RESUMO
Se revisan la fisiopatología y los mecanismos que producen la sofocación en el hematoma cervical y se determina que el único tratamiento con posibilidades de éxito vital es el inmediato drenaje del hematoma.
In this article are reviewed the physiopathology and the mechanisms that causes suffocation in the cervical hematoma. It is determined that the only treatment with possibilities of vital success is the immediate drainage of the hematoma.
Assuntos
Humanos , Asfixia/etiologia , Drenagem , Hematoma/fisiopatologia , Hematoma/terapia , Complicações Pós-Operatórias , Asfixia/fisiopatologia , Vértebras Cervicais/cirurgia , Pescoço/cirurgiaRESUMO
Perinatal asphyxia (PA) is one of the most frequent risk factors for several neurodevelopmental disorders (NDDs) of presumed multifactorial etiology. Dysfunction of neuronal connectivity is thought to play a central role in the pathophysiology of NDDs. Because underlying causes of some NDDs begin before/during birth, we asked whether this clinical condition might affect accurate establishment of neural circuits in the hippocampus as a consequence of disturbed brain plasticity. We used a murine model that mimics the pathophysiological processes of perinatal asphyxia. Histological analyses of neurons (NeuN), dendrites (MAP-2), neurofilaments (NF-M/Hp) and correlative electron microscopy studies of dendritic spines were performed in Stratum radiatum of the hippocampal CA1 area after postnatal ontogenesis. Protein and mRNA analyses were achieved by Western blot and RT-qPCR. Behavioral tests were also carried out. NeuN abnormal staining and spine density were increased. RT-qPCR assays revealed a ß-actin mRNA over-expression, while Western blot analysis showed higher ß-actin protein levels in synaptosomal fractions in experimental group. M6a expression, protein involved in filopodium formation and synaptogenesis, was also increased. Furthermore, we found that PI3K/Akt/GSK3 pathway signaling, which is involved in synaptogenesis, was activated. Moreover, asphyctic animals showed habituation memory changes in the open field test. Our results suggest that abnormal synaptogenesis induced by PA as a consequence of excessive brain plasticity during brain development may contribute to the etiology of the NDDs. Consequences of this altered synaptic maturation can underlie some of the later behavioral deficits observed in NDDs.
Assuntos
Asfixia/patologia , Hipocampo/fisiopatologia , Plasticidade Neuronal/fisiologia , Análise de Variância , Animais , Asfixia/fisiopatologia , Aprendizagem da Esquiva/fisiologia , Espinhas Dendríticas/metabolismo , Espinhas Dendríticas/patologia , Espinhas Dendríticas/ultraestrutura , Comportamento Exploratório/fisiologia , Feminino , Hipocampo/metabolismo , Hipocampo/patologia , Hipocampo/ultraestrutura , Microscopia Eletrônica , Proteínas do Tecido Nervoso/genética , Proteínas do Tecido Nervoso/metabolismo , Gravidez , Células Piramidais/metabolismo , Células Piramidais/patologia , RNA Mensageiro/metabolismo , Ratos , Ratos Sprague-Dawley , Transdução de Sinais/fisiologia , Frações Subcelulares/metabolismo , Frações Subcelulares/ultraestruturaRESUMO
BACKGROUND: One of the most important manifestations of perinatal asphyxia is the occurrence of seizures, which are treated with antiepileptic drugs, such as carbamazepine. These early seizures, combined with pharmacological treatments, may influence the development of dopaminergic neurotransmission in the frontal cortex. This study aimed to determine the extracellular levels of dopamine and its main metabolite DOPAC in 30-day-old rats that had been asphyxiated for 45 min in a low (8%) oxygen chamber at a perinatal age and treated with daily doses of carbamazepine. Quantifications were performed using microdialysis coupled to a high-performance liquid chromatography (HPLC) system in basal conditions and following the use of the chemical stimulus. RESULTS: Significant decreases in basal and stimulated extracellular dopamine and DOPAC content were observed in the frontal cortex of the asphyxiated group, and these decreases were partially recovered in the animals administered daily doses of carbamazepine. Greater basal dopamine concentrations were also observed as an independent effect of carbamazepine. CONCLUSIONS: Perinatal asphyxia plus carbamazepine affects extracellular levels of dopamine and DOPAC in the frontal cortex and stimulated the release of dopamine, which provides evidence for the altered availability of dopamine in cortical brain areas during brain development.
Assuntos
Ácido 3,4-Di-Hidroxifenilacético/metabolismo , Anticonvulsivantes/farmacologia , Asfixia/fisiopatologia , Carbamazepina/farmacologia , Dopamina/metabolismo , Lobo Frontal/efeitos dos fármacos , Animais , Asfixia/etiologia , Lobo Frontal/metabolismo , Masculino , Ratos , Ratos WistarRESUMO
Breathing and the activity of its generator (the pre-Bötzinger complex; pre-BötC) are highly regulated functions. Among neuromodulators of breathing, somatostatin (SST) is unique: it is synthesized by a subset of glutamatergic pre-BötC neurons, but acts as an inhibitory neuromodulator. Moreover, SST regulates breathing both in normoxic and in hypoxic conditions. Although it has been implicated in the neuromodulation of breathing, neither the locus of SST modulation, nor the receptor subtypes involved have been identified. In this study, we aimed to fill in these blanks by characterizing the SST-induced regulation of inspiratory rhythm generation in vitro and in vivo. We found that both endogenous and exogenous SST depress all preBötC-generated rhythms. While SST abolishes sighs, it also decreases the frequency and increases the regularity of eupnea and gasping. Pharmacological experiments showed that SST modulates inspiratory rhythm generation by activating SST receptor type-2, whose mRNA is abundantly expressed in the pre-Bötzinger complex. In vivo, blockade of SST receptor type-2 reduces gasping amplitude and consequently, it precludes auto-resuscitation after asphyxia. Based on our findings, we suggest that SST functions as an inhibitory neuromodulator released by excitatory respiratory neurons when they become overactivated in order to stabilize breathing rhythmicity in normoxic and hypoxic conditions.
Assuntos
Asfixia/fisiopatologia , Inalação/efeitos dos fármacos , Neurotransmissores/farmacologia , Centro Respiratório/efeitos dos fármacos , Somatostatina/farmacologia , Animais , Asfixia/metabolismo , Asfixia/mortalidade , Fenômenos Eletrofisiológicos , Hipóxia/metabolismo , Hipóxia/mortalidade , Hipóxia/fisiopatologia , Inalação/fisiologia , Camundongos , Neurônios/efeitos dos fármacos , Neurônios/patologia , Neurônios/fisiologia , Neurotransmissores/fisiologia , Periodicidade , Pletismografia , Receptores de Somatostatina/agonistas , Receptores de Somatostatina/genética , Centro Respiratório/fisiologia , Somatostatina/fisiologia , Taxa de Sobrevida , Regulação para CimaRESUMO
Perinatal asphyxia (PA) may cause long-term neurological and psychiatric diseases. We evaluated, by ethanolic phosphotungstic acid (E-PTA) staining, whether PA affects postsynaptic densities (PSDs), ultrastructure of neostriatum and hippocampus of 45-day-old post-PA male and female rats. PA was induced by placing the uterine horns containing the fetuses in a 37°C bath for 10, 15, 19 and 20 min and a 15°C bath for 20 min (hypothermia). Striatal synaptic disorganization and PSDs thickness increase were evident after 10 and 19 min of PA in male and female rats, respectively, but striatal female PSDs thickness was lower than in males. These changes were associated with increments of the PSDs area in both sexes at 19 and 20 min PA. Thickness and PSDs area from hippocampal PA males was affected more negatively than in females. Intrahypoxic hypothermia was able to protect the brain from effects of PA. In conclusion, early PA affects neostriatal and hippocampal PSDs in a time and sex-dependent manner, while hypothermia during asphyxia is able to prevent synaptic changes by providing protection from damage.
Assuntos
Asfixia/patologia , Hipocampo/ultraestrutura , Hipotermia Induzida , Neostriado/ultraestrutura , Sinapses/ultraestrutura , Animais , Animais Recém-Nascidos , Asfixia/fisiopatologia , Feminino , Masculino , Densidade Pós-Sináptica/ultraestrutura , Gravidez , Ratos , Ratos Sprague-DawleyRESUMO
Piglets appear to be neurologically sensitive to intrapartum asphyxia. Our aim was to investigate the short-term neurophysiologic consequences of intrapartum asphyxia in piglets. We studied 10 piglets suffering intrapartum asphyxia and 10 control piglets. Glucose and blood gas levels, tympanic membrane temperature, and body weight were measured within the first 2 min after birth. Animals were followed up for a 5-day period. As surrogated markers of piglets' neurological function, a viability score and the time elapsed from birth to the first contact with the maternal udder were recorded. In the control group, temperature and blood pH levels at birth were significantly higher (p < or = .001), whereas calcium, lactate and PCO2 levels were statistically lower (p < or = .05) than in the piglets experiencing intrapartum asphyxia. Lower temperature and blood pH levels as well as higher blood PCO2 and lactate levels were observed in piglets with lower viability scores and in piglets with prolonged times until first udder contact. At the end of the study, asphyxiated piglets weighed on average 200 g less (p = .023) than control piglets. In conclusion, intrapartum asphyxia in spontaneously born piglets was associated with signs of acute neurological dysfunction and lower weight gain, supporting the hypothesis that they may be used as a naturalistic model for the study of asphyxia in newborns.
Assuntos
Asfixia/fisiopatologia , Parto/fisiologia , Acidose Respiratória/diagnóstico , Acidose Respiratória/metabolismo , Acidose Respiratória/fisiopatologia , Animais , Animais Recém-Nascidos , Asfixia/diagnóstico , Asfixia/metabolismo , Gasometria/métodos , Glicemia/metabolismo , Glicemia/fisiologia , Eletrólitos/metabolismo , Feminino , Parto/metabolismo , Distribuição Aleatória , Suínos , Fatores de TempoRESUMO
PURPOSE: The usefulness of body movements that occur during sleep when assessing perinatal asphyxia and predicting its long-term consequences is contradictory. This study investigated whether neonatal rats manifest these movements in compensatory rebound after asphyxia, and if these alterations play an important role in its pathogenesis. METHODS: Eight neonatal rats (aged 6-48 h) were implanted with small EMG and EKG electrodes and sleep movements were recorded over a 30-minute control period. Recordings were continued during asphyxia caused by the enclosure of the animal in a polyvinyl sheet for 60 minutes, followed by a 30-minute recovery period. RESULTS: Heart rate was lowered to bradycardic level during asphyxia causing behavioral agitation and increased waking time during the initial phase (30 minutes). Sleep-related movements were also significantly reduced from 12.5 +/- 0.5 (median +/- SE/2min) to 9.0 +/- 0.44 in the final half of the period (Anova, p<0.05). Movement frequency increased in the recovery period to 15.0 +/- 0.49 (Anova, p<0.05). CONCLUSION: These data show that newborn rats present compensatory rebound of body movements during sleep which may help in the diagnosis of asphyxia and other problems related to sleep parameters.
Assuntos
Asfixia/fisiopatologia , Atividade Motora/fisiologia , Parassonias/fisiopatologia , Sono/fisiologia , Animais , Animais Recém-Nascidos , Asfixia/complicações , Modelos Animais de Doenças , Eletromiografia , Frequência Cardíaca , Parassonias/etiologia , Polissonografia , Ratos , Ratos Wistar , Fatores de TempoRESUMO
PURPOSE: The usefulness of body movements that occur during sleep when assessing perinatal asphyxia and predicting its long-term consequences is contradictory. This study investigated whether neonatal rats manifest these movements in compensatory rebound after asphyxia, and if these alterations play an important role in its pathogenesis. METHODS: Eight neonatal rats (aged 6-48h) were implanted with small EMG and EKG electrodes and sleep movements were recorded over a 30-minute control period. Recordings were continued during asphyxia caused by the enclosure of the animal in a polyvinyl sheet for 60 minutes, followed by a 30-minute recovery period. RESULTS: Heart rate was lowered to bradycardic level during asphyxia causing behavioral agitation and increased waking time during the initial phase (30 minutes). Sleep-related movements were also significantly reduced from 12.5 ± 0.5 (median ± SE/2min) to 9.0 ± 0.44 in the final half of the period (Anova, p<0.05). Movement frequency increased in the recovery period to 15.0 ± 0.49 (Anova, p<0.05). CONCLUSION: These data show that newborn rats present compensatory rebound of body movements during sleep which may help in the diagnosis of asphyxia and other problems related to sleep parameters.
OBJETIVO: A utilidade dos movimentos corporais (MC) que ocorrem durante o sono para diagnosticar e predizer as conseqüências, em longo prazo, da asfixia perinatal é contraditório. Este estudo investigou se ratos recém-nascidos (RN) manifestam MC em resposta compensatória à asfixia, e se estas alterações podem ter alguma importância na sua patogênese. MÉTODOS: Oito ratos RN (6-48h de vida) foram submetidos à implantação de pequenos eletrodos para registros da eletromiografia e eletrocardiografia. Os MC e a freqüência cardíaca (FC) foram registrados durante períodos de 30 min: fase controle (F1), fases de asfixia (F2; F3) e fase de recuperação pós-asfixia (F4). A asfixia foi promovida pelo envolvimento completo do animal com uma lâmina de polivinil. RESULTADOS: A FC diminuiu progressivamente durante F2 e F3 até a bradicardia. Em F2 houve grande agitação dos animais e aumento dos períodos de vigília. Em F3 houve redução significante dos MC de 12,5 ± 0,5 (Md ± SE/2min) para 9,0 ± 0,44 (P<0,05). A freqüência dos MC aumentou em F4 para 15,0 ± 0,49. CONCLUSÃO: Estes dados mostram que ratos RN com asfixia apresentam MC compensatórios durante o sono que podem ajudar no diagnóstico desta afecção e de outros problemas relacionados aos parâmetros do sono.
Assuntos
Animais , Ratos , Asfixia/fisiopatologia , Atividade Motora/fisiologia , Parassonias/fisiopatologia , Sono/fisiologia , Animais Recém-Nascidos , Asfixia/complicações , Modelos Animais de Doenças , Eletromiografia , Frequência Cardíaca , Polissonografia , Parassonias/etiologia , Ratos Wistar , Fatores de TempoRESUMO
There is clinical and experimental evidence indicating that neurocircuitries of the hippocampus are vulnerable to hypoxia/ischemia occurring at birth, inducing, upon re-oxygenation/re-circulation, delayed neuronal death, but also compensatory mechanisms, including neurogenesis. In the present report, perinatal asphyxia was induced by immersing foetuses-containing uterine horns removed from ready-to-deliver rats into a water bath at 37 degrees C for 20 min. Some pups were delivered immediately after the hysterectomy to be used as non-asphyxiated caesarean-delivered controls. The pups were sacrificed after seven days for preparing organotypic hippocampal cultures. The cultures were grown on a coverslip in a medium-containing culture tube inserted in a hole of a roller device standing on the internal area of a cell incubator at 35 degrees C, 10% CO2. At days in vitro (DIV) 25-27, cultures were fixed for assaying cell proliferation and neuronal phenotype with antibodies against 5-bromo-2'deoxyuridine (BrdU) and microtubule associated protein-2 (MAP-2), respectively. Confocal microscopy revealed that there was a 2-fold increase of BrdU-positive, but a 40% decrease of MAP-2-positive cells/mm3 in cultures from asphyxia-exposed, compared to that from control animals. Approximately 30% of BrdU-positive cells were also positive for MAP-2 (approximately 4800 cells), mainly seen in the dentate gyrus of the hippocampus, demonstrating a 3-fold increase of postnatal neurogenesis, when the total amount of double-labelled cells seen in cultures from asphyxia-exposed animals is compared to that from control animals.
Assuntos
Asfixia/fisiopatologia , Hipocampo/fisiopatologia , Neurônios/fisiologia , Animais , Animais Recém-Nascidos , Neurônios/citologia , Técnicas de Cultura de Órgãos , Fosfoproteínas Fosfatases/efeitos dos fármacos , Fosfoproteínas Fosfatases/metabolismo , RatosRESUMO
The present report summarizes studies combining an in vivo and in vitro approach, where asphyxia is induced in vivo at delivery time of Wistar rats, and the long term effects on hippocampus neurocircuitry are investigated in vitro with organotypic cultures plated at postnatal day seven. The cultures preserved hippocampus layering and regional subdivisions shown in vivo, and only few dying cells were observed when assayed with a viability test at day in vitro 27. When properly fixed, cultures from asphyxia-exposed animals showed a decreased amount of microtubule-associated protein-2 immunocytochemically positive cells (approximately 30%), as compared with that from controls. The decrease in microtubule-associated protein-2 immunocytochemistry was particularly prominent in Ammon's horn 1 and dentate gyrus regions (approximately 40%). 5-Bromo-2'deoxyuridine labeling revealed a two-fold increase in cellular proliferation in cultures from asphyxia-exposed, compared with that from control animals. Furthermore, confocal microscopy and quantification using the optical disector technique demonstrated that in cultures from asphyxia-exposed animals approximately 30% of 5-bromo-2'deoxyuridine-positive cells were also positive to microtubule-associated protein-2, a marker for neuronal phenotype. That proportion was approximately 20% in cultures from control animals. Glial fibrillary acidic protein-immunocytochemistry and Fast Red nuclear staining revealed that the core of the hippocampus culture was surrounded by a well-developed network of glial fibrillary acidic protein-positive cells and glial fibrillary acidic protein-processes providing an apparent protective shield around the hippocampus. That shield was less developed in cultures from asphyxia-exposed animals. The increased mitotic activity observed in this study suggests a compensatory mechanism for the long-term impairment induced by perinatal asphyxia, although it is not clear yet if that mechanism leads to neurogenesis, astrogliogenesis, or to further apoptosis.