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PubMed2006

Intrapulmonary percussive ventilation in tracheostomized patients: a randomized controlled trial.

OBJECTIVE: To investigate whether the addition of intrapulmonary percussive ventilation to the usual chest physiotherapy improves gas exchange and lung mechanics in tracheostomized patients. DESIGN AND SETTING: Randomized multicenter trial in two weaning centers in northern Italy. PATIENTS AND PARTICIPANTS: 46 tracheostomized patients (age 70 +/- 7 years, 28 men, arterial blood pH 7.436 +/- 0.06, PaO(2)/FIO(2) 238 +/- 46) weaned from mechanical ventilation. INTERVENTIONS: Patients were assigned to two treatment groups performing chest physiotherapy (control), or percussive ventilation (IMP2 Breas, Sweden) 10 min twice/day in addition to chest physiotherapy (intervention). MEASUREMENTS AND RESULTS: Arterial blood gases, PaO(2)/FIO(2) ratio, and maximal expiratory pressure were assessed every 5th day for 15 day. Treatment complications that showed up in 1 month of follow-up were recorded. At 15 days the intervention group had a significantly better PaO(2)/FIO(2) ratio and higher maximal expiratory pressure; after follow-up this group also had a lower incidence of pneumonia. CONCLUSIONS: The addition of percussive ventilation to the usual chest physiotherapy regimen in tracheostomized patients improves gas exchange and expiratory muscle performance and reduces the incidence of pneumonia.

Aged↗
PubMed1994

The role of opioids in newborn pig fluid percussion brain injury.

The present study was designed to characterize the relationship between cerebral opioid concentration, cerebral hemodynamics, and cerebral oxygenation following percussion brain injury in neonatal pigs. Previous research found that opioids represent a significant vasoactive component in the regulation of the neonatal piglet cerebral circulation. Anesthetized newborn (1-5 days old) pigs equipped with a closed cranial window were connected to a percussion device consisting of a saline-filled cylindrical reservoir with a metal pendulum. Brain injury of moderate severity (1.9-2.3 atm.) was produced by allowing the pendulum to strike a piston on the cylinder. Fluid percussion brain injury decreased pial arteriolar diameter (132 +/- 5 to 110 +/- 5 microns within 10 min). Cerebral blood flow also fell within 10 min of injury and continued to fall progressively for 3 h, resulting in a 46 +/- 4% decrease. Within 30 s of brain injury, there was a transient increase in cerebral hemoglobin-O2 saturation that was reversed to a progressive profound decrease in cerebral hemoglobin-O2 saturation for the next 3 h, as measured by near infrared spectroscopy. CSF opioid concentrations were increased 10 min after brain injury; dynorphin showed the largest proportional increase (5.8 +/- 0.9 fold). The CSF concentration for other opioids continued to increase over 180 min while the dynorphin concentration progressively decreased with time. In naloxone (1 mg/kg i.v.) pretreated piglets, the brain injury induced decrease in arteriolar diameter was attenuated (129 +/- 5 to 121 +/- 5 microns within 10 min). Similarly, the decrease in regional cerebral blood flow and cerebral hemoglobin-O2 saturation observed following brain injury were also blunted by naloxone.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2005

Environmental enrichment increases progenitor cell survival in the dentate gyrus following lateral fluid percussion injury.

Neurons in the hilus of the dentate gyrus are lost following a lateral fluid percussion injury. Environmental enrichment is known to increase neurogenesis in the dentate in intact rats, suggesting that it might also do so following fluid percussion injury, and potentially provide replacements for lost neurons. We report that 1 h of daily environmental enrichment for 3 weeks increased the number of progenitor cells in the dentate following fluid percussion injury, but only on the ipsilesional side. In the dentate granule cell layer, but not the hilus, most progenitors had a neuronal phenotype. The rate of on going cell proliferation was similar across groups. Collectively, these results suggest that the beneficial effects of environmental enrichment on behavioral recovery following FP injury are not attributable to neuronal replacement in the hilus but may be related to increased neurogenesis in the granule cell layer.

Animals↗
PubMed2006

A model of posttraumatic epilepsy induced by lateral fluid-percussion brain injury in rats.

Although traumatic brain injury is a major cause of symptomatic epilepsy, the mechanism by which it leads to recurrent seizures is unknown. An animal model of posttraumatic epilepsy that reliably reproduces the clinical sequelae of human traumatic brain injury is essential to identify the molecular and cellular substrates of posttraumatic epileptogenesis, and perform preclinical screening of new antiepileptogenic compounds. We studied the electrophysiologic, behavioral, and structural features of posttraumatic epilepsy induced by severe, non-penetrating lateral fluid-percussion brain injury in rats. Data from two independent experiments indicated that 43% to 50% of injured animals developed epilepsy, with a latency period between 7 weeks to 1 year. Mean seizure frequency was 0.3+/-0.2 seizures per day and mean seizure duration was 113+/-46 s. Behavioral seizure severity increased over time in the majority of animals. Secondarily-generalized seizures comprised an average of 66+/-37% of all seizures. Mossy fiber sprouting was increased in the ipsilateral hippocampus of animals with posttraumatic epilepsy compared with those subjected to traumatic brain injury without epilepsy. Stereologic cell counts indicated a loss of dentate hilar neurons ipsilaterally following traumatic brain injury. Our data suggest that posttraumatic epilepsy occurs with a frequency of 40% to 50% after severe non-penetrating fluid-percussion brain injury in rats, and that the lateral fluid percussion model can serve as a clinically-relevant tool for pathophysiologic and preclinical studies.

Animals↗
PubMed2002

Attenuation of the electrophysiological function of the corpus callosum after fluid percussion injury in the rat.

This study describes a new method used to evaluate axonal physiological dysfunction following fluid percussion induced traumatic brain injury (TBI) that may facilitate the study of the mechanisms and novel therapeutic strategies of posttraumatic diffuse axonal injury (DAI). Stimulated compound action potentials (CAP) were recorded extracellularly in the corpus callosum of superfused brain slices at 3 h, and 1, 3, and 7 days following central fluid percussion injury and demonstrated a temporal pattern of functional deterioration. The maximal CAP amplitude (CAPA) covaried with the intensity of impact 1 day following sham, mild (1.0-1.2 atm), and moderate (1.8-2.0 atm) injury (p < 0.05; 1.11 +/- 0.10, 0.82 +/- 0.11, and 0.49 +/- 0.08 mV, respectively). The CAPA in sham animals were approximately 1.1 mV and did not vary with survival interval (3 h, and 1, 3, and 7 days); however, they were significantly decreased at each time point following moderate injury (p < 0.05; 0.51 +/- 0.11, 0.49 +/- 0.08, 0.46 +/- 0.10, and 0.75 +/- 0.13 mV, respectively). The CAPA at 7 days in the injured group were higher than at 3 h, and 1 and 3 days. H&E and amyloid precursor protein (APP) light microscopic analysis confirmed previously reported trauma-induced axonal injury in the corpus callosum seen after fluid percussion injury. Increased APP expression was confirmed using Western blotting showing significant accumulation at 1 day (IOD 913.0 +/- 252.7; n = 3; p = 0.05), 3 days (IOD 753.1 +/- 159.1; n = 3; p = 0.03), and at 7 days (IOD 1093.8 = 105.0; n = 3; p = 0.001) compared to shams (IOD 217.6 +/- 20.4; n = 3). Thus, we report the characterization of white matter axonal dysfunction in the corpus callosum following TBI. This novel method was easily applied, and the results were consistent and reproducible. The electrophysiological changes were sensitive to the early effects of impact intensity, as well as to delayed changes occurring several days following injury. They also indicated a greater degree of attenuation than predicted by APP expression changes alone.

Action Potentials↗
PubMed1987

Traumatic brain injury in the rat: characterization of a midline fluid-percussion model.

Fluid-percussion models of traumatic brain injury produce injury by rapidly injecting fluid volumes into the epidural space. In the present study, we characterized the physiological, histopathological, and neurological responses in a new model of midline (vertex) fluid-percussion injury of graded severity in the rat. All levels of injury produced transient (acute) hypertension, which was followed by a significant and prolonged hypotension at the higher levels of injury. There was also postinjury suppression if EEG amplitudes, which was related to the severity of injury. However, there were no significant changes in brainstem auditory evoked potentials (BAERs) at any level of injury. Neurological scores over a 4-week postinjury period were directly correlated with the severity of injury. Survival rates were significantly decreased at the higher magnitudes of injury. The extent of postinjury hemorrhage and blood-brain barrier disruption (as evidenced by extravasation of Evans Blue Albumin complex) was related to the magnitude of injury. These data demonstrate that the midline (vertex) model of fluid-percussion injury in the rat reproduces many of the features of head injury observed in other models and species and may serve as a useful cost-effective model for the study of the pathophysiology and treatment of traumatic brain injury.

Animals↗
PubMed1997

Investigation of morphological change of lateral and midline fluid percussion injury in rats, using magnetic resonance imaging.

OBJECTIVE: Investigating the time course of morphological changes in experimental traumatic brain injury (TBI) in vivo helps to clarify the mechanism of TBI and develop new therapeutic modalities. We examined the morphological changes in experimental TBI, using magnetic resonance imaging (MRI) in a rat model. METHODS: We produced lateral fluid percussion injury (LFP) and midline fluid percussion injury (MFP) in rats, using the Yamaki fluid percussion device. The rats were divided into four groups: LFP, MFP, sham LFP, and sham MFP. MRI was performed with a 4.7-T magnetic resonance apparatus 2 days and 90 days after the induction of injury. T1-, T2-, and T2- weighted images were obtained using a surface coil. RESULTS: Hemorrhage, contusion, and brain edema in LFP models were detected on the 2nd day after injury, and the necrotic tissue was absorbed and replaced by cerebrospinal fluid on the 90th day. In MFP animals, we detected a small hemorrhage in the corpus callosum with minimal brain edema around the hemorrhage on the 2nd day after injury, and on the 90th day, enlarged ventricles and cisterns were observed, indicating brain atrophy. CONCLUSION: MRI, therefore, is useful for plotting morphological changes in experimental TBI in vivo. We report the novel and clinically important finding of brain atrophy after experimental TBI.

Animals↗
PubMed2005

High-frequency percussive ventilation.

OBJECTIVE: To review the technique and clinical application of high-frequency percussive ventilation in critically ill patients. DESIGN: Literature search and descriptive review. RESULTS: High-frequency percussive ventilation is a time-cycled, pressure-limited mode of ventilation that delivers subphysiologic tidal volumes at rates that can exceed 500 breaths/min. It offers the potential advantage over conventional ventilation of providing equal or improved oxygenation and ventilation at lower peak and end-expiratory pressures. This modality has been used to manage severe lung disease in the neonatal and pediatric population, treat inhalation injury in pediatric and adult patients, and as salvage therapy in adult patients with acute respiratory distress syndrome. CONCLUSIONS: High-frequency percussive ventilation has been shown to provide favorable gas exchange in several well-defined patient populations. It reliably improves oxygenation and provides adequate ventilation at lower peak pressures than conventional ventilation. Adequately powered, randomized, prospective studies demonstrating significant mortality benefit have not yet been performed.

Adult↗
PubMed1993

A model of measured percussive mechanical trauma and its effects on skin.

In this study, the role of mechanical trauma to skin in industrial dermatitis is considered. The percussive component of mechanical trauma to skin is investigated by modelling it, using an oscillating device which can supply a range of percussive trauma doses. The instrument is electronically controlled, and contains sensors which monitor the force and displacement throughout each impact. From this information, a value proportional to the dose delivered to the skin is calculated and used, rather than the driving power of the percussor. The rate of dose is also controlled. In this study, doses were delivered at a frequency of 7 Hz. Eight volunteers were given regimens of percussive trauma at regular intervals over a 5-day period. Half the group received a dose of 4 mJ/cm2 per impact, the other half received double this dose. The skin response was evaluated using non-invasive measurements of transepidermal water loss, skin thickness, and erythema. The results demonstrate that erythema, skin thickness and transepidermal water loss are all increased after mechanical challenge--erythema and water loss by amounts dependent upon the trauma dose applied. The transepidermal water loss results indicate that for the subjects used in our study, there was a trauma threshold reached after a cumulative dose of greater than 250 J/cm2.

Dermatitis, Occupational↗
PubMed2006

Lactate, not glucose, up-regulates mitochondrial oxygen consumption both in sham and lateral fluid percussed rat brains.

OBJECTIVE: Failure of energy metabolism after traumatic brain injury may be a major factor limiting outcome. Although glucose is the primary metabolic substrate in the healthy brain, the well documented surge in tissue lactate after traumatic brain injury suggests that lactate may provide an energy need that cannot be met by glucose. We hypothesized, therefore, that administration of lactate or the combination of lactate and supraphysiological oxygen may improve mitochondrial oxidative respiration in the brain after rat fluid percussion injury. We measured oxygen consumption (VO2) to determine what effects glucose, lactate, oxygen, and the combination of lactate and oxygen have on mitochondrial respiration in both injured and uninjured rat brain tissue. METHODS: Anesthetized Sprague-Dawley rats were intubated and ventilated with either 0.21 or 1.0 fraction of inspired oxygen (FIO2). Brain tissue from acute sham animals was subjected in vitro to 1.1 mM, 12 mM and 100 mM concentrations of glucose and L-lactate. In another group, injury (fluid percussion injury of 2.5 +/- 0.02 atmospheres) was induced over the left hemisphere. The VO2 of mug amounts of brain tissues were measured in a microrespirometry system (Cartesian diver). RESULTS: The VO2 was found to be independent of glucose concentrations, but dose-dependent for lactate. Moreover, the lactate dependent VO2s were all significantly higher than those generated by glucose. Injured rats on FIO2 0.21 had brain tissue VO2 rates that were significantly lower than those of shams or preinjury levels. In injured rats treated with FIO2 1.0, the reduction in VO2 levels was prevented. Injured rats that received an intravenous infusion of 100 mM lactate had VO2 rates that were significantly higher than those obtained with FIO2 1.0. Combined treatment further boosted the lactate generated VO2 rates by approximately 15%. CONCLUSION: Glucose sustains mitochondrial respiration at a low level "fixed" rate because, despite increasing its concentration nearly 100-fold, it cannot up-regulate VO2 after fluid percussion injury. Lactate produces a dose-dependent VO2 response, possibly enabling mitochondria to meet the increased energy needs of the injured brain.

Animals↗
PubMed1994

Comparison of intrapulmonary percussive ventilation and chest physiotherapy. A pilot study in patients with cystic fibrosis.

STUDY OBJECTIVE: To compare the intrapulmonary percussive ventilator (IPV) to chest physiotherapy (P&PD) with respect to acute changes in (1) pulmonary function and (2) sputum physical properties in patients with cystic fibrosis (CF). DESIGN: Randomized crossover. SETTING: Community-based CF referral center. PARTICIPANTS: Nine nonhospitalized person (range, 7 to 40 years; median, 12.4 years) with moderate to excellent Shwachman scores. INTERVENTIONS: Three treatment regimens: (1) 2.5 mg albuterol delivered via IPV (internal percussive component activated); (2) 2.5 mg. albuterol delivered via IPV (internal percussive component inactivated), followed by P&PD; and (3) 2.5 mg albuterol delivered via updraft nebulizer, followed by P&PD. MEASUREMENTS AND RESULTS: Outcome measures included pulmonary function testing (PFTs) and quantitative and qualitative sputum analysis. Among the three treatment groups, there were no significant differences in the change in predicted PFTs 1 h or 4 h after treatment, nor in the volume of sputum expectorated in the first 4 or in the subsequent 20 h. Among patients receiving IPV, more serious disease was associated with greater improvement in FEF25-75 1 h after treatment, but these differences disappeared by 4 h. There were no meaningful differences in viscoelastic characteristics of sputum expectorated after each treatments. Participants reported general satisfaction with no adverse effects while using IPV. CONCLUSIONS: This initial pilot study suggests (1) stable patients with CF tolerated one treatment of IPV without adverse sequelae, and (2) IPV was as effective as standard aerosol and P&PD in improving short-term PFT results and enhancing sputum expectoration.

Adolescent↗
PubMed1979

Physiologic effects of chest percussion and postural drainage in patients with stable chronic bronchitis.

The effects of a 30-minute period of chest percussion and postural drainage were compared to a sham treatment (infrared lamp) in 35 patients with stable chronic bronchitis and to a period of directed coughing in 11 of these same patients. There were no differences in subjective responses or arterial blood gas levels following therapy. Spirometric studies showed small improvements over baseline values following either treatment but no difference between active and sham treatments. The volume of sputum expectorated during percussion and drainage was significantly greater than during the infrared warming (5.5 vs 1.4 ml) or during the directed coughing (9.0 vs 3.5 ml). Although chest percussion and postural drainage are effective in augmenting the volume of expectorated sputum, no significant alternations in air flow or gas exchange after two hours were demonstrated.

Adult↗
PubMedDate not supplied

Coma associated with flaccidity produced by fluid-percussion concussion in the cat. I: Is it due to depression of activity within the brainstem reticular formation?

This study is the first attempt to characterize neurological and behavioural consequences of fluid-percussion concussive head injury in the cat. Both animals initially anaesthetized by N2O as well as unanaesthetized, chronically prepared animals were subjected to injury. Injury with a fluid-pressure wave of 1.9-2.5 atm (duration 21-24 ms) produced a brief generalized areflexia. Following this initial response, injury greater than 2.1 atm frequently produced a period associated with hypotonia of postural muscles and suppression of postural motor responses (flaccidity). A close association between flaccidity and other indices of coma such as absence of eye-opening responses was noted. These consequences of injury can occur without fatal apnoae, circulatory collapse or overt intraparenchymal haemorrhages. This result suggests that mechanical stress predominantly restricted to the brain stem in fluid percussion may be sufficient, at least in the cat, to produce coma associated with flaccidity which has been previously documented for acceleration concussion. There was no evidence that fluid percussion produced EEG depression similar to the effects of lesions in the mesencephalic reticular activating system (RAS). Thus, depression of general levels of brain activity including those within the RAS seems not be necessary for production of this form of reversible coma.

Animals↗
PubMed1985

A comparison of physiological responses to percussive brain trauma in dogs and sheep.

Physiological variables were monitored in dogs and sheep after exposure of the brain to a pressure wave produced by a fluid-percussion device. Mean systemic arterial pressure (SAP), mean pulmonary arterial pressure (PAP), and pulmonary wedge pressure (PWP) were recorded prior to and following trauma. Lung lymph flows (QLYM) were measured prior to and for 2 hours after trauma. Plasma catecholamine levels were quantitated prior to and at 30 seconds following trauma. In 16 dogs, SAP increased from 123 +/- 14.6 to 254 +/- 60.8 mm Hg (p less than 0.0001), PAP increased from 17 +/- 4.4 to 27 +/- 10.8 mm Hg (p less than 0.05), and PWP increased from 4 +/- 2.4 to 15 +/- 8.8 mm Hg (p less than 0.0001), all at 30 seconds posttrauma. All pressures returned to near baseline values within 6 minutes. The QLYM from the right lymph duct in 12 dogs increased from 0.82 +/- 0.77 to 2.7 +/- 2.1 and 1.88 +/- 1.82 ml/30 min, respectively, at 30 and 120 minutes. In five dogs the plasma concentrations of dopamine, epinephrine, and norepinephrine increased from 234 +/- 98 to 1906 +/- 1384, 609 +/- 641 to 19,813 +/- 10,234, and 388 +/- 194 to 3223 +/- 992 pg/ml, respectively (all p less than 0.01). In sheep there were no changes in SAP, PAP, PWP, QLYM, or catecholamine levels in response to percussive wave trauma up to 10 atm. Ratios of lung tissue water to dry weight were not significantly different from control animals in either species. The authors conclude that in dogs there is a profound sympathetic discharge resulting in dramatic elevations in plasma catecholamines, systemic and pulmonary artery hypertension, and an increase in pulmonary lymph flow. Sheep fail to demonstrate changes in any of these variables after severe percussive wave brain trauma.

Animals↗
PubMed2001

[Effects of fluid percussion injury on intracellular [Ca2+]i and pH in cultured rat neurons].

AIM: To study the change of intracellular [Ca2+]i and pH in cultured neurons after fluid percussion injury, and the therapeutic effect of drugs. METHODS: The neurons of Sprague Dawley rats were cultured for 8-14 days, then treated them with fluid percussion injury (2.5 kPa, 20 ms). Alterations of [Ca2+]i and pH in single neural cells following fluid percussion injury were measured by a laser scanning confocal microscope. After being injured for several hours the cultured neurons were treated with nimodipine or D-(-)-2-amino-5-phosphonovaleric acid (D-AP-5). Two hours later, the effects of drugs on intracellular [Ca2+]i and pH were studied. RESULTS: The Intracellular [Ca2+]i increased quickly after brain injury and reached peak in 12 hours. It then decreased gradually and became normal at 48 hours. The pH decreased slowly, reached minimum in 12 hours, and then kept at a lower level. It did not recover normal at 48 hours. Nimodipine and D-AP-5 decreased significantly the ascension of [Ca2+]i and the descent of pH. But nimodipine and D-AP-5 must be given within 10 hours after injury for a good therapeutic effect. CONCLUSION: According to the change of intracellular [Ca2+]i and pH, early use of nimodipine and D-AP-5, will get a better therapeutic effect.

2-Amino-5-phosphonovalerate↗
PubMed2005

[Expression of PDGF-B after fluid percussion brain injury in rats].

OBJECTIVE: To elucidate the changes of PDGF-B chain in the brain injured by fluid percussion. METHODS: The expression of PDGF-B protein was studied by immunohistochemistry and the results were assessed by image analysis system. RESULTS: Enhanced expression of PDGF-B protein induced by fluid percussion injury was seen at 1 h, and its marked up-regulation was noted at 4-7 days, and then the expression became decreased but it remained above the control levels till 14 days after injury. CONCLUSION: Fluid percussion brain injury induced expression of PDGF-B. The regular change pattern of PDGF-B level in time course seems to be of value in estimating the age of brain injury.

Animals↗
PubMed2007

Measurement of pulsatile tidal volume, pressure amplitude, and gas flow during high-frequency percussive ventilation, with and without partial cuff deflation.

OBJECTIVE: With a high-frequency percussive ventilator and a mechanical lung model, to measure tidal volume (V(T)), pulsatile pressure amplitude (difference between peak and nadir pulsatile pressure [DeltaP];), and mean airway pressure (P (aw)) at various pulsatile frequencies, pulsatile inspiratory-expiratory ratios (I:E(p)), and pressures (measured at the interface between the pulse-generator and the endotracheal tube [P(vent)]). METHODS: With the endotracheal tube inside an artificial trachea, we manipulated the high-frequency percussive ventilation settings and adjuncts, including pulsatile frequency, I:E(p), and P(vent) by manipulating pulsatile flow. We also studied the effects of partially deflating the endotracheal tube cuff. We measured P (aw), pulsatile pressure amplitude at the carina (DeltaP(c)), and pulsatile V(T) at the carina. With the cuff partly deflated, we measured the fraction of inspired oxygen (F(IO(2))) in the gas efflux above and below the cuff. RESULTS: Increasing the pulsatile frequency from 300 cycles/min to 600 cycles/min and changing the I:E(p) from 1:3 to 1:1 significantly reduced V(T) (p < 0.001). P (aw) and DeltaP(c) were unaffected by the change in pulsatile frequency or I:E(p), except when we did not preserve the pulsatile flow. The measured V(T) range was from 19.1 mL (at 600 cycles/min) to 47.3 mL (at 300 cycles/min). Partial cuff deflation did not significantly reduce P (aw) or DeltaP(c), but it did significantly reduce V(T) and F(IO(2)). CONCLUSION: During high-frequency percussive ventilation, the pulsatile frequency is inversely related to V(T). Partial cuff deflation reduces the delivered F(IO(2)).

Air Pressure↗
PubMed1985

On the concept of the center of percussion.

This paper briefly reviews the concept of the center of percussion of a rigid body, with special emphasis on the requirements for its existence, the two complementary methods used to determine its location, and the system parameters on which its location depends. A consistent generalization of this concept is then proposed for the case when the rigid body is initially moving arbitrarily in three-dimensional inertial space and is restrained in such a way that no impulsive reaction torque can be applied to the body at the point of restraint. The basic requirement for the existence of a center of percussion in this generalized case is identified, and the location of the center of percussion is obtained using one of the two complementary solution methodologies. Six special cases are considered when the existence requirement is satisfied, and these cases are illustrated using examples from common sport situations.

Biomechanical Phenomena↗