A Modified Fluid Percussion Device

Yamaki, Takashi; Murakami, Nobukuni; Iwamoto, Yoshihiro; Yoshino, Eiji; Nakagawa, Yoshio; Ueda, Satoshi; Horikawa, Jun; Tsujii, T

doi:10.1089/neu.1994.11.613

Cited by 23 publications

(17 citation statements)

References 16 publications

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“…The lateral fluid percussion model of experimental brain trauma of moderate severity (2.3 6 0.1 atm) was performed using equipment based on similar well-recognised and characterised systems (Dixon et al, 1987;McIntosh et al, 1989;Yamaki et al, 1994). Our model consists of a horizontally mounted 10ml syringe connected via a luer-loc and three-way connection to two identical lengths of plastic tubing, one connected to a pressure transducer and the other to the craniotomy site.…”

Section: Methodsmentioning

confidence: 99%

The Hypothalamo-Pituitary-Adrenal Axis Response to Experimental Traumatic Brain Injury

Grundy

Harbuz

Jessop

et al. 2001

Journal of Neurotrauma

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Alterations in the hypothalamo-pituitary-adrenal (HPA) axis following traumatic brain injury have not been documented in detail. We used fluid percussion injury (FPI) to evaluate the early changes in components of the HPA axis following experimental traumatic brain injury. Wistar rats were sacrificed at 2 or 4 h following sham or FPI surgery. In situ hybridization histochemistry was used to determine the expression of mRNAs of corticotrophin releasing hormone (CRH) and arginine vasopressin (AVP) in the hypothalamus and pro-opiomelanocortin (POMC) in the pituitary. A group of animals undergoing no surgery were used as control. Repeated blood sampling from an indwelling catheter demonstrated that plasma corticosterone (CORT) levels peaked 30 min following surgery in sham and FPI animals but there was no significant difference in CORT concentration between these groups at any time. Pituitary POMC expression was increased following sham and FPI surgery (compared with control non-operated animals) but with no significant difference between the two groups undergoing surgery. Hypothalamic CRH mRNA expression was significantly higher in animals undergoing FPI compared with sham surgery. Hypothalamic AVP mRNA expression was not significantly increased when compared with control nonoperated animals. These data indicate that the anaesthesia and/or surgery associated with FPI or sham surgery induces a generalised activation of the HPA axis. The selective increase in CRH mRNA in animals undergoing FPI may be due to specific effects of traumatic brain injury rather than a general stress response and may suggest an additional neurotransmitter role for CRH following head injury. The absence of an AVP response suggests that the effects of FPI may be mediated through the CRH-alone-containing subpopulation of neurons.

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Section: Methodsmentioning

confidence: 99%

The Hypothalamo-Pituitary-Adrenal Axis Response to Experimental Traumatic Brain Injury

Grundy

Harbuz

Jessop

et al. 2001

Journal of Neurotrauma

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“…The main advantages of the fluid percussion model are similar to that described for the CCI model in that it induces graded levels of brain injury and produces axonal injuries and contusions, as well as impaired neurologic motor function and cognitive deficits (Dixon et al, 1987;McIntosh et al, 1987;Yaghmai and Povlishock, 1992). It has also been modified and widely applied (Sullivan et al, 1976;Povlishock et al, 1983;Dixon et al, 1987;McIntosh et al, 1989;Yamaki et al, (1994) to other animal species including the rat, dog, rabbit, cat and swine and has been used in combination with microdialysis in the rat Busto et al, 1987;Kawamata et al, 1995;Katayama et al, 1990). Also, fluid flow characteristics (i.e.…”

Section: Fluid Percussion Injurymentioning

confidence: 99%

Animal models of traumatic brain injury: A critical evaluation

O’Connor

Smyth

Gilchrist

2011

Pharmacology & Therapeutics

142

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“…Recently, reports have shown that midline fluid percussion (MFP) injury in a rat model produced DAI in contrast to the lateral fluid percussion injury rat model (Yamaki et al 1994;Iwamoto et al 1997). Therefore, we used the surgical procedure for MFP injury in the rat model.…”

Section: Surgical Proceduresmentioning

confidence: 99%

The role of tumor necrosis factor-α in diffuse axonal injury following fluid-percussive brain injury in rats

Kita¹,

Tanaka²,

Тanaka³

et al. 2000

International Journal of Legal Medicine

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The immunolocalization of tumor necrosis factor-alpha (TNF alpha) after diffuse axonal injury (DAI) is demonstrated using a midline fluid percussion rat model (moderate brain injury of 1000 mm Hg was generated) and the effects of TNF alpha on the axolemmal permeability using horseradish peroxidase as a tracer. In addition, the accumulation of beta-amyloid precursor protein (beta-APP) was investigated, which has recently been shown to be a reliable marker for the diagnosis of DAI in cases with fatal head injury. TNF alpha levels in brain tissues from the impact site and the cortex including the corpus callosum, gradually increased during the first 1 h, rose to a maximal elevation at 3 h, gradually decreased at 6 h and decreased further at 24 h. Horseradish peroxidase (HRP) tracer experiments revealed that primary axonal damage appeared as early as 15 min after impact but rapidly recovered and that 1 h after impact, secondary axonal damage occurred in the corpus callosum and the brain stem. By immunoelectron microscopy it was seen that beta-APP accumulated in the axon from 1 h after impact demonstrating that there was functional axonal damage. TNF alpha reactions were detected in the lysosomes of microglia 30 min after impact and 1 h after impact these reactions were mainly detected in the glial cells (such as microglia, astrocytes and oligodendrocytes) in the corpus callosum and the brain stem. It is generally accepted that TNF alpha directly induces primary demyelination and oligodendrocyte apoptosis. Therefore, TNF alpha conveyed from the microglial cells is one cofactor contributing to the formation of the delayed axonal damage observed at these sites. The present study suggests that TNF alpha conveyed from the glial cells may contribute to the pathogenic mechanism of DAI formation following fluid percussive brain injury.

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A Modified Fluid Percussion Device

Cited by 23 publications

References 16 publications

The Hypothalamo-Pituitary-Adrenal Axis Response to Experimental Traumatic Brain Injury

The Hypothalamo-Pituitary-Adrenal Axis Response to Experimental Traumatic Brain Injury

Animal models of traumatic brain injury: A critical evaluation

The role of tumor necrosis factor-α in diffuse axonal injury following fluid-percussive brain injury in rats

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