OBJECTIVES: Desaturation leading to hypoxemia may occur during rapid sequence intubation (RSI). Apneic oxygenation (AO) was developed to prevent the occurrence of oxygen desaturation during the apnea period. The purpose of this study was to determine if the application of AO increases the average lowest oxygen saturation during RSI when compared to usual care (UC) in the emergency setting. METHODS: A randomized controlled trial was conducted at an academic, urban, Level I trauma center. All patients requiring intubation were included. Exclusion criteria were patients in cardiac or traumatic arrest or if preoxygenation was not performed. An observer, blinded to study outcomes and who was not involved in the procedure, recorded all times, while all saturations were recorded in real time by monitors on a secured server. Two-hundred patients were allocated to receive AO (n = 100) or UC (n = 100) by predetermined randomization in a 1:1 ratio. RESULTS: A total of 206 patients were enrolled. There was no difference in lowest mean oxygen saturation between the two groups (92, 95% confidence interval [CI] = 91 to 93 in AO vs. 93, 95% CI = 92 to 94 in UC; p = 0.11). CONCLUSION: There was no difference in lowest mean oxygen saturation between the two groups. The application of AO during RSI did not prevent desaturation of patients in this study population.
Hypoxia/prevention & control , Intubation, Intratracheal , Oxygen Inhalation Therapy/methods , Emergency Service, Hospital , Female , Humans , Male , Middle Aged , New York City , Oxygen/blood , Trauma Centers
Spinal muscular atrophy (SMA) is an autosomal-recessive disorder characterized by severe, often fatal muscle weakness due to loss of motor neurons. SMA patients have deletions and other mutations of the survival of motor neuron 1 (SMN1) gene, resulting in decreased SMN protein. Astrocytes are the primary support cells of the CNS and are responsible for glutamate clearance, metabolic support, response to injury, and regulation of signal transmission. Astrocytes have been implicated in SMA as in in other neurodegenerative disorders. Astrocyte-specific rescue of SMN protein levels has been shown to mitigate disease manifestations in mice. However, the mechanism by which SMN deficiency in astrocytes may contribute to SMA is unclear and what aspect of astrocyte activity is lacking is unknown. Therefore, it is worthwhile to identify defects in SMN-deficient astrocytes that compromise normal function. We show here that SMA astrocyte cultures derived from mouse spinal cord of both sexes are deficient in supporting both WT and SMN-deficient motor neurons derived from male, female, and mixed-sex sources and that this deficiency may be mitigated with secreted factors. In particular, SMN-deficient astrocytes have decreased levels of monocyte chemoactive protein 1 (MCP1) secretion compared with controls and MCP1 restoration stimulates outgrowth of neurites from cultured motor neurons. Correction of MCP1 deficiency may thus be a new therapeutic approach to SMA.SIGNIFICANCE STATEMENT Spinal muscular atrophy (SMA) is caused by the loss of motor neurons, but astrocyte dysfunction also contributes to the disease in mouse models. Monocyte chemoactive protein 1 (MCP1) has been shown to be neuroprotective and is released by astrocytes. Here, we report that MCP1 levels are decreased in SMA mice and that replacement of deficient MCP1 increases differentiation and neurite length of WT and SMN-deficient motor-neuron-like cells in cell culture. This study reveals a novel aspect of astrocyte dysfunction in SMA and indicates a possible approach for improving motor neuron growth and survival in this disease.
Astrocytes/metabolism , Chemokine CCL2/metabolism , Motor Neurons/metabolism , Muscular Atrophy, Spinal/metabolism , Survival of Motor Neuron 1 Protein/genetics , Animals , Astrocytes/cytology , Cells, Cultured , Chemokine CCL2/genetics , Female , Humans , Male , Mice , Motor Neurons/cytology , Spinal Cord/cytology , Spinal Cord/metabolism , Survival of Motor Neuron 1 Protein/metabolism
This unit describes methods for loading ion- and voltage-sensitive dyes into neurons, with a particular focus on the spinal cord as a model system. In addition, we describe the use of these dyes to visualize neural activity. Although the protocols described here concern spinal networks in culture or an intact in vitro preparation, they can be, and have been, widely used in other parts of the nervous system.
Central Nervous System/physiology , Electrophysiology/methods , Fluorescent Dyes/chemistry , Neurophysiology/methods , Staining and Labeling/methods , Animals , Central Nervous System/cytology , Humans , Microscopy, Fluorescence/methods , Nerve Net/cytology , Nerve Net/physiology , Neurons/cytology , Neurons/physiology , Spinal Cord/cytology , Spinal Cord/physiology
Para identificar los factores causales de la oliguria transitoria que se observa en los procedimientos laparoscópicos, 3 experimentos fueron llevados a cabo. En el primer experimento 12 perros fueron sometidos a insuflación abdominal a 15 mm de Hg. A seis de ellos se les suministró una dosis de la enzima convertidora de la angiotensina (ECA ENALAPRIL) y fueron comparados con los seis a los cuales sólo se les sometió a insuflación abdominal y sirvieron como control. La administración del inhibidor de la ECA no logró prevenir la disminución de la diuresis, la tasa de filtración ni el flujo efectivo renal plasmático. Debido a estos hallazgos pudimos inferir que la actividad del sistema renina angiotensina no era la responsable de la oliguria transitoria de la laparoscopia. En el segundo experimento un catéter ureteral fue colocado en la pelvis renal para evitar el efecto compresivo del neumoperitoneo a lo largo del trayecto ureteral, el otro uréter fue dejado sin catéter y sirvió como su propio control para los seis perros de esta fase experimental. La comparación entre ambos riñones de este grupo demostró que el efecto compresivo ureteral no era el responsable de la disminución de diuresis. TFG ni FEPR. En el experimento final de la compresión renal directa fue investigado, una bolsa de presión fue diseñada para introducir uno de los riñones en este nuevo grupo de seis animales e insuflado a 15 mm de Hg dejando el riñon contralateral como su propio control. Durante el periódo experimental se encontró una diferencia significativa entre ambos riñones con un 63 por ciento de disminución en la diuresis (P<0.05) una disminución del 21 por ciento para la TFG (P<0.01) y una disminución del 25 por ciento en el FEPR (P<0.05). Luego de desinsuflar el riñon experimental todos los parámetros regresaron a niveles basales. Estos resultados soportan de manera irregular la importancia contribución de la compresión renal directa a la génesis de la oliguria inducida por la laparoscopia
Animals , Dogs , Oliguria/etiology , Laparoscopy , Insufflation
