Lactato como marcador temprano de hipoxia cerebral en pacientes neurológicos bajo anestesia general: una revisión sistemática / Lactate as an early marker of cerebral hypoxia in neurological patients under general anesthesia: a systematic review

Resumen: Las complicaciones neurológicas perioperatorias secundarias a hipoxia durante procedimientos de sedación y anestesia general son frecuentes en cirugía cardiovascular y en pacientes con comorbilidades. Sin embargo, hasta el momento no existe un consenso para el diagnóstico de estas posibles complicaciones. En pacientes con trauma encefálico severo y/o hemorragia subaracnoidea el lactato cerebral no fue útil para predicción de hipoxia cerebral; pese a ello, la relación de lactato/piruvato podría ser una herramienta para diagnóstico intraoperatorio de hipoxia cerebral aguda. Los estudios sugieren que éste debe asociarse a otros marcadores y/o a monitoreo multimodal. Es necesario realizar estudios que evalúen su valor predictivo para hipoxia cerebral.

Abstract: Perioperative neurological complications secondary to hypoxia during sedation and general anesthesia procedures are frequent in cardiovascular surgery, and in patients with comorbidities. However, so far there is no consensus for the diagnosis of these possible complications. In patients with head trauma severe and/or subarachnoid hemorrhage cerebral lactate was not useful for predicting cerebral hypoxia, however the lactate/pyruvate ratio could be a tool for intraoperative diagnosis of acute cerebral hypoxia. Studies suggest that it must be associated with other markers or multimodal monitoring. Further studies are needed to evaluate lactate predictive value for the diagnosis of cerebral hypoxia.

Prolongación del intervalo QT durante hipotermia terapéutica en un recién nacido con encefalopatía hipóxico isquémica: a propósito de un caso / Prolongation of the QT interval during therapeutic hypothermia in a newborn with hypoxic-ischemic encephalopathy: A case report / Prolongamento do intervalo QT durante hipotermia terapêutica em recém-nascido com encefalopatia hipóxico-isquêmica: relato de caso

Resumen: El síndrome de QT largo adquirido puede ser secundario a la hipotermia, tanto accidental como terapéutica. Es poco el conocimiento sobre el efecto de ésta en la actividad eléctrica cardíaca, sobre todo en recién nacidos, y sus potenciales complicaciones. Se presenta el caso clínico de un recién nacido con diagnóstico de encefalopatía hipóxico isquémica que presenta una prolongación del intervalo QT durante el tratamiento con hipotermia. Se discute la evolución del paciente, que es consistente con lo referido en la literatura sobre el tema: buena evolución, ausencia de arritmias graves o alteraciones hemodinámicas, y normalización del electrocardiograma luego de finalizado el tratamiento.

Summary: Acquired long QT syndrome may be secondary to hypothermia, both accidental and therapeutic. There is not enough knowledge about the effect of hypothermia in cardiac activity and its potential complications, especially in newborns. We present the clinical case of a newborn with a diagnosis of hypoxic ischemic encephalopathy who has a prolonged QT interval during treatment with hypothermia. The evolution of the patient is discussed, which is consistent with what is referred to in the literature on the subject: Good evolution, absence of serious arrhythmias or hemodynamic alterations, and normalization of the ECG after the end of treatment.

Resumo: A síndrome do QT longo adquirida pode ser secundária à hipotermia, tanto acidental quanto terapêutica. Pouco se sabe sobre seu efeito na atividade elétrica cardíaca, principalmente em recém-nascidos, e suas possíveis complicações. Apresentamos o relato de caso clínico de um recém-nascido com diagnóstico de encefalopatia hipóxica isquêmica que apresenta prolongamento do intervalo QT durante o tratamento com hipotermia. Discutimos a evolução do paciente, a que é consistente com a literatura sobre o assunto: boa evolução, ausência de arritmias graves ou alterações hemodinâmicas e normalização do ECG após o término do tratamento.

Differential Effects of Pentoxifylline on Learning and Memory Impairment Induced by Hypoxic-ischemic Brain Injury in Rats

OBJECTIVE: Hypoxic-ischemic (HI) brain injury in the human perinatal period often leads to significant long-term neurobehavioral dysfunction in the cognitive and sensory-motor domains. Using a neonatal HI injury model (unilateral carotid ligation followed by hypoxia) in postnatal day seven rats, the present study investigated the long-term effects of HI and potential behavioral protective effect of pentoxifylline. METHODS: Seven-day-old rats underwent right carotid ligation, followed by hypoxia (FiO2 = 0.08). Rats received pentoxifylline immediately after and again 2 hours after hypoxia (two doses, 60–100 mg/kg/dose), or serum physiologic. Another set of seven-day-old rats was included to sham group exposed to surgical stress but not ligated. These rats were tested for spatial learning and memory on the simple place task in the Morris water maze from postnatal days 77 to 85. RESULTS: HI rats displayed significant tissue loss in the right hippocampus, as well as severe spatial memory deficits. Low-dose treatment with pentoxifylline resulted in significant protection against both HI-induced hippocampus tissue losses and spatial memory impairments. Beneficial effects are, however, negated if pentoxifylline is administered at high dose. CONCLUSION: These findings indicate that unilateral HI brain injury in a neonatal rodent model is associated with cognitive deficits, and that low dose pentoxifylline treatment is protective against spatial memory impairment.

Paradoxical Motor and Cognitive Function Recovery in Response to Zolpidem in a Patient with Hypoxic-ischemic Brain Injury: A Case Report

We report an extremely rare case of a patient with hypoxic-ischemic brain injury who recovered consciousness and motor and cognitive functions due to paradoxical response after zolpidem administration. A 32-year-old woman who had attempted suicide by hanging was admitted. The patient had stabilized in a state of drowsy mentality, quadriparesis, dysphagia, and impaired cognition. Brain magnetic resonance imaging was suggestive of hypoxic ischemic brain injury and unilateral infarction in the right posterior cerebral artery territory. Due to sleep disturbance, zolpidem was administered, and paradoxically consciousness level and function returned to near-normal during the duration of the drug-effect. In addition to previous reports, our case characteristically showed remarkable motor and cognitive function recovery, not only consciousness level. The drug-effect time was gradually decreased after 18 months and absent after 3 years. We have reviewed related literature and discussed possible neuropharmacological and neurobiological mechanism.

Sustained erroneous near-infrared cerebral oxygen saturation in alert icteric patient with vanishing bile duct syndrome during and after liver transplantation: A case report

Monitoring cerebral oxygenation using a near infrared spectroscopy (NIRS) device is useful for estimating cerebral hypoperfusion and is available during liver transplantation (LT). However, high serum bilirubin concentration can interfere with NIRS because bilirubin absorbs near infrared light. We report a patient who underwent LT with a diagnosis of vanishing bile duct syndrome, whose regional cerebral oxygen saturation (rSO₂) remained below 15% even with alert mental status and SpO2₂ value of 99%. The rSO₂ values were almost fixed at the lowest measurable level throughout the intra- and postoperative period. We report a case of erroneously low rSO₂ values during the perioperative period in a liver transplant recipient which might be attributable to skin pigmentation rather than higher serum bilirubin concentration.

Neuroprotective effects of erythropoietin against hypoxic injury via modulation of the mitogen-activated protein kinase pathway and apoptosis / 소아과

PURPOSE: Hypoxic-ischemic encephalopathy is a significant cause of neonatal morbidity and mortality. Erythropoietin (EPO) is emerging as a therapeutic candidate for neuroprotection. Therefore, this study was designed to determine the neuroprotective role of recombinant human EPO (rHuEPO) and the possible mechanisms by which mitogen-activated protein kinase (MAPK) signaling pathway including extracellular signal-regulated kinase (ERK1/2), JNK, and p38 MAPK is modulated in cultured cortical neuronal cells and astrocytes. METHODS: Primary neuronal cells and astrocytes were prepared from cortices of ICR mouse embryos and divided into the normoxic, hypoxia (H), and hypoxia-pretreated with EPO (H+EPO) groups. The phosphorylation of MAPK pathway was quantified using western blot, and the apoptosis was assessed by caspase-3 measurement and terminal deoxynucleotidyl transferase dUTP nick end labeling assay. RESULTS: All MAPK pathway signals were activated by hypoxia in the neuronal cells and astrocytes (P<0.05). In the neuronal cells, phosphorylation of ERK-1/-2 and apoptosis were significantly decreased in the H+EPO group at 15 hours after hypoxia (P<0.05). In the astrocytes, phosphorylation of ERK-1/-2, p38 MAPK, and apoptosis was reduced in the H+EPO group at 15 hours after hypoxia (P<0.05). CONCLUSION: Pretreatment with rHuEPO exerts neuroprotective effects against hypoxic injury reducing apoptosis by caspase-dependent mechanisms. Pathologic, persistent ERK activation after hypoxic injury may be attenuateed by pretreatment with EPO supporting that EPO may regulate apoptosis by affecting ERK pathways.

Caracterización de la población con epilepsia atendida en un hospital infantil en Manizales 2013-2014 / Characterization of patients with epilepsy treated in a children's hospital in Manizales 2013-2014

Resumen Objetivo: caracterizar la población con diagnóstico de epilepsia en el Hospital Infantil Universitario Rafael Henao Toro, en Manizales (Colombia), desde el punto de vista del comportamiento de la enfermedad, factores de riesgo, tratamiento y particularidades demográficas. Métodos: estudio de corte transversal realizado mediante la revisión de historias clínicas.Resultados: de 172 pacientes, 51,2 % fueron del género masculino; las crisis focales fueron las más frecuentes con 59,1 %; la comorbilidad más usual fue el retraso del desarrollo psicomotor (30,9 %), aunque si se tiene en cuenta la asociación con otras enfermedades la cifra asciende al 57,9 %; la monoterapia más utilizada fue el ácido valpróico (39,8 %). La epilepsia infantil se asoció con estados hipertensivos maternos en un 8,7 %; el 21,7 % presentó encefalopatía hipóxica-isquémica; 24,1 % tenían antecedentes familiares de epilepsia; en 15,1 % de los casos hubo bajo peso y 16,7 % de talla baja al nacer. Conclusión: los hallazgos de la presente investigación, en general, coinciden con lo reportado en otros estudios efectuados en poblaciones análogas.

Abstract Objective:To characterize the diagnosed with epilepsy population at the "Hospital Infantil Universitario Rafael Henao Toro", in the city of Manizales (Colombia) from the behavior of the disease, risk factors, treatment and demographic characteristics. Methods: Cross-sectional study of the population referred to and performed by reviewing medical records. Results: of 172 patients, 51,2% were male gender; focal seizures were the most frequent with 59.1%; the most common comorbidity was delayed psychomotor development (30.9%), although if is consider the association with other diseases the figure is 57.9%; the most commonly monotherapy used was Valproic Acid (39.8%). Childhood epilepsy was associated with maternal hypertensive disorders in 8,7%; 21.7% had hypoxic-ischemic encephalopathy; 24.1% had a family history of epilepsy; in 15.1 % of cases was underweight and 16.7% of short stature at birth. Conclusion: The findings of this research, in general, agree with those reported in other studies in similar populations.

Perinatal brain lesions and epilepsy: prematurity and cerebral hypoxia evolving with west syndrome / Lesões cerebrais perinatais e epilepsia: prematuridade e hipóxia cerebral evoluindo com Síndrome de West / Lesiones cerebrales perinatales y epilepsia: prematuridad e hipoxia cerebral evolucionando con Síndrome de West

Introduction: West syndrome (WS) is the most frequent epileptic encephalopathy in the first year of life and is strongly correlated with prenatal and perinatal brain injury. Objective: To analyze the relationship between prematurity and birth asphyxia (cerebral hypoxia) with WS. Methods: This is an observational and cross-sectional study. All the patients with WS treated at Pediatric Neurology Service of Pequeno Príncipe Children?s Hospital from January 2010 to January 2015 were analyzed. The patients underwent magnetic resonance imaging (MRI) of the brain and electroen- cephalogram (EEG). Results: Thirty-eight patients with WS, 23 (60.53%) females; ages ranging from 9 to 27 months (±16.6 months). Twenty (52.63%) patients had a history of hypoxia/anoxia perinatal, 8 (21.05%) were premature, 8 (21.05%) had brain malformations, 4 (10.53%) had Down syndrome, 4 (10.53%) had tuberous sclerosis, and 2 (5.26%) had no comorbidities. MRI showed: 9 (23.68%) multi-cystic encephalomalacia, 4 (10.53%) periventricular leukomalacia, 4 (10.53%) periventricular leukomalacia with cerebral atrophy, 4 (10.53%) periventricular nodules, 3 (7.89%) brain atrophy, 2 (5.26%) pachygyria associated with agenesis of corpus callosum, one (2.63%) agenesis of the corpus callosum, one (2.63%) right frontal dysplasia, one (2.63%) left frontal dysplasia, one (2.63%) right frontoparietal dysplasia, one (2.63%) left frontoparietal dysplasia, and one (2.63%) pachygyria. Conclusion: The history of hypoxia/anoxia perinatal and prematurity is very frequent in WS. Improved care during pregnancy and childbirth is very important to reduce perinatal brain injury, premature birth, and neurological morbidity.

Introdução: A síndrome de West (SW) é a mais frequente encefalopatia epiléptica do primeiro ano de vida e está fortemente relacionada com lesões cerebrais pré-natais e perinatais. Objetivo: Analisar a relação entre prematuridade e asfixia perinatal (hipóxia cerebral) e SW. Métodos: Este é um estudo observacional e transversal. Todos os pacientes com SW tratados no Serviço de Neurologia Pediátrica do Hospital Infantil Pequeno Príncipe entre janeiro de 2010 e janeiro de 2015 foram analisados. Os pacientes foram submetidos a ressonância magnética (RM) do encéfalo e eletroencefalograma (EEG). Resultados: Trinta e oito pacientes com SW, 23 (60,53%) do sexo feminino; idade entre 9 a 27 meses (±16,6 meses). Vinte (52,63%) pacientes tinham história de hipóxia/anóxia perinatal, 8 (21,05%) eram prematuros, 8 (21,05%) tinham malformações cerebrais, 4 (10,53%) tinham síndrome de Down, 4 (10,53%) tinham esclerose tuberosa e 2 (5,26%) não apresentavam nenhuma comorbidade. A RM mostrou: 9 (23,68%) casos de encefalomalácia multicística, 4 (10,53%) leucomalácia periventricular, 4 (10,53%) leucomalácia periventricular com atrofia cerebral, 4 (10,53%) nódulos periventriculares, 3 (7,89%) atrofia cerebral, 2 (5,26%) paquigiria associada à atrofia de corpo caloso, um (2,63%) agenesia de corpo caloso, um (2,63%) displasia frontal direita, um (2,63%) displasia frontal esquerda, um (2,63%) displasia frontoparietal direita, um (2,63%) displasia frontoparietal esquerda e um (2,63%) paquigiria. Conclusão: A história de hipóxia/anóxia perinatal e prematuridade é muito frequente na SW. A melhora dos cuidados durante a gestação e o parto é muito importante para reduzir lesões cerebrais perinatais, nascimentos prematuros e consequentemente, a morbidade neurológica.

Introducción: El síndrome de West (SW) es la más frecuente encefalopatía epiléptica del primer año de vida y está fuertemente relacionado con lesiones cerebrales prenatales y perinatales. Objetivo: Analizar la relación entre prematuridad y asfixia perinatal (hipoxia cerebral) y SW. Métodos: Este es un estudio observacional y transversal. Fueron analizados todos los pacientes con SW tratados en el Servicio de Neurología Pediátrica del Hospital Infantil Pequeno Príncipe entre enero de 2010 y enero de 2015. Los pacientes fueron sometidos a resonancia magnética (RM) del encéfalo y electroence- falograma (EEG). Resultados: Treinta y ocho pacientes con SW, 23 (60,53%) del sexo femenino; edad entre 9 a 27 meses (±16,6 meses). Veinte (52,63%) pacientes tenían historia de hipoxia/anoxia perinatal, 8 (21,05%) eran prematuros, 8 (21,05%) tenían malformaciones cerebrales, 4 (10,53%) tenían síndrome de Down, 4 (10,53%) tenían esclerosis tuberosa y 2 (5,26%) no presentaban ninguna comorbilidad. La RM mostró: 9 (23,68%) casos de encefalomalacia multiquística, 4 (10,53%) con leucomalacia periventricular, 4 (10,53%) con leucomalacia periventricular con atrofia cerebral, 4 (10,53%) con nódulos periventriculares, 3 (7,89%) con atrofia cerebral, 2 (5,26%) con paquigiria asociada a la atrofia de cuerpo calloso, uno (2,63%) con agenesia de cuerpo calloso, uno (2,63%) con displasia frontal derecha, uno (2,63%) con displasia frontal izquierda, uno (2,63%) con displasia frontoparietal derecha, uno (2,63%) con displasia frontoparietal izquierda y uno (2,63%) con paquigiria. Conclusión: La historia de hipoxia/anoxia perinatal y prematuridad es muy frecuente en SW. La mejora de los cuidados durante la gestación y el parto es muy importante para reducir lesiones cerebrales perinatales, nacimientos prematuros y consiguientemente, la morbilidad neurológica.

Modelo experimettal de hipoperfusión cerebral poduce déficit de la memoria y aaprendizaje y modificaciones en la expresión de genes / Experimental Model of Cerebral Hypoperfusion Produced Memory-learning Deficits, and Modifications in Gene Expression

A escala mundial, la isquemia cerebral constituye una de las principales causas de muerte, por lo que los modelos animales de isquemia cerebral son extensamente usados tanto en el estudio de la pato-fisiología del fenómeno isquémico; como en la evaluación de agentes terapéuticos con posible efecto protector o regenerador. Los objetivos de este estudio fueron examinar la presencia de daño neuronal en diferentes áreas cerebrales como consecuencia del evento isquémico; así como evaluar consecuencias de este proceder sobre los procesos de memoria-aprendizaje. Los grupos de estudios incluyeron un grupo experimental de animales isquémicos, 30 ratas a las que se les ocluyó ambas arterias carótidas comunes, y un grupo control. Fue evaluada la expresión de genes isquémicos e inflamatorios por técnicas de qPCR 24 horas post lesión, la morfología del tejido cerebral en áreas de corteza, estriado e hipocampo, siete días post lesión y los procesos de memoria y aprendizaje, 12 días post lesión. Los estudios morfológicos evidenciaron que el proceder induce la muerte de poblaciones celulares en corteza, estriado e hipocampo; la isquemia modificó la expresión los genes gfap, ho-1, il-6, il-17 e ifn-γ, lo cual puede ser utilizado como un marcador de proceso isquémico temprano. Adicionalmente, el daño isquémico causó un deterioro en la memoria espacial. Esta caracterización nos permite contar con un modelo experimental donde desarrollar futuros estudios sobre la patofisiología de los eventos isquémicos y la evaluación de estrategias terapéuticas.

Cerebral ischemia is a major cause of death, for this reason animal models of cerebral ischemia are widely used to study both the pathophysiology of ischemic phenomenon and the evaluation of possible therapeutic agents with protective or regenerative properties. The objectives of this study were to examine the presence of neuronal damage in different brain areas following the ischemic event, and assess consequences of such activities on the processes of memory and learning. The study group included an experimental group ischemic animals (30 rats with permanent bilateral occlusion of the carotids), and a control group. Was evaluated gene expression and inflammatory ischemic by qPCR techniques 24h post injury, brain tissue morphology in areas of cortex, striatum and hippocampus seven days post injury and processes of memory and learning, 12 days post injury. The morphological studies showed that the procedure induces death of cell populations in cortex, striatum and hippocampus, ischemia modified gfap gene expression and ho, il-6, il-17 and ifn-γ, which can be used as a marker of early ischemic process. Additionally, the ischemic injury caused spatial memory decline. This characterization gives us an experimental model to develop future studies on the pathophysiology of ischemic events and assessing therapeutic strategies.

Expression of NF-κB subunits P50 and c-Rel protein in primary cortical neurons after oxygen glucose deprivation/reoxygenation / 第二军医大学学报

Objective: To investigate the expression of nuclear factor-κB (NF-κB) subunits P50 and c-Rel protein in primary cortical neurons of Wistar rats at different time points of oxygen glucose deprivation/ reoxygenation(OGD/R). Methods: The neurons dissociated from the cortex of the neonatal rats were primary cultured and were identified by immunocytochemistry. OGD/R model was established. The study was divided into 6 groups according to different processing methods,including normal group,OGD 4 h treated,OGD 4 h/R 2 h treated,OGD 4 h/R 6 h treated,OGD 4 h/R 12 h treated and OGD 4 h/R 24 h treated groups. The expression of NF-κB P50 and c-Rel protein in neurons was examined by immunocytochemistry method and Western blotting. Results: (1) Immunocytochemistry detection targeting neuron specific enolase (NSE) and beta-III tubulin confirmed that the cultured cells were neurons. (2) The expression of NF-κB P50 protein was significantly higher in OGD 4 h group than in control group(P<0.05); the expression continued to increase in OGD 4 h/R 2 h andOGD 4 h/R 6 h groups, and reached its peak 6 h after reoxygenation (P<0.01),then began to decrease,but the expression in OGD 4 h/R 12 h group was significantly different from that of the control group (P<0.05); there was no significant difference between OGD 4 h/R 24 h group and control group. (3) The expression of NF-κB c-Rel protein was similar between OGD 4 h group and the control group; the expression increased in OGD 4 h/R 2 h and OGD 4 h/R 12 h groups and reached its peak 12 h after reoxygenation(P<0.01),and did not recover to the normal level in OGD 4 h/ R 24 h group (P<0.05). Conclusion: Oxygen glucose deprivation/reoxygenation can activate NF-κB subunits P50 and c-Rel in the primary cortical neurons in rats in a time-associated manner.

Research of Mild Hypothermia on Expression of AKT after Hypoxia-Ischemia Brain Damage / 医学研究杂志

Objective To study the effect of local mild hypothermia on AKT protein expression after rats focal cerebral ischemia-reperfusion injury.Methods By using the model of rat focal cerebral ischemia-reperfusion injury,the middle cerebral arteries(MCA)of SD rats were occluded for 2 h,and reperfused for2h,12h,24h,72h.Immunohistochemical analysis was used to detect expression of AKT.Results AKT expressed after ischemia 2h,the expression was significantly increased after ischemia reperfusion with peak expression at 72h in model group on normal temperature.In mild hypothermia group,the AKT expression was higher than that in normal temperature group when at the same time point.Conclusion Brain hypoxia-ischemia could induce the expression of AKT.Mild hypothermia could promote the expression of AKT.The expression of AKT could be one of the protected way of brain hypoxia-ischemia.

Role of Tissue-Type Plasminogen Activator in Neonatal Rat with Hypoxia-Ischemia Brain Damage / 实用儿科临床杂志

Objective To explore the role of tissue-type plasminogen activator(tPA) in neonatal rat with hypoxia-ischemia brain damage(HIBD).Methods Seven-day-old Wistar rat pups were used for the Vannucci model of HIBD.Reverse transcription-polymerase chain reaction(RT-PCR),terminal deoxynucleotidyl transferase mediated dUTP nick end labeling(TUNEL),double immunostaining and immunoblot analysis were adapted to determin the expression of tPA at acute phase after HIBD and neural cell apoptosis and the blood-brain-barrier(BBB) damage.Results Neonatal hypoxia-ischemia triggers persistent induction of the plasminogen system.The increase of tPA activity induced the degradation of laminin and occludin which would aggravate the BBB damage.The number of neural cell apoptosis after HIBD increased progressively with the reperfusion time.Conclusions The increase of tPA at the acute phase after HIBD can help clot to dissolve,while its extravascular proteolysis will induce cell apoptosis and BBB damage which will aggravate brain injury.

Effects of exogenous brain-derived neurotrophic factors on concentrations of cerebral endogenous opioid peptides in neonatal rats subject to with hypoxic-ischemic brain injury / 中华物理医学与康复杂志

Objective To explore the effects of brain derived neurotrophic factors (BDNF) on concentrations of cerebral endogenous opioid peptides(EOP)in neonatal rats subject to with hypoxic ischemic brain injury (HIBI). Methods Seven day old Sprague Dawley rats were randomly divided into a HIBI+BDNF group (group A),a HIBI group (group B) and a sham operation group (group C). Models of HIBI were established by use of permanent ligation of the left common carotid artery followed by 2.5 hours ofinhalation of 8%O 2+92%N 2, then 0.5 ?g BDNF was injected into the parietal cerebral ventricle in group A immediately. Contents of dynorphin A 1 13 like, ? endorphin like and leu enkaphalin like immunoreactivities (ir DynA 1 13 , ir ? EP and ir LEK) in cortex and hippocampus were measured at 0, 60, 120 min after administration of BDNF. Results The concentrations of ir DynA 1 13 and ir ? EP in the cortex and hippocampus in group B were increased significantly than those in group C at most time points( P

Effects of different interval intracerebroventricular administration of brain-derived neurotrophic factor on hypoxic ischemic encephalopathy in neonatal rats / 中国药理学通报

AIM: To observe the effects of different interval administration of exogenous brain derived neurotrophic factor (BDNF) on hypoxic-ischemic encephalopathy in neonatal rats. METHODS: BDNF (0.5 μg) was microinjected intracerebroventricularly at 0, 1 and 4 h after the hypoxic-ischemic encephalopathy in 7 d neonatal Sprague-Dawley rats undergone by ligation of left common carotid artery followed by a 2.5 h inhalation of humidified 8% 02 + 92% N2 at 37°C immediately after the injury, respectively. Changes of brain edema, levels of malondialehyde (MDA) and neuronal apoptosis at the left cortex and hippocampus were investigated 24 h after the injury. RESULTS: The most prominent effect of BDNF was seen in 0 h group with a marked decreases in brain edema and levels of MDA and a significantly alleviated neuronal apoptosis while it was lowered obviously when administered at 4 h after the insult. CONCLUSION: BDNF exerts a prominent protective effect on hypoxic-ischemic encephalopathy in neonatal rats when given as early as possible after the injury rather than later administration.

EFFECTS OF INTRACEREBROVENTRICULAR INJECTION OF BDNF ON HYPOXIC ISCHEMIC ENCEPHALOPATHY IN NEONATAL RATS / 解放军医学杂志

To explore the effects of brain derived neurotrophic factor (BDNF) on hypoxic ischemic encephalopathy in neonatal rats,0 2, 0 5 or 2 0?g of BDNF was injected into cerebroventricles of 7d neonatal Sprague Dawley rats with hypoxic ischemic encephalopathy by ligation of left common carotid artery and 2 5h inhalation of humidified 8% O 2 +92% N 2 at 37℃. Its effects on brain edema, levels of malondialehyde (MDA) and neuronal apoptosis at the left cortex and hippocampus were observed. The results showed that brain edema was markedly alleviated in 0 5?g group compared to the vehicle group 24h after BDNF injection. Levels of MDA in the left hemisphere in 2 0?g group were significantly higher than those in either vehicle group or 0 5?g group. Neuronal apoptosis decreased to a different extent in the three groups while obviously in both 0 2?g and 0 5?g groups. It is suggested that BDNF exerts a prominent protective effect on hypoxic ischemic encephalopathy in neonatal rats, but this effect is lowered when overdose is injected.

Expression of NF-?B subunits P50 and c-Rel protein in primary cortical neurons after oxygen glucose deprivation/reoxygenation / 第二军医大学学报

Objective:To investigate the expression of nuclear factor-?B(NF-?B)subunits P50 and c-Rel protein in primary cortical neurons of Wistar rats at different time points of oxygen glucose deprivation/reoxygenation(OGD/R).Methods:The neurons dissociated from the cortex of the neonatal rats were primary cultured and were identified by immunocytochemistry.OGD/R model was established.The study was divided into 6 groups according to different processing methods,including normal group,OGD 4 h treated,OGD 4 h/R 2 h treated,OGD 4 h/R 6 h treated,OGD 4 h/R 12 h treated and OGD 4 h/R 24 h treated groups.The expression of NF-?B P50 and c-Rel protein in neurons was examined by immunocytochemistry method and Western blotting.Results:(1)Immunocytochemistry detection targeting neuron specific enolase(NSE)and beta-Ⅲ tubulin confirmed that the cultured cells were neurons.(2)The expression of NF-?B P50 protein was significantly higher in OGD 4 h group than in control group(P

Enhancing Effect of Exogenous Gangliosides on Learning and Memory in Hypoxic-ischemic Brain Damage Rats / 中华围产医学杂志

Objective To investigate the effect of exogenous GAs on learning and memory capability of hypoxic-ischemic(HI) brain damage rats. Methods After ligation of the right carotid artery of 7-day old male SD rats and waiting for 4 hours of recovery, the rats were exposed to 8% oxygen-92% nitrogen gas mixture for 2 hours. The HI animals were randomly divided into 3 groups. GAs-treated group 1: animals were injected i.p. GAs immediately after HI every 12 hours for 4 doses with 50 mg/kg, followed by a 2 weeks consecutive daily injections at dose of 30 mg/kg/day. GAs treated group 2: rats received GAs 50 mg/kg immediately after HI every 12 hours for 4 doses, followed by injection of saline in the same volums for 2 weeks. Control group: rats received saline in the equivalent volums and duration. The behavioral test starded when the animals were 24 days old. Discriminative learning ability and memory retention were tested in the tri-equal-arms maze . The locomotor activity and alternative behavior was observed. The degree of neuronal damage were assessed after behavioral test. Results (1)The number of trails to reach the learning criteria were (39?17), (32?14)and (20?13) for control group, GAs-treated group 2 and GAs-treated group 1, respectively. The percentages of memory retention for control group, GAs-treated group 2 and GAs-treated group 1 were (62?10)%, (64?11)% and (70?9)%, respectively. Two weeks consecutive daily injection of GAs had facilitatory effects on learning ability and memory retention of HI rats(P0.05). Conclusion Gangliosides can enhance the learning ability and memory retention in neonate rats with HI.

Anesthetic Management of Patient with Renal Cell Carcinoma Extending into the Right Atrium Using Adjunctive Deep Hypothermic Circulatory Arrest: A case report / 대한마취과학회지

Renal cell carcinoma is associated with inferior vena cava tumor spread in 4~10% of cases and with extension of the tumor thrombus into the right atrium in less than 1% of cases. Because inferior vena caval involvement does not affect the ultimate survival in patients with nonmetastatic renal cell carcinoma, aggressive surgical resection is indicated. We experienced a case of complete tumor excision with radical nephrectomy and inferior vena caval and right atrial thrombectomy using adjunctive cardiopulmonary bypass(CPB) and deep hypothermic circulatory arrest(DHCA). During total circulatory arrest(TCA), we protected brain from ischemic insult using deep hypothermia, retrograde cerebral perfusion, thiopental, and high dose steroid. The patient recovered uneventfully except minor neuropsychiatric symptom for 3 weeks after operation.

Effects of GSRb3 on GABA in brain tissue of rats with injury of hypoxia / 临床神经病学杂志

Objective To observe the influence of ginsenoside Rb3(GSRb3) on ?-aminobutyric acid (GABA) in brain tissue of rats with injury of hypoxia.Methods 20 rats were randomly divided into A, B, C, D and E group. The models of cerebral anoxia in group A and C were made by hypopiesia and hypoxia, and the models of hypoxia-reoxgenation were made in group B and D. 24 h and 1 h before establishment of models, ginsenoside Rb3 was injected peritoneally in rats of group C and D, respectively. The number and form of GABA-like immunoreactive neurons in hippocampus CA1 area of rats after brain hypoxia-reoxgenation were investigated with immunohistochemistry.Results (1)Compared with group E, GABA-like immunoreactive neuron density in CA1 area of group A and B decreased, presented with light staining and absence of prominency. GABA-like immunoreactive neuron density in CA1 area in group C and D was significantly higher than that in group A and B, but the shape was similar to group E. (2) The number of GABA-like immunoreactive neuron in CA1 area was 7.7?2.83 (group A), 10.1?2.08 (group B), 30.9?2.02 (group C), 33.1?4.2 (group D) and 16.9?1.05 (group E), respectively. The numbers were lower in group A and B than in group E, however higher in group C and D than in group E(all P

Effects of different interval intracerebroventricular administration of brain-derived neurotrophic factor on hypoxic ischemic encephalopathy in neonatal rats / 中国药理学通报

AIM To observe the effects of different interval administration of exogenous brain derived neurotrophic factor (BDNF) on hypoxic ischemic encephalopathy in neonatal rats. METHODS BDNF (0 5 ?g) was microinjected intracerebroventricularly at 0, 1 and 4 h after the hypoxic ischemic encephal opathy in 7 d neonatal Sprague Dawley rats undergone by ligation of left common carotid artery followed by a 2 5 h inhalation of humidified 8% O 2+92% N 2 at 37℃ immediately after the injury, respectively. Changes of brain edema, levels of malondialehyde (MDA) and neuronal apoptosis at the left cortex and hippocampus were investigated 24 h after the injury. RESULTS The most prominent effect of BDNF was seen in 0 h group with a marked decreases in brain edema and levels of MDA and a significantly alleviated neuronal apoptosis while it was lowered obviously when administered at 4 h after the insult. CONCLUSION BDNF exerts a prominent protective effect on hypoxic ischemic encephalopathy in neonatal rats when given as early as possible after the injury rather than later administration.