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PubMed2002

High frequency percussive ventilation and conventional ventilation after smoke inhalation: a randomised study.

Inhalation injury and bacterial pneumonia represent some of the most important causes of mortality in burn patients. Thirty-five severely burned patients were randomised on admission for conventional ventilation (CV; control group) versus high frequency percussive ventilation (HFPV; study group). HFPV is a ventilatory mode, introduced 10 years ago which combines the advantages of CV with some of those of high frequency ventilation. Arterial blood gases, ventilatory and hemodynamic variables were recorded for 5 days at 2h intervals. Incident complications were classically managed. A statistical analysis (Student's t-test and Wilcoxon signed rank test) demonstrated a significant higher PaO(2)/FiO(2) from days 0 to 3 in the HFPV group. No significant differences were observed for the other parameters. Our findings suggest that HFPV can improve blood oxygenation during the acute phase following inhalation injury allowing reduction of FiO(2). No significant differences were observed between groups for mortality nor incidence of infectious complications in this study.

Acute-Phase Reaction↗
PubMed1998

The usefulness of combined high-frequency percussive ventilation during acute respiratory failure after smoke inhalation.

Inhalation injury and bacterial pneumonia represent some of the most important causes of mortality in burn patients. We describe 11 severely burned patients with acute respiratory failure due to inhalation injury who did not respond adequately to conventional respiratory support. High-frequency percussive ventilation (HFPV) is a recent ventilatory mode, which combines the advantages of conventional ventilation with some of those of high-frequency ventilation. Seven patients developed pulmonary infection during the acute phase; one patient died of multiple organ failure on day 25. All the other patients survived; two developed bronchiolitis obliterans symptoms before discharge. No side-effects were noted and haemodynamic tolerance of HFPV was excellent. Our findings suggest that HFPV can improve pulmonary function and gas exchange in these catastrophic pulmonary failures following inhalation injury.

Acute Disease↗
PubMed2002

Environmental enrichment attenuates cognitive deficits, but does not alter neurotrophin gene expression in the hippocampus following lateral fluid percussion brain injury.

Environmental enrichment attenuates neurological deficits associated with experimental brain injury. The molecular events that mediate these environmentally induced improvements in function after injury are largely unknown, but neurotrophins have been hypothesized to be a neural substrate because of their role in cell survival and neural plasticity. Furthermore, exposure to complex environments in normal animals increases neurotrophin gene expression. However, following an ischemic injury, environmental enrichment decreases neurotrophin mRNA levels. Whether these contrasting findings are attributable to differences between injured and uninjured animals or are dependent upon the specific type of brain injury has not been determined. We examined the effects of 14 days of environmental enrichment following a lateral fluid percussion brain injury on behavior and gene expression of brain-derived neurotrophic factor, its high-affinity receptor, TrkB, and neurotrophin-3 in the rat hippocampus. Environmental enrichment attenuated learning deficits in the injured animals, but neither the injury nor housing conditions influenced neurotrophin/receptor mRNA levels. From these data we suggest that following brain trauma, improvements in learning associated with environmental enrichment are not mediated by alterations in brain-derived neurotrophic factor, TrkB or neurotrophin-3 gene expression.

Animals↗
PubMed2002

The percussion reactions involved in brain function.

A hypothesis is presented describing the operation of mammalian brains on the basis of rapid percussion chemical reactions and shock waves generated by such reactions. It is shown that the products of these are various chemical compounds identified as present in the brain. The manner in which the brain deals with various external optical, sonic pressure, and chemical phenomena is described. The origin and possible relief of disabling conditions related to brain action are discussed on the basis of the hypothesis.

Animals↗
PubMed1999

Evaluation of micro tip pressure transducers for the measurement of intracerebral pressure transients induced by fluid percussion.

We describe the application of MIKRO TIP miniature pressure transducers (MPT) for the in vivo measurement of intracerebral stresses induced by traumatic brain injury (TBI). In order to test the linearity of these transducers pressure pulses of different amplitudes (duration approximately 10ms) were generated in a closed calibration chamber. A piezoelectric pressure transducer (PPT) served as the reference measure. A linear correlation was found within the pressure range between 0.57 and 5.09 bar (R2 = 0.998). The frequency transmission characteristics of the MPTs are comparable to the PPT. In three juvenile swines (6 weeks of age) pressures within the brain tissue were induced by fluid percussion (FP) and were measured in the anterior, middle, and posterior cranial cavity as well as in the extracranial part of the medulla oblongata. The data obtained in our experiments agree with the basic biomechanics of FP known from studies in cats and rabbits. Due to their small size, MPTs can be applied in living animals. Stereotaxic positioning of these catheters at any site of the brain and spinal cord requires only minimal surgery. Therefore, MPTs are useful in evaluating animal models of brain injury and in generating input data for computational models of head injury as well as to validate the mathematical results of such models with experimental data.

Animals↗
PubMed2001

Changes in mACh, NMDA and GABA(A) receptor binding after lateral fluid-percussion injury: in vitro autoradiography of rat brain frozen sections.

Adult rats were subjected to a moderate lateral fluid percussion injury (FPI), followed by survival periods of 2 and 12 h. Regional NMDA subtype glutamate, muscarinic acetylcholine and GABA(A) receptor binding in various brain regions was analysed by quantitative in vitro autoradiography and short-lived positron emission tomography tracers [11C]cyano-dizocilpine, 4-N-[11C]methylpiperidylbenzilate (4-N-[11C]MPB), and [11C]flumazenil, respectively. The binding potential (BP, Bmax/KD) was calculated. The data with [11C]cyano-dizocilpine showed a significant decrease in BP bilaterally for the frontoparietal cortex and hippocampus at both time points, in comparison with that of the sham-operated controls. At 12 h the decrease was significantly more prominent for the ipsilateral cortex and hippocampus than for the contralateral side. The BP of 4-N-[11C]MPB was significantly decreased after 2 h for the trauma-side hippocampus, and after 12 h it had decreased for the trauma-site cortex and the bilateral hippocampus. The [11C]flumazenil exhibited a significant decrease in BP for the trauma-site cortex and the underlying hippocampus by 2 h after the traumatic brain injury. After 12 h a significantly decreased BP was observed only for the trauma-site cortex. The finding of a decreased BP demonstrates the involvement of these receptor systems in the development of cellular dysfunction, which is widespread and not limited to the site of lateral FPI.

Animals↗
PubMed2003

Percussion chisel.

A new percussion chisel exclusively designed for neurosurgical use is presented that can be applied easily and safely. It is particularly useful in the removal of bony membranes through a transsphenoidal approach.

Equipment Design↗
PubMed1986

A percussion lithotripter.

A mechanical lithotripter producing a percussion action on biliary stones is described. This device seems to be robust and flexible at the same time. Every biliary stone is easily crushed by this lithotripter. Sixty-seven patients have been endoscopically treated with the aid of this probe.

Aged↗
PubMed2000

Secondary hypoxemia exacerbates the reduction of visual discrimination accuracy and neuronal cell density in the dorsal lateral geniculate nucleus resulting from fluid percussion injury.

The purpose of this study was to determine the impact of secondary hypoxemia on visual discrimination accuracy after parasagittal fluid percussion injury (FPI). Rats lived singly in test cages, where they were trained to repeatedly execute a flicker-frequency visual discrimination for food. After learning was complete, all rats were surgically prepared and then retested over the following 4-5 days to ensure recovery to presurgery levels of performance. Rats were then assigned to one of three groups [FPI + Hypoxia (IH), FPI + Normoxia (IN), or Sham Injury + Hypoxia (SH)] and were anesthetized with halothane delivered by compressed air. Immediately after injury or sham injury, rats in groups IH and SH were switched to a 13% O2 source to continue halothane anesthesia for 30 min before being returned to their test cages. Anesthesia for rats in group IN was maintained using compressed air for 30 min after injury. FPI significantly reduced visual discrimination accuracy and food intake, and increased incorrect choices. Thirty minutes of immediate posttraumatic hypoxemia significantly (1) exacerbated the FPI-induced reductions of visual discrimination accuracy and food intake, (2) further increased numbers of incorrect choices, and (3) delayed the progressive recovery of visual discrimination accuracy. Thionine stains of midbrain coronal sections revealed that, in addition to the loss of neurons seen in several thalamic nuclei following FPI, cell loss in the ipsilateral dorsal lateral geniculate nucleus (dLG) was significantly greater after FPI and hypoxemia than after FPI alone. In contrast, neuropathological changes were not evident following hypoxemia alone. These results show that, although hypoxemia alone was without effect, posttraumatic hypoxemia exacerbates FPI-induced reductions in visual discrimination accuracy and secondary hypoxemia interferes with control of the rat's choices by flicker frequency, perhaps in part as a result of neuronal loss and fiber degeneration in the dLG. These results additionally confirm the utility of this visual discrimination procedure as a sensitive, noninvasive means of assessing behavioral function after experimental traumatic brain injury.

Animals↗
PubMed2001

Free radical scavenger posttreatment improves functional and morphological outcome after fluid percussion injury in the rat.

Reactive oxygen species (ROS) are thought to contribute to the secondary injury process after traumatic brain injury (TBI). ROS scavenging compounds have shown neuroprotective properties in various models of experimental brain injury, including TBI. Administration of nitrone radical scavengers has emerged as a promising pharmacological concept in focal experimental ischemia due to their low toxicity and neuroprotective properties, with a time window of several hours. The aim of this study was to test the neuroprotective efficacy of two nitrones, the readily blood-brain barrier (BBB) penetrating alpha-phenyl-N-tert-butyl nitrone (PBN) and the poorly BBB penetrating sulfo-derivative, 2-sulfo-phenyl-N-tert-butyl nitrone (S-PBN) after moderate (2.20-2.45 atm) lateral fluid percussion injury (FPI) in rats. Twenty-six rats received a 24-h intravenous infusion (30 mg/kg/h) of saline, PBN, or an equimolar dose of S-PBN beginning 30 min after FPI. Eight sham-operated animals were used as controls. Cognitive function was assessed using the Morris Water Maze at day 11-15 after TBI, neurological status at day 1, 4, and 8 and morphological outcome at day 15. PBN and S-PBN treatment significantly reduced the loss of ipsilateral hemispheric tissue whereas only S-PBN tended to reduce the cortical lesion volume. PBN treatment caused a significant improvement in the neurological score as compared to saline-treated animals, while S-PBN alone attenuated the cognitive deficit. Our results suggest that nitrone radical scavengers are neuroprotective when administered 30 min after FPI in rats. Differences in pharmacokinetics may account for the observed individual neuroprotective profiles of the two nitrones.

Animals↗
PubMed2001

Small shifts in craniotomy position in the lateral fluid percussion injury model are associated with differential lesion development.

Previous studies have shown that location and direction of injury may affect outcome in experimental models of traumatic brain injury. Significant variability in outcome data has also been noted in studies using the lateral fluid percussion brain injury model (FPI) in rats. In recent studies from our laboratory, we observed considerable variability in localization and severity of tissue damage as a function of small changes in craniotomy position. To further address this issue, we examined the relationship between craniotomy position and brain lesion size/location in rats subjected to moderate FPI (2.28 +/- 0.18 atmospheres). With placement of a 5-mm craniotomy adjacent to the sagittal suture, there was both ipsilateral and contralateral damage as detected at 3 weeks posttrauma using T2-weighted magnetic resonance imaging (MRI). The MRI lesions were generally restricted to the hippocampus and subcortical layers. Shifting of the craniotomy site laterally was associated with increased ipsilateral tissue damage and a greater cortical component that correlated with distance from the sagittal suture. In contrast, the contralateral MRI lesion did not change significantly in size or location unless the center of the craniotomy was placed more than 3.5 mm from the sagittal suture, under which condition contralateral damage could no longer be detected. Ipsilateral tissue damage as determined from the MRI scans was linearly correlated to motor outcome but not with cognitive outcome as assessed by the Morris Water Maze. We conclude that craniotomy position is critical in determining extent and location of tissue injury produced during the lateral FPI model in rats. Addressing such potential variability is essential for studies that address either injury mechanisms or therapeutic treatments.

Animals↗
PubMed2001

Age-dependency of 45calcium accumulation following lateral fluid percussion: acute and delayed patterns.

This study was designed to determine the regional and temporal profile of 45calcium (45Ca2+) accumulation following mild lateral fluid percussion (LFP) injury and how this profile differs when traumatic brain injury occurs early in life. Thirty-six postnatal day (P) 17, thirty-four P28, and 17 adult rats were subjected to a mild (approximately 2.75 atm) LFP or sham injury and processed for 45Ca2+ autoradiography immediately, 6 h, and 1, 2, 4, 7, and 14 days after injury. Optical densities were measured bilaterally within 16 regions of interest. 45Ca2+ accumulation was evident diffusely within the ipsilateral cerebral cortex immediately after injury (18-64% increase) in all ages, returning to sham levels by 2-4 days in P17s, 1 day in P28s, and 4 days in adults. While P17s showed no further 45Ca2+ accumulation, P28 and adult rats showed an additional delayed, focal accumulation in the ipsilateral thalamus beginning 2-4 days postinjury (12-49% increase) and progressing out to 14 days (26-64% increase). Histological analysis of cresyl violet-stained, fresh frozen tissue indicated little evidence of neuronal loss acutely (in all ages), but considerable delayed cell death in the ipsilateral thalamus of the P28 and adult animals. These data suggest that two temporal patterns of 45Ca2+ accumulation exist following LFP: acute, diffuse calcium flux associated with the injury-induced ionic cascade and blood brain barrier breakdown and delayed, focal calcium accumulation associated with secondary cell death. The age-dependency of posttraumatic 45Ca2+ accumulation may be attributed to differential biomechanical consequences of the LFP injury and/or the presence or lack of secondary cell death.

Acute Disease↗
PubMed2001

Effects of binge ethanol administration on the behavioral outcome of rats after lateral fluid percussion brain injury.

This study examined the effects of 4 weeks of binge ethanol administration (BEAn) on the behavioral outcome in rats after lateral fluid percussion (FP) brain injury. Rats were intragastrically given 7.5 mL/kg of either 40% ethanol in 5% glucose solution (3 g ethanol/kg; binge ethanol group), or 5% glucose solution (vehicle group), twice on Thursday and Friday of 3 consecutive weeks. Then rats from both groups were subjected to either lateral FP brain injury of moderate severity (1.8 atm) or to sham operation. Postinjury behavioral measurements revealed that brain injury caused significant spatial learning disability in both groups. There were no significant differences in mean search latencies in the sham animals between the vehicle and binge ethanol groups. On the other hand, the mean search latency of the binge ethanol group was significantly higher than that of the vehicle group in trial blocks 2 and 4. There were no significant differences in the target visits (expressed as mean zone difference [MZD]) during the probe trial between the injured animals of binge ethanol and vehicle groups. However, there was only a minor trend towards worsened MZD score in the binge-injured animals. Histologic analysis of injured animals from both injured ethanol and vehicle groups revealed similar extents of ipsilateral cortical and observable hippocampal damage. These results suggest that 4 weeks of binge ethanol treatment followed by ethanol intoxication at the time of injury worsens some aspects of the spatial learning ability of rats. This worsening is probably caused by subtle, undetectable morphologic damage by binge ethanol administration.

Animals↗
PubMed2002

Effect of posttraumatic hyperglycemia on contusion volume and neutrophil accumulation after moderate fluid-percussion brain injury in rats.

The purpose of this study was to evaluate the effects of posttraumatic hyperglycemia on contusion volume and neutrophil accumulation following moderate traumatic brain injury (TBI) in rats. A parasagittal fluid-percussion (F-P) brain injury (1.8-2.1 atm) was induced in male Sprague-Dawley rats. Rats were then randomized into four trauma groups (n = 7/group) by the timing of dextrose injection (2.0 gm/kg/ip), which included (1) early (E) group: 5 min after TBI; (2) delayed (D) group: 4 h after TBI; (3) 24-h group: 24 h after TBI; or (4) control (C) group: no dextrose injection. A sham operated control group also received dextrose to document physiological parameters (n = 4). Rats were perfusion fixed 3 days following TBI, and the brains were processed for routine histopathological and immunocytochemical analysis. Contusion areas and volumes, as well as the frequency of myeloperoxidase immunoreactive polymorphonuclear leukocytes (PMNLs) were determined. Dextrose injections significantly increased blood glucose levels (p < 0.005) in all treated groups. Although acute hyperglycemia following TBI did not significantly affect total contusion volume, contusion area was significantly elevated in the early treatment group. In addition, early posttraumatic hyperglycemia enhanced neutrophil accumulation in the area of the cortical contusion (p < 0.005). In contrast, delayed induced hyperglycemia (i.e., 4 h, 24 h) did not significantly affect histopathological outcome or neutrophil accumulation. Taken together, these findings indicate that acute but not delayed hyperglycemia aggravates histopathological outcome and increased accumulation of PMNLs. Posttraumatic hyperglycemia in the acute phase may worsen traumatic outcome by enhancing secondary injury processes, including inflammation.

Animals↗
PubMed2002

Cyclosporin A improves brain tissue oxygen consumption and learning/memory performance after lateral fluid percussion injury in rats.

Traumatic brain injury (TBI) triggers a complex pathophysiological cascade, leading to cell death. A major factor in the pathogenesis of TBI is neuronal overloading with calcium, causing the opening of mitochondrial permeability transition pores (MPTP), which consequently inhibit normal mitochondrial function. The immunosuppressant Cyclosporin A (CsA) has been shown to block MPTPs, and to be neuroprotective in ischemia and TBI. However, the translation of these effects on mitochondrial function, into behavioral endpoints has not been investigated thoroughly. Therefore, we tested the effect of a low, clinically evaluated, CsA dose of 0.125 mg/kg (infused for 3 h) and a higher "known" neuroprotective dose of 18.75 mg/kg on brain tissue O(2) consumption, and on motor and cognitive performance following lateral fluid percussion injury (FPI) in rats. CsA at both concentrations abolished the 25% decrease in O(2) consumption (VO(2)), seen in saline-treated animals at 5 h post-FPI. Furthermore, the lower dose of CsA also ameliorated acute motor deficits (days 1-5 post-FPI) and learning and memory impairments in a Morris water maze test on days 11-15 post-FPI. Although, the higher dose of CsA improved cognitive performance, it worsened acute motor functional recovery. These results suggest, that the CsA-induced preservation of mitochondrial function, as assessed by tissue O(2) consumption, directly translated into improvements in motor and cognitive behavior.

Animals↗
PubMed2002

Effects of enriched environment and fluid percussion injury on dendritic arborization within the cerebral cortex of the developing rat.

We have recently demonstrated that fluid percussion injury (FPI) sustained early in life prevents the neural plasticity response associated with rearing in an enriched environment (EE). In order to determine if this reduction in plasticity capacity is reflected in alterations in dendritic arborization, the present study examined dendritic changes in response to EE, FPI, and FPI followed by EE. Twenty postnatal day 19-20 rat pups were subjected to FPI or sham injury and were subsequently housed in EE (17 days) or standard conditions. Brains were processed according to the Golgi-Cox method and were analyzed using dendritic density (Sholl) and dendritic branching analyses in frontal, parietal, and occipital cortices. Rearing in EE induced an increase in dendritic density, primarily within the occipital cortex. FPI induced an increase in dendritic density, primarily in regions remote from the injury site, namely contralateral parietal cortex and ipsilateral and contralateral occipital cortex. In injured animals subsequently housed in EE, FPI appeared to inhibit the experience-dependent dendritic density effects of EE. However, an unexpected enhancement of dendritic density was seen in the ipsilateral occipital cortex, indicating a unique response of this region based on its distance-specific sensitivity to injury-induced plasticity and its region-specific sensitivity to experience-dependent plasticity. These results suggest that dendritic changes mediate the anatomical and behavioral changes characteristic of impaired developmental plasticity following FPI, and that these changes are dependent on location within the cerebral cortex.

Animals↗
PubMed2003

Relationship between intracranial pressure and cortical spreading depression following fluid percussion brain injury in rats.

Traumatic brain injury (TBI) is known to be accompanied by an increase in intracranial pressure (ICP) and in some cases, by spontaneous generation of cortical spreading depression (CSD) cycles. However, the role of CSD in the pathophysiology of cerebral contusion is still unknown. A multiparametric monitoring assembly was placed on the right hemisphere of the rat brain to evaluate ICP, DC potential, extracellular K(+), cerebral blood flow (CBF), and electrocorticogram in 27 rats during 5 h. Fluid percussion brain injury (FPBI) with the magnitude of the impact 2.9, 3.3, 4.1, and 5.0 atmospheres was induced to the left parietal cortex in animal groups A, B, C, and D, respectively. A slow increase in ICP was evident, and was pronounced in group C and especially in group D, where four of nine animals died during the monitoring. At the end of the 5 h experiment, the mean ICP levels were 6.75 +/- 2.87, 8.40 +/- 2.70, 12.75 +/- 4.03, 29.56 +/- 9.25, and the mean total number of CSD cycles was 2.00 +/- 1.41, 4.29 +/- 4.23, 11.71 +/- 13.29, and 20.11 +/- 19.26 in groups A, B, C, and D, respectively. The maximal level of intensity of CSD cycle generation after FPBI was obtained in group D, where almost constant activity was maintained until the end of the experiment. A significant coefficient of correlation between ICP level and total number of CSD cycles was found for all ICP measurements (r = 0.47-0.63, p < 0.05, n = 27), however more significant (p < 0.001) was the coefficient during the period of monitoring between 2 and 4 h after FPBI. Our results suggest that numerous repeating CSD cycles are typical phenomena in moderate and especially severe forms of FPBI. The rising number of CSD cycles under condition of an ICP level >/=20 mm Hg may demonstrate, with high probability, the unfavorable development of TBI, caused by growing secondary hypoxic insult.

Animals↗
PubMed2003

Increased hippocampal CA3 vulnerability to low-level kainic acid following lateral fluid percussion injury.

This study was designed to determine whether a secondary increase in neuronal activity induced by a low dose of kainic acid (KA), a glutamate analogue, exacerbates the anatomical damage in hippocampal regions following a mild lateral fluid percussion (LFP) brain injury. KA (9 mg/kg) was injected intraperitoneally in LFP-injured rats (n = 16) 1 h post-trauma. The neuronal loss in the CA3, CA4, and hilar regions at 7 days was quantified by two-dimensional cell counts. Hippocampal activation 15 min following KA injection was assessed by measuring local glucose metabolic rates (lCMR(glc)). Following LFP + KA, the ipsilateral side exhibited a 62.7%, 75.7%, and 52.1% decrease in the number of CA3, CA4 and hilar neurons, respectively, compared to naive rats (n = 3). These CA3 and CA4 neuronal counts were also significantly decreased compared to LFP + saline (n = 5) and sham + KA (n = 9) groups. The median Racine Score, used to rate the severity of behavioral seizures, was 4 in LFP + KA and 2 in sham + KA groups (p < 0.015), suggesting a reduction in seizure threshold following injury. lCMRglc in CA3 following LFP + KA was 121.8 +/- 2.0 (mean +/- SE) ipsilaterally and 71.5 +/- 5.4 contralaterally (p < 0.0012). No changes were found in the BBB permeability as measured by [(14)C]aminoisobutyric acid in CA3, CA4, and hilar regions. We conclude that the presence of low-level KA 1 h after LFP dramatically increases the extent of hippocampal activation and induces a striking loss of ipsilateral CA3 and CA4 pyramidal neurons. Neuronal excitation during a time of cellular vulnerability may trigger or amplify the cycle of secondary damage in functionally impaired, but potentially viable, tissue.

Animals↗