Electrocardiogram changes in acute cerebral infarction patients

INTRODUCTION In the acute phase of the disease, patients may be worsen because of the secondary arrhythmia. We observed electrocardiogram (ECG) of patients with cerebral in- farction and compared with healthy people, analyzed the heart rate (HR), PR inter…     

Electrocardiogram cerebral infarction changes in acute patients

BACKGROUND: Comparison of different stroke locations had been focused in past researches in electrocardiogram (ECG) changes of cerebral stroke patients. Some researches neglected the heart disease in the illness history. OBJECTIVE: To discuss ECG changes in different infarction locations and size of acute cerebral infarction and compare with healthy people. DESIGN: Contrast observation. SETTING: Shanghai Ninth People's Hospital. PARTICIPANTS: A total of 57 patients with cerebral infarction were selected from the Neurological Department of Ninth People's Hospital of Shanghai from March 2003 to September 2005. They were diagnosed according to the criteria revised in the 4th National Cerebral Disease Conference and brain images. Patients who had heart disease were excluded. There were 32 males and 25 females, who were 65-84 years old. Among them, 23 cases were involved in right hemisphere, 34 cases in left one, 23 in base ganglion, 11 in brain stem, 9 in frontal lobe and 14 in other parts. According to their infarction size (plus size in every different scan), they were divided into three different groups: large-size group (n = 10) with size larger than 3.5 cm3, medium-size group (n = 13) with size between 1.5-3.5 cm3, and small-size group (n = 34) with size smaller than 1.5 cm3. Another 50 healthy subjects were regarded as control group. There were 29 males and 21 females aged 40-82 years. All these cases knew and agreed of the examination. METHODS: Patients received 12-lead ECG examinations within the first 6-24 hours of onset while control group received it at the same time. The HR, PR, QTc, QRS, T wave and ST changes were compared between the two groups. MAIN OUTCOME MEASURES: The ECG changes and differences in two hemispheres, in different infarction locations and sizes. RESULTS: All 57 patients and 50 healthy subjects were involved in the final analysis. ① ECG changes in infarction group and control group. There were no differences in HR, QRS time and cases with opposite T wave of infarction group compared with control group (P > 0.05). PR and QTc [(0.167±0.010), (0.383±0.029) s] in infarction group were longer than those in control group [(0.159±0.008), (0.361±0.022) s, t = 1.982, 2.363, P < 0.05, 0.01]. ST changes cases were 77% (44/57), which was more than those in control group [46% (23/50), χ2 = 11.072, P < 0.01]. ② Comparison of infarction in two hemispheres. HR, PR interval, QRS time, cases with opposite T wave and ST changes showed no differences (P > 0.05), and QTc interval in right hemisphere infarction was longer than left one [(0.391±0.054), (0.380±0.034) s, t =1.673, P < 0.05]. ③ ECG changes in different infarction locations. HR, PR interval, QTc interval, QRS time, cases with opposite T wave and ST changes showed no statistically significantly differences (P > 0.05). ④ ECG changes in different infarction sizes. HR, PR interval, QRS time showed no differences (P > 0.05). QTc interval in large size group was longer than the others [(0.399±0.044), (0.388±0.073), (0.378±0.124) s, F = 3.19, P < 0.05]. Cases with opposite T wave and ST changes in large size group were 80% (8/10), 100% (10/10), which were higher than those in medium size group [46% (6/13), 69% (9/13)] and small size group [44% (15/34), 35% (12/34), χ２ = 8.495, 10.538, P < 0.05, 0.01]. CONCLUSION: ① PR interval and QTc interval prolonged in cerebral infarction patients. Furthermore, QTc interval was more obvious in large size infarction group and right hemisphere infarction group. ② Infarction location did not affect the changes of ECG.     

Regulation of α-synuclein expression in Down syndrome

The triplication of genes located on chromosome 21 is known to cause a wide spectrum of pathology seen in Down syndrome (DS), including leukemia, seizures, stroke, and mental retardation. Studies on RNA and protein expression of genes in DS brain have demonstrated the role of triplicated genes in several DS phenotypes. Significant changes in the expression of nontriplicated genes have also been observed. However, little information is available regarding the role of nonchromosome 21 genes in DS pathology. We have found that α-synuclein (SNCA), a presynaptic protein whose gene is located on chromosome 6 in the Ts65Dn mouse model for DS, is significantly reduced in the cortex and other brain regions. We hypothesize that this alteration may play a critical role in the reduced synaptic function observed in DS. We have found an increase in the level of neurosin, a key negative regulator of SNCA in Ts65Dn cortex. We have also found increased levels of protein phosphatase 2A, a negative regulator of the activation of tyrosine hydroxylase and a key enzyme in the biosynthetic pathway for dopamine in Ts65Dn cortex. These findings reveal potential target sites for intervention in the treatment of DS pathology.     

Neuronal quantity and ultrastructure in extracorticospinal tract of newborn rabbits with cerebral palsy

BACKGROUND: The liver enzyme system and blood brain barrier function of newborn rabbits are incomplete. High level of bilirubin can lead to cerebral palsy (CP) of newborn rabbits. The pathological and ultrastructural changes of brains of immature rabbits may differ from those of mature rabbits. OBJECTIVE: To observe the changes in dopaminergic neuron amount and ultrastructure in the extracorticospinal tract of animal models of CP induced by hyperbilirubinemia. DESIGN: A randomized controlled observation. SETTING: Rehabilitation Medical College of Jiamusi University; Laboratory for Pediatric Neurology Rehabilitation of Jiamusi University. MATERIALS: Thirty newborn 2- to 5- day inbred Japanese rabbits, weighing about 50 g, of either gender, were provided by Experimental Animal Center, Jilin University. Bilirubin and tyrosine hydroxylase (TH) antibody were purchased from Sigma Corporation, USA. METHODS: This experiment was carried out in the laboratory for children neuro-rehabilitation, Jiamusi University between September 2002 and December 2005. ①Thirty rabbits were randomly divided into 2 groups: control group (n =10) and model group (n =20). ②Bilirubin of 100 mg/kg was given to the rabbits of model group through intraperitoneal injection, once every other day, 3 times totally; The same amount of normal saline was given to the rabbits of control group. After injection, the newborn rabbits had been fed by maternal milk for 45 days. ③TH-positive neurons in substantia nigra and corpora striatum in each area of 0.15 mm×0.15 mm were counted. Ultrastructures of substantia nigra and corpora striatum were observed under the electron miscroscope. The concentration of bilirubin in brain tissue of CP rabbits of model group was measured with high performance liquid chromatogram. MAIN OUTCOME MEASURES: Quantitative analysis results and ultrastructure of TH-positive neurons in substantia nigra and corpora striatum in two groups. RESULTS: Thirty newborn rabbits were involved, 6 rabbits from model group died and 4 were failed in modeling, finally, 20 rabbits were involved in the result analysis. ① The concentration of bilirubin in brain tissue of newborn rabbits of model group was (59.9±17.04) mg/L, which was significantly higher than that of control group [(42.79±3.57) mg/L, P < 0.01]. ② TH positive neurons amount in the substantia nigra and corpora striatum of newborn rabbits in the model group was 30.30±9.58, 4.70±2.79, which was significantly less than that in the control group respectively (45.20±12.74, 11±2.45, P < 0.01). ③The concentration of bilirubin in brain tissue was significantly negatively correlated with TH-positive neurons in substantia nigra(r =-0.69, P < 0.01); The concentration of bilirubin in brain tissue was also significantly negatively correlated with TH-positive neurons in corpora striatum(r =-0.59, P < 0.01). TH-positive neurons in substantia nigra were positively correlated with those in corpora striatum (r =0.77, P < 0.01).④ Under the electron microscope, the nerve cells in substantia nigra and corpora striatum of newborn rabbits of model group were significantly changed in ultrastructure as compared with control group. CONCLUSION: Ultrastructure of extracorticospinal tract of newborn rabbits with CP is significantly changed, presenting the injury of dopaminergic neuron and decrease of neuronal amount.     

Effect of Panaxtriol Saponins on synaptophysin and postsynaptic density-95 expression at different periods of cerebral infarction*☆

BACKGROUND： The change in expression of synaptophysin （Syp） and postsynaptic density-95 （PSD-95） alters after cerebral infarction, and the plasticity of synapses contributes greatly to nerve function recovery. Chinese medicinal substances may play an important role in the expression of Syp and PSD-95. OBJECTIVE： To observe the effect of Panaxtriol Saponins （PTS）, an active component in Sanqi tongshu capsules, on the expression of Syp and PSD-95 after cerebral infarction at different time points in rats, so as to examine the cerebral function remodeling mechanism. DESIGN, TIME AND SETTING： A randomized and controlled observation which was performed in Dongzhimen Hospital, Beijing University of Traditional Chinese Medicine from January to March, 2007. MATERIALS： Twenty-six healthy male Sprague Dawley rats were used to establish middle cerebral artery occlusion based on the Longa method. Sanqi tongshu capsules （containing 100 mg PTS per tablet） were provided by the Chengdu Huashen Group and nimodipine tablets （30 mg） by Tianjin Zhongyang Pharmaceutical Co., Ltd. METHODS： Twenty-six rats were randomly divided into an operation group （n = 21 ） and a control group （n = 5）. The operation group underwent the EZ Longa procedure to make the middle cerebral artery occlusion model. After surgery rats were randomly divided into a model group, a PTS group and a nimodipine group, with seven rats in each group. Rats were intragastrically administrated with saline （2 mL/d） in the model group, with Sanqi tongshu capsule （5.4 mg/100 g/d） in the PTS group, and with nimodipine （1.73 mg/100 g/d） in the nimodipine group. Rats in the control group did not undergo model establishment and drug administration. MAIN OUTCOME MEASURES： The expressions of Syp and PSD-95 were measured by immunohistochemical and image analysis at days 3, 7 and 28 after the operation. RESULTS： The expression of Syp and PSD-95 in the operation group was significantly lower than in the control group at days 3, 7     

Neuronal and glial accumulation of α- and β-synucleins in human lipidoses

A number of the lysosomal storage diseases that have now been characterized are associated with intra-lysosomal accumulation of lipids, caused by defective lysosomal enzymes. We have previously reported neuronal accumulation of both α- and β-synucleins in brain tissue of a GM2 gangliosidosis mouse model. Although α-synuclein has been implicated in several neurodegenerative disorders including Parkinson’s disease, dementia with Lewy bodies and multiple system atrophy, its functions remain largely unclear. In our present study, we have examined a cohort of human lipidosis cases, including Sandhoff disease, Tay–Sachs disease, metachromatic leukodystrophy, β-galactosialidosis and adrenoleukodystrophy, for the expression of α- and β-synucleins and the associated lipid storage levels. The accumulation of α-synuclein was found in brain tissue in not only cases of lysosomal storage diseases, but also in instances of adrenoleukodystrophy, which is a peroxisomal disease. α-synuclein was detected in both neurons and glial cells of patients with these two disorders, although its distribution was found to be disease-dependent. In addition, α-synuclein-positive neurons were also found to be NeuN-positive, whereas NeuN-negative neurons did not show any accumulation of this protein. By comparison, the accumulation of β-synuclein was detectable only in the pons of Sandhoff disease cases. This differential accumulation of α- and β-synucleins in human lipidoses may be related to functional differences between these two proteins. In addition, the accumulation of α-synuclein may also be a condition that is common to lysosomal storage diseases and adrenoleukodystrophies that show an enhanced expression of this protein upon the elevation of stored lipids.     

Changes of biochemical indexes in patients with acute cerebral infarction after treatment with simvastatin

BACKGROUND: At present, it is believed that the important causes of cerebral infarction are the disorders of lipid metabolism and endothelial function, and the outcomes of clinical treatment can be improved by regulating serum lipids and antiinflammation, etc. OBJECTIVE: To observe the effect of simvastatin, inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, on the levels of serum lipids, serum enzymic indexes and inflammatory metabolic indexes in patients with cerebral infarction. DESIGN: A comparative observation. SETTING: Department of Geriatrics, Longquanshan Hospital of Liuzhou City. PARTICIPANTS: Forty-eight patients with acute cerebral infarction were selected from the Department of Geriatrics of Longquanshan Hospital of Liuzhou from March 2004 to February 2006, including 24 males and 24 females, the mean age was (54±12) years, average disease course was (10.0±4.5) days. They were all accorded with the diagnostic standard for cerebral infarction set by the Fourth National Academic Meeting for Cerebrovascular Disease in 1999, and cerebral hemorrhage was excluded by cranial CT scanning. The 48 patients were randomly divided into control group (n =24) and treatment group (n =24). Informed consents were obtained from all the participants. METHODS: ① All the patients were treated according to the symptoms, besides those in the treatment group were given simvastatin (Harbin Pharm. Group Sanjing Pharmaceutical Shareholding, Co.,Ltd., No. H20010454; Batch number: 20040218; 5 mg/tablet). The initial dosage was 10 mg per day for 4 weeks, and then increased to 30 mg per day for another 4 weeks. ② Before treatment and within 1 week after treatment, the total cholesterol, triglyceride, high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), aspartate aminotransferase (AST), creatine kinase and C reactive protein in serum were determined with Beckman-cx7 automatic biochemical analytical apparatus in both groups. ③ The differences of intergroup and intragroup data were compared with the independent-samples t test and paired samples t test. MAIN OUTCOME MEASURES: Changes of total cholesterol, triglyceride, HDL-C, LDL-C, AST, creatine kinase and C reactive protein before and treatment in both groups. RESULTS: All the 48 patients with cerebral infarction were involved in the analysis of results. ① Changes of serum lipids: The levels of serum lipids were close between the two groups before treatment (P > 0.05). After treatment, the HDL-C level in the treatment group was obviously higher than that in the control group and that before treatment [(1.34±0.12), (0.92±0.33), (0.93±0.21) mmol/L, t =7.922, 11.699, P < 0.01], and the levels of total cholesterol, triglyceride and LDL-C were obviously lower than those in the control group and those before treatment (t =2.780-7.591, P < 0.01). ② Changes of serum enzymic indexes and C reactive protein in serum: The levels of enzymes and C reactive protein in serum had no obvious differences between the two groups before treatment (P > 0.05). The levels of AST, creatine kinase and C reactive protein in serum after treatment were obviously lower than those before treatment in both groups (t =7.259-17.996, P < 0.01). The levels of levels of creatine kinase and C reactive protein in serum after treatment in the treatment group were obviously lower than those in the control group [(3.061±0.522) μkat/L, (4.6±3.1) mg/L; (4.348±0.580) μkat/L, (12.3±4.8) mg/L, t =7.910, 6.463, P < 0.01]. CONCLUSION: Compared with common treatment according to symptoms, the additional administration of simvastatin is better for improving the serum lipids, serum enzymic indexes of patients with cerebral infarction at acute period, and benefit for repairing their inflammatory damages.     

TNF-α and TNF-β gene polymorphisms in cerebral infarction

Tumor necrosis factor (TNF) is an important cytokine in the inflammation process of atherosclerosis. Two biallelic polymorphisms in the TNF-α (TNF-α-308) and TNF-β (TNF-β +252) genes have been reported to be associated with TNF production and susceptibility to inflammatory diseases. We investigated two genetic polymorphisms in the TNF locus (TNF-α-308 G→A and TNF-β +252 A→G) as risk factors for cerebral infarction (CI) by determining its prevalence in 294 survivors of CI, and in 581 age-, gender-, and race-matched controls. A significant association was found for the TNF-α and TNF-β genotypes in CI patients compared with controls. A significant increase was found for the TNF-α A allele in controls compared with CI patients (X ²=7.593, p=0.006, odds ratio =1.74, confidence interval =1.17-2.59). In addition, the TNF-α GG genotype increased the relative risk for CI in subjects with the TNF-β AA genotype (X ² = 4.998, P=0.025). As a result, compared to controls, the frequency of the TNF-α AA genotype was decreased, whereas that of TNF-β AA was increased in CI patients. The former implies an association with resistance, whereas the latter suggests an association with susceptibility to the disease. These results show that the TNF-α-308 and TNF-β + 252 locus plays an important role in the etiopathogenesis of CI.     

Penumbra around chronic cerebral infarction?

In a series of 13 patients with cerebrovascular occlusive disease regional cerebral blood flow (rCBF) measurements (two-dimensional intravenous ¹³³Xe clearance method) and quantitative EEG analysis (sensorimotor rhythms) as well as electronic measurement of handforce were performed before and during intravenous infusion of 1 μg kg/min of one of the lipophilic dihydropyridine calcium channel blocker nimodipine (Nimotop®). The aim of the study was to test the hypothesis of the existence of hypoperfusion (ischaemic penumbra) in the surroundings of chronic cerebral infarcts. All 3 parameters improved in one patient. Sensorimotor rhythms increased in 5 patients, rCBF in 3. EEG and rCBF improved in 2 patients. In 3 instances, a redistribution of rCBF in favour of the peri-infarct zone was noted (significant increase of rCBF from 35 ± 2 sem to 53 ± 4 ml/100 g/min (p > 0.01), whereas rCBF fell from 61 ± 5 to 46 ±2 ml/100 g/min on a collimator remote from the infarct but in the infarcted hemisphere. The parallel improvement of rCBF and EEG in brain regions surrounding chronic infarcts in 3 patients was interpreted as functional improvement as a consequence of nimodipine-induced normalization of peri-infarct hypoperfusion, i.e. reversal of flow-dependent neuronal silence and/or dysfunction.     

Effects of phycocyanin on apoptosis and expression of superoxide dismutase in cerebral ischemia reperfusion injury

IN T R O D U C T IO NSuperoxide dism utase (SO D )is an im portantendogenous free radica scavenger, itelim inates superoxide anion free radicals through dis proportionation, and itprotects the nerve cells in the process ofcere bralischem ia reperfusion in…     

Dynamic changes in fibrinogen levels of patients with acute cerebral infarction after taking defibrase*☆

BACKGROUND： At present, as a therapeutic drug mainly for reducing fibrinogen （FIB） levels, the dynamic influence of defibrase on the FIB levels of patients with acute cerebral infarction has not been clearly ascertained. OBJECTIVE： To observe the dynamic changes in FIB levels of patients with acute cerebral infarction at different time points after taking defibrase. DESIGN, TIME AND SETTING： Randomized controlled clinical trial. The study was conducted in the Department of Neurology, the Second Affiliated Hospital of Jinan University, from June to November 2006. PARTICIPANTS： Sixty patients with acute cerebral infarction, who had been treated by the Neurological Department of the Second Affiliated Hospital of Jinan University from June to November 2006, were selected, including 37 males and 23 females, aged 35-75 years. All cases met the diagnostic criteria formulated by the Fourth National Cerebrovascular Disease Conference within 12 hours of onset. All the patients were confirmed with definite hemiparesis and cerebral infarction without coma, and were randomly divided into two groups： a treatment group （n =40） and a control group （n =20）. Patients＇ families had the right to be informed and agree with the treatment, which had permission from the Hospital Ethics Committee. METHODS： Patients in the control group were given routine treatment with 30 mL fleabane and 0.75 g cytidine diphosphate added to 500 mL saline solution once a day for 14 consecutive days. Patients in the treatment group were given routine treatment and Haiwang defibrase injection （purchased from Changchu Guoao Bio-Pharmaceutical Co. Ltd., Approval document number H10983237） within 12 hours of infarction. Defibrase doses of 15, 12.5 and 10 U were given over 2 hours according to the patients＇ pre-treatment plasma FIB levels of ≥ 4.50 g/L, 3.50 4.49 g/L and 1.00 3.49 g/L, respectively. Plasma FIB levels in the treatment group were measured before, and once every six hours for 48 hours after administration of defib     

CSF β-endorphin and leu-enkephalin levels in the acute and chronic stages of cerebral infarction

Summary To investigate the role of endogenous opioid peptides in the pathophysiology of cerebral ischaemia, the CSF levels of immunoreactive -endorphin and leu-enkephalin in 16 patients with cerebral infarction were measured. Both the CSF -endorphin and leu-enkephalin levels in the acute stage of cerebral infarction were significantly higher than the values in the chronic stage. The CSF concentrations of the two peoptides revealed a positive correlation in the acute but not the chronic stage. The increased endogenous opioid peptides in the CSF in the acute stage may modify the evolution of cerebral infarction.     

Reciprocal Effects of α-Synuclein Overexpression and Proteasome Inhibition in Neuronal Cells and Tissue

Defects in the 20S/26S proteasome and conformational changes in α-synuclein (α-syn) are implicated in the development of sporadic and familial cases of PD. The objective of this study was to evaluate whether α-syn affects proteolysis by the proteasome and, reciprocally, whether proteasome inhibition affects α-syn solubility and localization. Although α-syn directly inhibited purified 20S proteasomes reversibly in vitro, its overexpression in neuroblastoma (SH-SY5Y and SK-N-BE), embryonic kidney (HEK293) cells, or mouse brain did not affect proteasome activity. Proteasome inhibition with MG132 and epoxomicin in SH-SY5Y cells failed to induce α-syn aggregation, although it increased membrane bound forms of endogenous and overexpressed wild-type, but not mutant, α-syn. Concomitantly this treatment generated cytoplasmic α-syn inclusions devoid of polyubiquitin in a small percentage of cells. The combination of proteasome inhibition with serum deprivation, which induced oxidative stress and autophagy, caused the appearance of high molecular weight α-syn species, such as those found in Lewy bodies. Our data suggest that high concentrations of α-syn do not affect proteasome function in vivo, whereas proteasome inhibition can modify synuclein solubility, most prominently under conditions of cell stress which occur during aging. These results have implications for the convergence of age-related oxidative stress and impaired protein degradation in neurodegeneration.     

Neuroprotective effect of high-dose hyperbaric oxygenation on rats with acute cerebral infarction in super-early stage

BACKGROUND: Previously, only single short-time low-dose hyperbaric oxygenation (HBO) protocol was administrated to treat acute ischemic stroke in early stage and the conflicting results were obtained. There are few studies to report the outcome of administering long-time (can cover all the natural pathologic progression period) high-dose HBO to treat the disease. OBJECTIVE: To evaluate the therapeutic effect between two kinds of high-dose hyperbaric oxygenation on super-early stage of acute permanent middle cerebral artery occlusion (MCAO) in rats. DESIGN: A randomized controlled experimental study. SETTING: Beijing Tiantan Hospital, Capital Medical University; Beijing Research Institute of Neurosurgery. MATERIALS: Seventy-four male SD rats, aged 2.5 months old, weighing （280±20）g, were provided by the Animal Institute, Chinese Academy of Medical Sciences. Hyperbaric oxygenation device was hyperbaric air cabin in which there was a self-made pure oxygen animal experimental cabin (made in China). METHODS: This experiment was carried out in the municipal laboratory of Beijing Tiantan Hospital affiliated to Capital Medical University and Beijing Research Institute of Neurosurgery. ① Experimental intervention: All the rats were developed into models of permanent MCAO by suture embolism. Then, they were randomly divided into two HBO groups (9 hours and 18 hours) and control group, with 24 rats in each as well as 3-hour ultrastructure control group, with 2 rats. After being modeled for 3 hours, rats in the two HBO groups stayed in the hyperbaric cabin for 9 hours and 18 hours, separately. Rats in the 9-hour HBO group inhaled pure oxygen at hours 1, 3, 5, 7 and 9, and hyperbaric air at hours 2, 4, 6 and 8. Rats in the 18-hour HBO group inhaled pure oxygen at hours 1, 3, 5, 7, 9, 11, 13, 15 and 17, and hyperbaric air at hours 2, 4, 6, 8, 10 12, 14, 16 and 18. After being created into models, rats in the control group and 3-hour ultrastructure control group breathed room air. ② Experimental evaluation: Neurologic functions of rat models in the 9-hour and 18-hour HBO groups as well as control group were scored by Bederson and Garica two neurological grading systems at hours 14 and 28 and on day 5; Infarct volume of rat models in the two HBO groups and control group was measured at hour 24 and on day 5 with NIH image processing software Image J; The pathological changes of brain tissue in the brain infarct region and its opposite region of rat models in the two HBO groups and 3-hour ultrastructure control group were observed with a Philips EM 208S transmission electron microscope. MAIN OUTCOME MEASURES: ① Neurobehavioral outcome. ② Rat brain infarct volume. ③ Ultrastructure of brain tissue in the ischemic penumbra of infarct models at the different time points RESULTS: ① Neurobehavioral outcome: After treatment, Garica score in the 9-hour and 18-hour HBO groups was significantly higher than that in the control group (P < 0.01). Bederson score on day 5 after modeling in the 9-hour and 18-hour HBO groups was significantly lower than that in the control group (P < 0.01). ② Cerebral infarct volume: Cerebral infarct volume in the 9-hour and 18-hour HBO groups was significantly smaller than that in the control group at hour 24 and on day 5 after modeling (P < 0.01). In the 18-hour HBO group, infarct volume on day 5 after modeling was significantly larger than that at hour 24 after modeling (P < 0.05). ③In the 3-hour ultrastructure control group, astrocyte edema and neuron damage around the capillary in the infarct cerebral tissue significantly relieved in the rats which were subjected to HBO. CONCLUSION: High dose of HBO is highly efficient in reducing infarct volume and improving neurobehavioral outcome of rats with acute cerebral infarction, and also has an important role in inhibiting the pathological progression of ischemic brain tissue after cerebral infarction.     

Combined intra-arterial thrombolysis and neuprotectant agents reduce cerebral infarction in rabbits with experimental acute cerebral ischemia

INTRODUCTION The cerebrovascular disease is one of leading causes, threatening human health and imposing a heavy burden on families and society overall [1,2]. The large sample multi-center randomized controlled re- searches achieved by the National Instit…