in human patients have independently been associated with dysregulated levels of monoamines,especially epinephrine,although few preclinical studies have examined the epinephrine level in the central nervous system after traumatic brain injury.Epinephrine has been shown to regulate the activities of spinal motoneurons as well as increase the heart rate,blood pressure,and blood flow to the hindlimb muscles.Therefore,the purpose of the present study was to determine the impact of repeated blast-induced traumatic brain injury on the epinephrine levels in seve ral function-s pecific central nervous system regions in rats.Following three repeated blast injuries at 3-day intervals,the hippocampus,motor cortex,locus coeruleus,vestibular nuclei,and lumbar spinal cord were harvested at post-injury day eight and processed for epinephrine assays using a high-sensitive electrochemical detector cou pled with high-performance liquid chromatography.Our results showed that the epinephrine levels were significantly decreased in the lumbar spinal cord tissues of blast-induced traumatic brain injury animals compared to the levels detected in age-and sex-matched sham controls.In other function-specific central nervous system regions,although the epinephrine levels were slightly altered following blast-induced tra u matic brain injury,they were not statistically significant.These results suggest that blast injury-induced significant downregulation of epinephrine in the lumbar spinal cord could negatively impact the motor and cardiovascular function.This is the first repo rt to show altered epinephrine levels in the spinal cord following repetitive mild blast-induced traumatic brain injury.

Neuroprotection of hyperbaric oxygen therapy in sub-acute traumatic brain injury:not by immediately improving cerebral oxygen saturation and oxygen partial pressure

Although hyperbaric oxygen （HBO） therapy can promote the recovery of neural function in patients who have suffered traumatic brain injury （TBI）, the underlying mechanism is unclear. We hypothesized that hyperbaric oxygen treatment plays a neuroprotective role in TBI by increasing regional transcranial oxygen saturation （rSO2） and oxygen partial pressure （PaO2）. To test this idea, we compared two groups： a control group with 20 healthy people and a treatment group with 40 TBI patients. The 40 patients were given 100% oxygen of HBO for 90 minutes. Changes in rSO2 were measured. The controls were also examined for rSO2 and PaO2, but received no treatment, rSO2 levels in the patients did not differ significantly after treatment, but levels before and after treatment were significantly lower than those in the control group. PaO2 levels were significantly decreased after the 30-minute HBO treatment. Our findings suggest that there is a disorder of oxygen metabolism in patients with sub-acute TBI. HBO does not immediately affect cerebral oxygen metabolism, and the underlying mechanism still needs to be studied in depth.

Effects of pituitary adenylate cyclase activating polypeptide on CD4^+/CD8^+T cell levels after traumatic brain injury in a rat model

BACKGROUND： The effect of pituitary adenylate cyclase activating polypeptide （PACAP） during traumatic brain injury （TBI） and whether it can modulate secondary injury has not been reported previously. The present study evaluated the potential protective effects of ventricular infusion of PACAP in a rat model of TBI.METHODS： Male Sprague Dawley rats were randomly divided into 3 treatment groups （n=6, each）： sham-operated, vehicle （normal saline）＋TBI, and PACAP＋TBI. Normal saline or PACAP （1 μg/5 μL） was administered intracerebroventricularly 20 minutes before TBI. Right parietal cortical contusion was produced via a weight-dropping method. Brains were extracted 24 hours after trauma. Histological changes in brains were examined by HE staining. The numbers of CD4＋ and CD8＋ T cells in blood and the spleen were detected via flow cytometry.RESULTS： In injured brain regions, edema, hemorrhage, inflammatory cell infiltration, and swollen and degenerated neurons were observed under a light microscope, and the neurons were disorderly arrayed in the hippocampi. Compared to the sham group, average CD4＋ CD8＋ lymphocyte counts in blood and the spleen were significantly decreased in rats that received TBl＋vehicle, and CD4- CD8＋ were increased. In rats administered PACAP prior to TBI, damage was attenuated as evidenced by significantly increased CD4＋, and decreased CD8＋, T lymphocytes in blood and the spleen.CONCLUSION： Pretreatment with PACAP may protect against TBI by influencing periphery T cellular immune function.

A brief report on MRI investigation of experimental traumatic brain injury

Traumatic brain injury is a major cause of death and disability. This is a brief report based on a symposium presentation to the 2014 Chinese Neurotrauma Association Meeting in San Francisco, USA. It covers the work from our laboratory in applying multimodal MRI to study experimental traumatic brain injury in rats with comparisons made to behavioral tests and histology. MRI protocols include structural, perfusion, manganese-enhanced, diffusion-tensor MRI, and MRI of blood-brain barrier integrity and cerebrovascular reactivity.

Protective effects of dl-3n-butylphthalide against diffuse brain injury

DI-3n-butyiphthalide can effectively treat cerebral ischemia; however, the mechanisms underlying the effects of dl-3n-butylphthalide on microcirculation disorders following diffuse brain injury remain unclear. In this study, models of diffuse brain injury were established in Sprague-Dawley rats with the vertical impact method. DI-3n-butylphthalide at 80 and 160 mg/kg was given via intraperitoneal injection immediately after diffuse brain injury. Ultrastructural changes in the cerebral cortex were observed using electron microscopy. Cerebral blood flow was measured by laser Doppler flowmetry, vascular density was marked by tannic acid-ferric chloride staining, vascular permeability was es- timated by the Evans blue method, brain water content was measured using the dry-wet method, and rat behavior was measured by motor function and sensory function tests. At 6, 24, 48, and 72 hours after administration of dl-3n-butylphthalide, reduced cerebral ultrastructure damage, in- creased vascular density and cerebral blood flow, and improved motor and sensory functions were observed. Our findings demonstrate that dl-3n-butylphthalide may have protective effects against diffuse brain injury by ameliorating microcirculation disorder and reducing blood-brain barrier dam- age and cerebral edema.

Magnetic resonance imaging and cell-based neurorestorative therapy after brain injury

Restorative cell-based therapies for experimental brain injury, such as stroke and traumatic brain injury,substantially improve functional outcome. We discuss and review state of the art magnetic resonance imaging methodologies and their applications related to cell-based treatment after brain injury. We focus on the potential of magnetic resonance imaging technique and its associated challenges to obtain useful new information related to cell migration, distribution, and quantitation, as well as vascular and neuronal remodeling in response to cell-based therapy after brain injury. The noninvasive nature of imaging might more readily help with translation of cell-based therapy from the laboratory to the clinic.

Bloodletting Puncture at Hand Twelve Jing-Well Points Relieves Brain Edema after Severe Traumatic Brain Injury in Rats via Inhibiting MAPK Signaling Pathway

Objective:To investigate whether blood-brain barrier(BBB)served a key role in the edema-relief effect of bloodletting puncture at hand twelve Jing-well points(HTWP)in traumatic brain injury(TBI)and the potential molecular signaling pathways.Methods:Adult male Sprague-Dawley rats were assigned to the shamoperated(sham),TBI,and bloodletting puncture(bloodletting)groups(n=24 per group)using a randomized number table.The TBI model rats were induced by cortical contusion and then bloodletting puncture were performed at HTWP twice a day for 2 days.The neurological function and cerebral edema were evaluated by modified neurological severity score(mNSS),cerebral water content,magnetic resonance imaging and hematoxylin and eosin staining.Cerebral blood flow was measured by laser speckles.The protein levels of aquaporin 4(AQP4),matrix metalloproteinases 9(MMP9)and mitogen-activated protein kinase pathway(MAPK)signaling were detected by immunofluorescence staining and Western blot.Results:Compared with TBI group,bloodletting puncture improved neurological function at 24 and 48 h,alleviated cerebral edema at 48 h,and reduced the permeability of BBB induced by TBI(all P<0.05).The AQP4 and MMP9 which would disrupt the integrity of BBB were downregulated by bloodletting puncture(P<0.05 or P<0.01).In addition,the extracellular signal-regulated kinase(ERK)and p38 signaling pathways were inhibited by bloodletting puncture(P<0.05).Conclusions:Bloodletting puncture at HTWP might play a significant role in protecting BBB through regulating the expressions of MMP9 and AQP4 as well as corresponding regulatory upstream ERK and p38 signaling pathways.Therefore,bloodletting puncture at HTWP may be a promising therapeutic strategy for TBI-induced cerebral edema.

Effects of intestinal mucosal blood flow and motility on intestinal mucosa

AIM： To investigate the role of intestinal mucosal blood flow （IMBF） and motility in the damage of intestinal mucosal barrier in rats with traumatic brain injury. METHODS： Sixty-four healthy male Wistar rats were divided randomly into two groups： traumatic brain injury （TBI） group （n = 32）, rats with traumatic brain injury; and control group （n = 32）, rats with sham-operation. Each group was divided into four subgroups （n = 8） as 6, 12, 24 and 48 h after operation. Intestinal motility was measured by the propulsion ratio of a semi-solid colored marker （carbon-ink）. IMBF was measured with the laser-Doppler technique. Endotoxin and D-xylose levels in plasma were measured to evaluate the change of intestinal mucosal barrier function following TBI. RESULTS： The level of endotoxin was significantly higher in TBI group than in the control group at each time point （0.382 ± 0.014 EU/mL vs 0.102 ± 0.007 EU/mL, 0.466 ± 0.018 EU/mL vs 0.114 ± 0.021 EU/mL, 0.478± 0.029 EU/mL vs 0.112 ±- 0.018 EU/mL and 0.412± 0.036 EU/mL vs 0.108 ±0.011 EU/mL, P 〈 0.05）. D-xylose concentrations in plasma in TBI group were significantly higher than in the control group （6.68 ± 2.37 mmol/L vs 3.66 ±1.07 retool/L, 8.51 ± 2.69 mmol/L vs 3.15 ＋ 0.95 mmol/L, 11.68 ±3.24 mmol/L vs 3.78 ± 1.12 mmol/L and 10.23 ± 2.83 mmol/L vs 3.34 ± 1.23 mmol/L, P 〈 0.05）. The IMBF in TBI group was significantly lower than that in the control group （38.5 ± 2.8 PU vs 45.6 ± 4.6 PU, 25.2 ± 3.1 PU vs 48.2 ± 5.3 PU, 21.5 ± 2.7 PU vs 44.9 ± 2.8 PU, 29. 4 ± 3.8 PU vs 46.7 ± 3.2 PU） （P 〈 0.05）. Significant decelerations of intestinal propulsion ratio in T8I groups were found compared with the control group （0.48% ± 0.06% vs 0.62%± 0.03%, 0.37% ±0.05% vs 0.64% ± 0.01%, 0.39% ± 0.07% vs 0.63% =1= 0.05% and 0.46% ± 0.03% vs 0.65% ± 0.02%） （P 〈 0.05）. CONCLUSION： The intestinal mucosal permeability is increased obviously in TBI rats. Decrease of intestinal motility and IMBF occur early in TBI, both are important pathogenic factors for stress-related damage of the intestinal mucosal barrier in TBI.

How does the motor relearning program improve neurological function of brain ischemia monkeys?

The motor relearning program can significantly improve various functional disturbance induced by ischemic cerebrovascular diseases. However, its mechanism of action remains poorly understood. In injured brain tissues, glial fibrillary acidic protein and neurofilament protein changes can reflect the condition of injured neurons and astrocytes, while vascular endothelial growth factor and basic fibroblast growth factor changes can indicate angiogenesis. In the present study, we induced ischemic brain injury in the rhesus macaque by electrocoagulation of the M1 segment of the right middle cerebral artery. The motor relearning program was conducted for 60 days from the third day after model establishment. Immunohistochemistry and single-photon emission CT showed that the numbers of glial fibrillary acidic protein-, neurofilament protein-, vascular endothelial growth factor- and basic fibroblast growth factor-positive cells were significantly increased in the infarcted side compared with the contralateral hemisphere following the motor relearning program. Moreover, cerebral blood flow in the infarcted side was significantly improved. The clinical rating scale for stroke was used to assess neurological function changes in the rhesus macaque following the motor relearning program. Results showed that motor function was improved, and problems with consciousness, self-care ability and balance function were significantly ameliorated. These findings indicate that the motor relearning program significantly promoted neuronal regeneration, repair and angiogenesis in the surroundings of the infarcted hemisphere, and improve neurological function in the rhesus macaque following brain ischemia.

In vivo observation of cerebral microcirculation after experimental subarachnoid hemorrhage in mice

Acute brain injury caused by subarachnoid hemorrhage is the major cause of poor prognosis. The pathology of subarachnoid hemorrhage likely involves major morphological changes in the microcirculation. However, previous studies primarily used fixed tissue or delayed injury models. Therefore, in the present study, we used in vivo imaging to observe the dynamic changes in cerebral microcirculation after subarachnoid hemorrhage. Subarachnoid hemorrhage was induced by perforation of the bifurcation of the middle cerebral and anterior cerebral arteries in male C57/BL6 mice. The diameter of pial arterioles and venules was measured by in vivo fluorescence microscopy at different time points within 180 minutes after subarachnoid hemorrhage. Cerebral blood flow was examined and leukocyte adhesion/albumin extravasation was determined at different time points before and after subarachnoid hemorrhage. Cerebral pial microcirculation was abnormal and cerebral blood flow was reduced after subarachnoid hemorrhage. Acute vasoconstriction occurred predominantly in the arterioles instead of the venules. A progressive increase in the number of adherent leukocytes in venules and substantial albumin extravasation were observed between 10 and 180 minutes after subarachnoid hemorrhage. These results show that major changes in microcirculation occur in the early stage of subarachnoid hemorrhage. Our findings may promote the development of novel therapeutic strategies for the early treatment of subarachnoid hemorrhage.

不同针灸介入时机对大脑中动脉供血区急性脑梗死神经功能预后的影响

目的观察不同针灸介入时机对大脑中动脉供血区急性脑梗死神经功能预后的影响。方法回顾性选取2020年1月—2022年8月收治的116例大脑中动脉供血区急性脑梗死患者的临床资料进行分析,根据针灸介入时机分为两组。两组均进行静脉溶栓及常规药物治疗,观察组61例患者于发病72 h内给予针灸治疗,对照组55例患者于发病2周时给予针灸治疗。检测两组不同时间点侧支循环代偿情况、脑损伤标志物的水平,评估两组不同时间点简易精神状态检查(Mini-mental state examination,MMSE)评分、神经功能评分、Barthel指数(Barthel index,BI)评分、肢体运动功能评分、中医症状评分的差异,统计两组疗效。结果治疗前,两组侧支循环代偿情况比较,差异无统计学意义(P>0.05)。治疗4周和随访时,两组患侧大脑前动脉平均血流速度与对侧大脑中动脉平均血流速度的比值(Ratio of the average flow ve⁃locity of the affected anterior cerebral artery to the average flow velocity of the contralateral middle cerebral artery,iVACA/cVM⁃CA)较治疗前升高,观察组同时间点较对照组更高(P<0.05);两组患侧大脑后动脉平均血流速度与对侧大脑中动脉平均血流速度的比值(Ratio of the average flow velocity of the affected posterior cerebral artery to the average flow velocity of the contralateral middle cerebral artery,iVPCA/cVMCA)与治疗前比较,差异无统计学意义(P>0.05)。治疗前,两组脑损伤标志物比较,差异无统计学意义(P>0.05)。治疗4周和随访时,两组脑源性神经营养因子(Brain-derived neurotrophic factor,BDNF)较治疗前升高,观察组同时间点较对照组更高(P<0.05);两组钙结合蛋白β(Calcium binding proteinβ,S100β)、神经胶质纤维酸性蛋白(Glial fibrillary acid protein,GFAP)较治疗前下降,观察组同时间点较对照组更低(P<0.05)。治疗前,两组Fugl-Meyer评分、中医症状评分等相关评分比较,差异无统计学意义(P>0.05)。治疗4周和随访时,两组MMSE评分、BI评分及上肢和下肢Fugl-Meyer评分较治疗前升高,观察组同时间点较对照组更高(P<0.05);两组美国国立卫生院神经功能缺损(National institutes of health stroke scale,NIHSS)评分、中医症状评分较治疗前下降,观察组同时间点较对照组更低(P<0.05)。观察组总有效率为88.52%(54/61)高于对照组的72.73%(40/55),差异有统计学意义(P<0.05)。结论发病72h内采用针灸治疗可改善大脑中动脉供血区急性脑梗死脑损伤标志物的表达,改善脑血流,促进神经功能的恢复,有利于疾病的康复。

亚低温治疗重型颅脑损伤患者的前瞻性对照研究

目的前瞻性对照分析亚低温治疗对重型颅脑损伤患者的影响。方法选取83例重型颅脑损伤患者,入院时间2022-01—2023-09。所有患者随机数字表法分为对照组40例(标准大骨瓣减压术治疗)与亚低温组43例(标准大骨瓣减压术+亚低温治疗),评价2组患者治疗前后基本生命体征、血气指标、脑血流指标、神经功能,观察并发症发生率。结果治疗后,2组rSO_(2)、CPP升高,亚低温组高于对照组[(86.24±3.87)mmHg比(79.64±3.48)mmHg,(69.24±4.25)比(62.34±4.31)],ICP均降低,亚低温组低于对照组[(26.18±2.25)mmHg比(31.28±2.28)mmHg],差异均有统计学意义(P<0.05);治疗前后比较,亚低温组体温明显降低[(36.37±0.27)℃比(34.15±0.31)℃,P<0.05],对照组体温无显著变化[(36.45±0.21)℃比(36.56±0.16)℃,P>0.05];2组患者SaO、PaO_(2)水平均明显升高,亚低温组高于对照组[(95.64±2.16)%比(92.31±2.13)%,(86.27±5.10)mmHg比(81.31±5.14)mmHg],PaCO_(2)均下降,亚低温组低于对照组(36.15±3.11)mmHg比(42.72±3.23)mmHg],差异均有统计学意义(P<0.05);2组患者Qm、Vm均升高,亚低温组高于对照组[(15.63±4.38)mL/s比(11.49±3.61)mL/s,(42.67±5.18)cm/s比(38.56±4.26)cm/s],DR均降低,亚低温组低于于对照组[(263.36±22.57)kPa/s比(295.27±26.64)kPa/s],差异均有统计学意义(P<0.05);2组患者GCS评分均升高,亚低温组高于对照组(9.24±1.18)分比(7.56±1.26)分,NIHSS评分降低,亚低温组低于对照组[(22.65±3.39)分比(25.63±3.53)分],6个月后GOS评分亚低温组高于对照组(4.25±0.24)分比(3.85±0.14)分,差异均有统计学意义(P<0.05);2组患者并发症发生率无统计学差异(16.67%比33.33%,P>0.05)。结论重型颅脑损伤患者行基础颅脑手术后联合亚低温辅助治疗能够改善患者脑氧代谢及脑血流,从而促进神经功能恢复,改善预后。

双侧去骨瓣减压开颅手术治疗重型对冲性颅脑外伤的效果及对脑氧代谢指标的影响

目的:探讨双侧去骨瓣减压开颅手术治疗重型对冲性颅脑外伤的效果及对脑氧代谢指标的影响。方法:选取2020年1月—2023年1月福建医科大学附属龙岩第一医院收治的60例重型对冲性颅脑外伤患者。根据抽签法将其分为对照组和观察组,各30例。对照组给予标准大骨瓣开颅减压术,观察组给予双侧去骨瓣减压开颅手术。比较两组手术疗效、神经功能、脑氧代谢指标、炎症因子及并发症。结果:术后2周,观察组总有效率高于对照组,差异有统计学意义(P<0.05)。术后2周,两组美国国立卫生研究院卒中量表(NIHSS)评分降低,观察组NIHSS评分低于对照组,术后3 d,两组神经元特异性烯醇化酶(NSE)水平降低,静脉血氧饱和度(SvO2)水平升高,观察组NSE水平低于对照组,SvO2水平高于对照组,差异有统计学意义(P<0.05)。术前及术后3 d,两组白细胞介素-2(IL-2)、白细胞介素-4(IL-4)水平比较,差异无统计学意义(P>0.05);术后3 d,两组IL-2水平降低,IL-4水平升高,差异有统计学意义(P<0.05)。两组并发症发生率比较,差异无统计学意义(P>0.05)。结论:双侧去骨瓣减压开颅手术治疗重型对冲性颅脑外伤患者的效果更好,可减轻神经功能损伤,改善患者脑氧代谢情况,并发症少。

标准大骨瓣开颅减压术与传统骨瓣开颅减压术在重型颅脑损伤治疗的应用比较

目的 对比标准大骨瓣开颅减压术(standard large trauma craniotomy,SLTC)与传统骨瓣开颅减压术对重型颅脑损伤(severe traumatic brain injury,sTBI)患者的影响。方法 回顾性分析48例sTBI患者病例资料,按治疗措施不同分为对照组(24例,传统骨瓣开颅减压术)和观察组(24例,SLTC)。比较两组颅内压、脑氧代谢指标、并发症、预后情况。结果 术后7d,观察组颅内压为(14.30±1.59)mmHg,桡动脉-颈内静脉球部血氧含量差(arterial jugular vein oxygen content difference,Da-jvO_(2))为(50.39±3.01)ml/L,均低于对照组(18.41±2.01)mmHg、(55.22±3.72)ml/L;静脉血氧含量(oxygen saturation in venous blood,CjvO_(2))为(97.54±11.38)ml/L,动脉血氧含量(arterial oxygen content,CaO_(2))为(162.22±11.57)ml/L,高于对照组(88.75±9.21)ml/L、(153.24±9.75)ml/L;术后6个月,观察组格拉斯哥预后评分(Glasgow Outcome Scale,GOS)为(4.13±0.28)分,高于对照组(3.52±0.26)分,差异具有统计学意义(P<0.05);两组并发症相比,差异无统计学意义(P>0.05)。结论 SLTC能够更有效降低sTBI患者颅内压,调节脑氧代谢,有助于改善患者预后,有一定应用价值,值得临床进行推广应用。

右美托咪定对重型颅脑外伤术后脑氧代谢的影响

【目的】研究右美托咪定对重型颅脑外伤(STBI)术后患者脑氧代谢的影响。【方法】采用前瞻性随机对照研究。入组患者按随机数字表法分为右美托咪定组(A组)和对照组(B组),最终纳入病例69例,A组37例,B组32例;所有患者术后即转入ICU,给予降低颅内压、维持呼吸、循环功能、防治感染、维持内环境稳定、营养支持、保护脏器功能等综合治疗;A组同时给予右美托咪定0.5μg/(kg·h)静脉泵入,持续72 h;所有患者持续监测心率(HR)、呼吸(R)、平均动脉压(MAP)、脉搏氧饱和度(Sp O2);颈内静脉逆行穿刺置管至颈静脉球部,并分别于入ICU后即刻(0 h)、12、24、48及72 h检测动脉及颈静脉球部血气分析,测得颈静脉球部血氧饱和度(Sjv O2),并计算颈内动脉与颈内静脉血氧含量差(AVDO2)及脑氧摄取率(CERO2);随访90 d,观察28 d病死率及90 d格拉斯哥预后评分(GOS);比较两组上述指标的差异性。【结果】入ICU即刻(0 h)两组HR、R、MAP、Sjv O2、AVDO2、CERO2比较无统计学差异(P>0.05);重复测量资料方差分析发现:A组HR、R、MAP整体水平均低于B组(均为P<0.001);随时间延长,A组患者HR、R、MAP均较B组明显下降(均为P<0.001);A组Sjv O2整体水平高于B组(P=0.005),AVDO2、CERO2整体水平均低于B组(P=0.035;P=0.001);随时间延长,A组患者Sjv O2较B组明显升高,而AVDO2明显降低(P=0.001;P<0.001)。A组90 d预后良好率明显高于B组(P=0.036)。【结论】右美托咪定可以降低STBI患者交感神经系统兴奋性,降低脑氧耗,改善脑氧代谢紊乱,从而发挥脑保护效应,改善患者临床预后。

三七总皂甙对实验性脑缺血脑血流及血脑屏障的影响作用

目的 观察三七总皂甙对脑缺血后再灌流期间血脑屏障及脑血流的影响。方法 利用大鼠局灶性脑缺血再灌流和全脑缺血再灌流损伤两种实验模型。结果 与相应对照组比较 ,不论是全脑缺血还是局灶性脑缺血 1h后再灌流 3d ,应用三七总皂甙的各组动物及水肿明显减轻 ,血脑屏障通透性改善 ,大脑局部血流量显著增加。结论 三七总皂甙对脑缺血后脑水肿、血脑屏障。

亚低温治疗对重型颅脑损伤患者颅内压及脑血液生化学指标的影响

目的：探讨亚低温治疗对重型颅脑损伤患者颅内压（ICP）及脑血液生化学指标的影响。方法：回顾性收集81例重型颅脑损伤患者,根据治疗方法的不同分为观察组（n=48）和对照组（n=33）,所有患者入院后给予重型颅脑损伤常规治疗,在此基础上,观察组患者给予亚低温治疗,治疗时间为72h。动态监测所有患者入院时及治疗开始第1~7天ICP,入院时和治疗第7天脑血流指标动态阻力（DR）、脉搏波速（Wv）、脑部平均血流量（Qmean）、平均血流速度（Vmean）和脑氧代谢指标脑氧摄取率（CERO2）、颈内静脉血氧饱和度（SjvO2）、CjvO2、CaO2。结果：随着时间的延长,两组患者ICP呈逐渐下降的趋势,差异有统计学意义（F=17.982、6.324,P〈0.05）;第2天开始,观察组ICP显著低于对照组,持续至第7天,差异均有统计学意义（P均〈0.05）;与入院时比较,两组第7天DR、Wv、CaO2均显著降低,Qmean、Vmean、CjvO2、CERO2、SjvO2显著升高,差异有统计学意义（P〈0.05）;与对照组第7天比较,观察组DR、Wv、CaO2显著低于对照组,Qmean、Vmean、CjvO2、CERO2、SjvO2显著高于对照组,差异有统计学意义（P〈0.05）。结论：亚低温治疗可以显著降低重型颅脑损伤患者颅内压,改善脑血流和脑氧代谢,具有重要的临床意义。