Traumatic brain injury in the rat: Characterization of a lateral fluid-percussion model

McIntosh, Tracy K.; Vink, Robert; Noble, Linda; Yamakami, Iwao; Fernyak, Susan; Soares, Holly; Ai, Faden

doi:10.1016/0306-4522(89)90247-9

Cited by 1,046 publications

(671 citation statements)

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“…Los primeros modelos de percusión por fluido, desarrollados en gatos y conejos 49,103 y posteriormente en ratas 30,78 , consistían en la aplicación de un impacto sobre la línea media del cerebro. Posteriormente la localización del impacto fue modificada, para producir un daño focal en un solo hemisferio, denominándose modelo de LFP 79 . Desde entonces, el modelo LFP se ha usado extensivamente en las investigaciones del daño cerebral traumático siendo uno de los modelos de lesión focal más empleados.…”

Section: Modelo De Percusión Lateral Por Fluido -Lateral Fluid Percusunclassified

“…En el otro extremo del cilindro se coloca un péndulo que generará un pulso de presión sobre el fluido contenido dentro del tubo y que deformará el cerebro inmediatamente bajo la duramadre expuesta (Figura 3). La intensidad del trauma causado dependerá de la presión ejercida con el pulso de fluido 79,113 .…”

Section: Figura 2 Exposición Del Cráneo Para La Realización De Una Cunclassified

“…La localización de la craneotomía en este modelo es un factor determinante del tipo de daño cerebral causado y al que por tanto se debe prestar especial atención. Según la descripción original, el modelo consiste en la realización de una craneotomía de 4.8 mm de diámetro centrada en el hueso parietal, 4 mm lateral a la sutura sagital 79 . Se ha observado que si la craneotomía se sitúa a menos de 3.5 mm de la sutura sagital, se produce un daño en ambos córtex, ipsilateral y contralateral a la percusión, que es observable tanto en los estudios convencionales histológicos como en las imágenes de resonancia magnética.…”

Section: Figura 2 Exposición Del Cráneo Para La Realización De Una Cunclassified

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Modelos experimentales de traumatismo craneoencefálico

et al. 2009

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Recibido:225 Neurocirugía 2009; 20: Resumen Objetivo. El objetivo de este trabajo es proporcionar una revisión de los diversos modelos experimentales de traumatismo craneoencefálico (TCE) que se han desarrollado para la investigación del daño cerebral traumático tanto en condiciones in vivo como in vitro, así como detallar los principales conocimientos fisiopatológicos obtenidos a partir de su aplicación. Se expone de forma sintética tanto el tipo de lesión cerebral traumática que cada modelo reproduce como los detalles técnicos necesarios para su utilización por investigadores en el campo del trauma cerebral.Desarrollo. El pronóstico de los pacientes que han sufrido un TCE ha mejorado gracias a las medidas iniciales de estabilización hemodinámica y control de la vía aérea, pero no existe todavía ningún tratamiento específico y eficaz para detener o limitar las lesiones cerebrales causadas por el traumatismo, exceptuando las medidas de control de la presión arterial y la presión intracraneal. Entender la fisiopatología del TCE es el paso básico y fundamental para desarrollar posibles abordajes terapéuticos con aplicación clínica. El daño cerebral traumático en humanos es una patología heterogénea y muy compleja. Por ello, cada modelo experimental se ha desarrollado con el objetivo de reproducir un tipo concreto de las diferentes lesiones cerebrales observadas en pacientes tras un TCE. El uso de estos modelos ha permitido ampliar el conocimiento sobre la fisiopatología del daño cerebral traumático, incluyendo las alteraciones inducidas a nivel celular y molecular.Conclusión. Los modelos experimentales suponen actualmente la mejor herramienta para el estudio de los mecanismos subyacentes a las lesiones cerebrales traumáticas, pero su simplicidad y por lo tanto su incapacidad de reproducir exactamente el daño heterogéneo observado en la práctica clínica puede ser uno de los motivos que explique la discrepancia en la respuesta terapéutica entre los estudios experimentales y clínicos.PALABRAS CLAVE: TCE. Daño cerebral traumático. Edema cerebral. Contusión cerebral. Modelos experimentales. Experimental models of traumatic brain injury SummaryAim. To provide a summary of the different experimental models of traumatic brain injury (TBI) designed under both in vivo and in vitro conditions. A comprehensible review of the specific types of brain lesions induced, as well as the technical details to reproduce each model at the laboratory is given.Development. Outcome of patients suffering from a TBI has significantly improved with the rapid application of vital supporting measures in addition to a strict control of blood and intracranial pressure at the intensive care units. However no specific treatment for post-traumatic brain lesions has proven as efficacious in the clinical settings. A deeper knowlegde of the physiopathological events associated with TBI is necessary for the development of new specific therapies. Due to the heterogeneity of the human TBI, each experimental model has been designed to reproduce a diffe...

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Section: Modelo De Percusión Lateral Por Fluido -Lateral Fluid Percusunclassified

Section: Figura 2 Exposición Del Cráneo Para La Realización De Una Cunclassified

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Modelos experimentales de traumatismo craneoencefálico

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“…A stainless-steel screw was placed anterior to the coronal suture to further anchor the luer-loc and dental cement to the skull bone. Ninety minutes after anesthesia, a subset of the animals (n = 26) were attached to the fluid percussion (FP) device via the luer-lok and subjected to a moderate severity brain injury (2.7 ± 0.3 atm) by the rapid (22 ms) delivery of a pressurized pulse of saline striking the intact dura, deforming the underlying brain tissue as originally described (McIntosh et al, 1989). The luerlok was then removed and the wound was closed.…”

Section: Surgery and Fluid Percussion Brain Injurymentioning

confidence: 99%

Selective temporal and regional alterations of Nogo-A and small proline-rich repeat protein 1A (SPRR1A) but not Nogo-66 receptor (NgR) occur following traumatic brain injury in the rat

Marklund

Fulp

Shimizu

et al. 2006

Experimental Neurology

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Axons show a poor regenerative capacity following traumatic central nervous system (CNS) injury, partly due to the expression of inhibitors of axonal outgrowth, of which Nogo-A is considered the most important. We evaluated the acute expression of Nogo-A, the Nogo-66 receptor (NgR) and the novel small proline-rich repeat protein 1A (SPRR1A, previously undetected in brain), following experimental lateral fluid percussion (FP) brain injury in rats. Immunofluorescence with antibodies against Nogo-A, NgR and SPRR1A was combined with antibodies against the neuronal markers NeuN and microtubule-associated protein (MAP)-2 and the oligodendrocyte marker RIP, while Western blot analysis was performed for Nogo-A and NgR. Brain injury produced a significant increase in Nogo-A expression in injured cortex, ipsilateral external capsule and reticular thalamus from days 1-7 post-injury (P < 0.05) compared to controls. Increased expression of Nogo-A was observed in both RIP-and NeuN positive (+) cells in the ipsilateral cortex, in NeuN (+) cells in the CA3 region of the hippocampus and reticular thalamus and in RIP (+) cells in white matter tracts. Alterations in NgR expression were not observed following traumatic brain injury (TBI). Brain injury increased the extent of SPRR1A expression in the ipsilateral cortex and the CA3 at all post-injury time-points in NeuN (+) cells. The marked increases in Nogo-A and SPRR1A in several important brain regions suggest that although inhibitors of axonal growth may be upregulated, the injured brain is also capable of expressing proteins promoting axonal outgrowth following TBI. KeywordsNogo-A; Nogo-66 receptor; Small proline-rich repeat protein 1A (SPRR1A); Traumatic brain injury; Oligodendrocytes

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“…Once induced, the animal was placed in a stereotactic frame. A scalp incision was made, the scalp and temporal muscle were reflected, and a 5.0 mm craniectomy was made in the skull over the left parietal cortex, midway between bregma and lambda as originally described (McIntosh et al, 1989). A female Luer-Lok fitting was cemented into the open craniectomy site, and then used to attach the animal to the FP injury device.…”

Section: Fluid Percussion Injurymentioning

confidence: 99%

Development of Posttraumatic Hyperthermia after Traumatic Brain Injury in Rats is Associated with Increased Periventricular Inflammation

Thompson

Hoover

Tkacs

et al. 2005

J Cereb Blood Flow Metab

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Posttraumatic hyperthermia (PTH) is a noninfectious elevation in body temperature that negatively influences outcome after traumatic brain injury (TBI). We sought to (1) characterize a clinically relevant model and (2) investigate potential cellular mechanisms of PTH. In study I, body temperature patterns were analyzed for 1 week in male rats after severe lateral fluid percussion (FP) brain injury (n ¼ 75) or sham injury (n ¼ 17). After injury, 27% of surviving animals experienced PTH, while 69% experienced acute hypothermia with a slow return to baseline. A profound blunting or loss of circadian rhythmicity (CR) that persisted up to 5 days after injury was experienced by 75% of brain-injured animals. At 2 and 7 days after injury, patterns of cell loss and inflammation were assessed in selected brain thermoregulatory and circadian centers. Significant cell loss was not observed, but PTH was associated with inflammatory changes in the hypothalamic paraventricular nucleus (PVN) by one week after injury. In brain-injured animals with altered CR, reactive astrocytes were bilaterally localized in the suprachiasmatic nucleus (SCN) and the PVN. Occasional IL-1b þ / ED-1 þ macrophages/microglia were observed in the PVN and SCN exclusively in brain-injured animals developing PTH. In animals with PTH there was a significant positive correlation (r ¼ 0.788, Po0.01) between the degree of postinjury hyperthermia and the total number of cells positive for inflammatory markers within selected thermoregulatory and circadian nuclei. In study II, a separate group of animals underwent the same injury and temperature monitoring paradigm as in study I, but had additional physiologic data obtained, including vital signs, arterial blood gases, white blood cell counts, and C-reactive protein levels. All parameters remained within normal ranges after injury. These data suggest that PTH and the alteration in CR of temperature may be due, in part, to acute reactive astrocytosis and inflammation in hypothalamic centers responsible for both thermoregulation and CR.

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Traumatic brain injury in the rat: Characterization of a lateral fluid-percussion model

Cited by 1,046 publications

References 19 publications

Modelos experimentales de traumatismo craneoencefálico

Modelos experimentales de traumatismo craneoencefálico

Selective temporal and regional alterations of Nogo-A and small proline-rich repeat protein 1A (SPRR1A) but not Nogo-66 receptor (NgR) occur following traumatic brain injury in the rat

Development of Posttraumatic Hyperthermia after Traumatic Brain Injury in Rats is Associated with Increased Periventricular Inflammation

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