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Biomedical subjects

A Marmarou

Publications and source records attributed to A Marmarou.

At least 73 records · Page 4Linked to original sources
PubMed1997

Contribution of vasogenic and cellular edema to traumatic brain swelling measured by diffusion-weighted imaging.

The contribution of brain edema to brain swelling in cases of traumatic brain injury remains a critical problem. The authors believe that cellular edema, the result of complex neurotoxic events, is the major contributor to brain swelling and that vasogenic edema, secondary to blood-brain barrier compromise, may be overemphasized. The objective of this study, therefore, was to quantify temporal water content changes and document the type of edema that forms during the acute and late stages of edema development following closed head injury (CHI). The measurement of brain water content was based on magnetic resonance imaging-determined values of tissue longitudinal relaxation time (T1-weighted imaging) and their subsequent conversion to percentage of water, whereas the differentiation of edema formation (cellular vs. vasogenic) was based on the measurement of the apparent diffusion coefficient (ADC) by diffusion-weighted imaging. A new impact-acceleration model was used to induce CHI. Thirty-six adult Sprague-Dawley rats were separated into two groups: Group I, control (six animals); and Group II, trauma (30 animals). Fast ADC measurements (localized, single-voxel) were obtained sequentially (every minute) up to 1 hour postinjury. The T1-weighted images, used for water content determination, and the diffusion-weighted images (ADC measurement with conventional diffusion-weighted imaging) were obtained at the end of the 1st hour postinjury and on Days 1, 3, 7, 14, 28, and 42 in animals from the trauma and control groups. In the animals subjected to trauma, the authors found a significant increase in ADC (10 +/- 5%) and brain water content (1.3 +/- 0.9%) during the first 60 minutes postinjury. This is consistent with an increase in the volume of extracellular fluid and vasogenic edema formation as a result of blood-brain barrier compromise. This transient increase, however, was followed by a continuing decrease in ADC that began 40 to 60 minutes postinjury and reached a minimum value on Days 7 to 14 (10 +/- 3% reduction). Because the water content of the brain continued to increase during the first 24 hours postinjury (1.9 +/- 0.9%), it is suggested that the decreased ADC indicated cellular edema formation, which started to develop soon after injury and became dominant between 1 and 2 weeks postinjury. The study provides supportive evidence that cellular edema is the major contributor to posttraumatic swelling in diffuse CHI and defines the onset and duration of the increase in cellular volume.

Acceleration↗
PubMed1997

Impact acceleration injury in the rat: evidence for focal axolemmal change and related neurofilament sidearm alteration.

Recently we reported that traumatic brain injury evokes local changes in the axolemma's permeability, in concert with local cytoskeletal changes involving neurofilament (NF) compaction and sidearm loss, all of which contribute to the genesis of reactive axonal change. Since it was of concern that these events may be either injury model- or species-specific, we sought to address these phenomena in a different but well-characterized animal model and species. Further, to provide more compelling insight into the potential for NF compaction and sidearm alteration, we also employed antibodies specific for the NF rod domains, which are readily visualized only when the NF sidearms are disturbed. Rats were subjected to impact acceleration injury. To assess the potential for altered axolemmal permeability, 5 animals received intrathecal horseradish peroxidase (HRP), normally excluded by the intact axolemma. To assess the potential for NF sidearm alteration, another 14 animals were processed for the visualization of antibodies targeting the NF rod domain at 5 minutes (min) to 24 hours (h) postinjury. All animals were evaluated at the LM and EM levels. Those animals receiving intrathecal HRP showed immediate focal alterations in the axolemma's permeability to the normally excluded tracer. Over a 2 h period, these axons demonstrated NF compaction. Antibodies targeted to the rod domains revealed focal intra-axonal immunoreactivity in sites closely correlated with those showing altered axolemmal permeability. These same sites also demonstrated evidence of NF compaction and sidearm loss/perturbation. Collectively, these findings suggest that occurrence of altered axolemmal permeability and concomitant cytoskeletal change are features common to traumatic brain injury in various animal models and species. Further, these studies underscore the utility of antibodies targeting the rod domain for the early detection of traumatically induced reactive change.

Animals↗
PubMed1996

Conduct of head injury trials in the United States: the American Brain Injury Consortium (ABIC).

This article provides a brief description of the American Brain Injury Consortium (ABIC), a group of clinical scientists focused on the design and implementation of clinical trials in the United States to improve outcome of the brain injured patient. The structure of the consortium, guidelines for participation, relationship with pharmaceutical industry, and the instruments used for acquisition and analysis of data gathered are described.

Brain Injuries↗
PubMed1996

Effects of increased intra-abdominal pressure upon intracranial and cerebral perfusion pressure before and after volume expansion.

OBJECTIVE: To study the effects of elevated intra-abdominal pressure (IAP) upon intracranial (ICP) and cerebral perfusion pressure (CPP) before and after intravascular volume resuscitation. MATERIALS AND METHODS: Intra-abdominal pressure was increased in five anesthetized swine by inflating an intraperitoneal balloon until the IAP was 25 mm Hg above baseline. Intravascular volume was then expanded and finally abdominal decompression was performed. Changes in ICP and systemic and pulmonary hemodynamic parameters secondary to increasing IAP were measured. The effect upon CPP was derived from these measurements. PaO2 and PaCO2 were maintained relatively constant by increasing ventilatory rate. MEASUREMENTS AND MAIN RESULTS: Elevated IAP significantly increased ICP (7.6 +/- 1.2 vs. 21.4 +/- 1.0), pleural pressure and central venous pressure; whereas cardiac index and CPP (82.2 +/- 6.3 vs. 62.0 +/- 10.0) decreased significantly. Intravascular volume expansion further significantly increased ICP (27.8 +/- 1.0), and significantly increased both mean arterial pressure (83.4 +/- 14.0 versus 103.4 +/- 8.9) and CPP (75.6 +/- 9.0). Abdominal decompression returned ICP (11.2 +/- 1.8) toward baseline and further increased CPP (79.8 +/- 9.7). CONCLUSIONS: Elevated IAP increases ICP and decreases CPP and cardiac index. Volume expansion further increases ICP yet improves CPP via its greater positive effect upon mean arterial pressure (*p < 0.05, analysis of variance. All measurements are mean +/- SEM in mm Hg).

Abdomen↗
PubMed1996

Characterization of edema by diffusion-weighted imaging in experimental traumatic brain injury.

The objective of this study was to use diffusion-weighted magnetic resonance imaging (DWI) to help detect the type of edema that develops after experimental trauma and trauma coupled with hypotension and hypoxia (THH). Reduction in the apparent diffusion coefficients (ADCs) is thought to represent cytotoxic edema. In a preliminary series of experiments, the infusion edema model and middle cerebral artery occlusion models were used to confirm the direction of ADC change in response to purely extracellular and cytotoxic edema, respectively. The ADCs increased (p<0.05) in the case of extracellular edema and decreased (p<0.001) in cytotoxic edema. Following these initial experiments, a new impact acceleration model was used to induce traumatic brain injury. Thirty-six adult Sprague-Dawley rats were separated into four groups; sham, trauma alone, hypoxia and hypotension (HH), and THH. Following trauma, a 30-minute insult of hypoxia (PaO2 of 40 mm Hg) and hypotension (mean arterial blood pressure (MABP) of 30 mm Hg) were imposed and the animals were resuscitated. The DWI was carried out at four 1-hour intervals postinjury, and MABP, intracranial pressure (ICP), cerebral perfusion pressure (CPP), and cerebral blood flow (CBF) were monitored. The ADCs in the control and HH groups remained unchanged. The ADCs in the THH group rapidly decreased from a control level of 0.68 +/- 0.05 x 10(-3) mm2/second to 0.37 +/- 0.09 x 10(-3) mm2/second by 3 hours posttrauma (p < 0.001). In this group, the decreased CBF and CPP during secondary insult remained low despite resuscitation, with the ICP increasing to 56 +/- 7 mm Hg by 3 hours. In the trauma alone group, the rise in ICP reached a maximum value (28 +/- 3 mm Hg) at 30 minutes with a significant and sustained increase in CBF despite a gradual decrease in CPP. The ADCs in this group were not significantly reduced. The data lead the authors to suggest that the rise in ICP following severe trauma coupled with secondary insult in this model is predominately caused by cytotoxic edema and that ischemia plays a major role in the development of brain edema after head injury.

Animals↗
PubMed1996

Ventriculostomy infections: the effect of monitoring duration and catheter exchange in 584 patients.

The investigators undertook a retrospective analysis of ventriculostomy infections to evaluate their relationship to monitoring duration and prophylactic catheter exchange. In 1984, the results of an epidemiological study of ventriculostomy-related infection were published. One of the conclusions of the paper was that the incidence of ventriculostomy-related infections rose after 5 days of monitoring. This led to the recommendation that catheters be prophylactically changed at 5-day intervals if prolonged monitoring was required. A recent randomized prospective study on central venous catheters showed no reduction in infection with prophylactic catheter exchanges. This has led the authors to reexamine their experience with ventriculostomy infections. Data on 584 severely head injured patients with ventriculostomies were prospectively collected in two data banks, The Traumatic Coma Data Bank and The Medical College of Virginia Neurocore Data Bank. These data were retrospectively analyzed for factors associated with ventriculostomy related infections. It was found that there is a relationship of ventriculitis to monitoring duration but it is not simple or linear. There is a rising risk of infection over the first 10 days, but infection then becomes very unlikely despite a population that continues to be at risk. Patients in whom catheters were replaced prior to 5 days did not have a lower infection rate than those whose catheters were exchanged at more than 5-day intervals. Based on these data, it is recommended that ventriculostomy catheters for intracranial pressure monitoring be removed as quickly as possible, and in circumstances in which prolonged monitoring is required, there appears to be no benefit from catheter exchange.

Adolescent↗
PubMed1996

Posttraumatic ventriculomegaly: hydrocephalus or atrophy? A new approach for diagnosis using CSF dynamics.

Cerebrospinal fluid (CSF) dynamics were correlated to the changes in ventricular size during the first 3 months posttrauma in patients with severe head injury (Glasgow Coma Scale score < or = 8, 75 patients) to distinguish between atrophy and hydrocephalus as the two possible causes of posttraumatic ventriculomegaly. Using the bolus injection technique, the baseline intracranial pressure (ICP), pressure volume index, and resistance for CSF absorption (R0) provided a three-dimensional profile of CSF dynamics that was correlated with ventricular size and Glasgow Outcome Scale (GOS) score at 3, 6, and 12 months posttrauma. Patients were separated into five different groups based on changes in ventricular size, presence of atrophy, and CSF dynamics. Group 1 (normal group, 41.3%) demonstrated normal ventricular size and normal ICP. Group 2 (benign intracranial hypertension group, 14.7%) showed normal ventricular size and elevated ICP. Group 3 (atrophy group, 24%) displayed ventriculomegaly, normal ICP, and normal R0. Group 4 (normal-pressure hydrocephalus group, 9.3%) had ventriculomegaly, normal ICP, and high R0. Group 5 (high-pressure hydrocephalus group, 10.7%) showed ventriculomegaly and elevated ICP with or without high R0. The GOS score in the nonhydrocephalic groups (Groups 1, 2, and 3) was better than in the hydrocephalic groups (Groups 4 and 5). It is concluded from these results that 44% of head injury survivors may develop posttraumatic ventriculomegaly. Posttraumatic hydrocephalus, as identified by abnormal CSF dynamics, was diagnosed in 20% of survivors and their outcome was significantly worse. This study demonstrates the importance of using CSF dynamics as an aid in diagnosis of posttraumatic hydrocephalus and identifying those patients who may benefit from shunt placement.

Atrophy↗
PubMed1996

Magnetic resonance imaging-monitored acute blood-brain barrier changes in experimental traumatic brain injury.

The authors posit that cellular edema is the major contributor to brain swelling in diffuse head injury and that the contribution of vasogenic edema may be overemphasized. The objective of this study was to determine the early time course of blood-brain barrier (BBB) changes in diffuse closed head injury and to what extent barrier permeability is affected by the secondary insults of hypoxia and hypotension. The BBB disruption was quantified and visualized using T1-weighted magnetic resonance (MR) imaging following intravenous administration of the MR contrast agent gadolinium-diethylenetriamine pentaacetic acid. To avoid the effect of blood volume changes, the maximum signal intensity (SI) enhancement was used to calculate the difference in BBB disruption. A new impact-acceleration model was used to induce closed head injury. Forty-five adult Sprague-Dawley rats were separated into four groups: Group I, sham operated (four animals), Group II, hypoxia and hypotension (four animals), Group III, trauma only (23 animals), and Group IV, trauma coupled with hypoxia and hypotension (14 animals). After trauma was induced, a 30-minute insult of hypoxia (PaO2 40 mm Hg) and hypotension (mean arterial blood pressure 30 mm Hg) was imposed, after which the animals were resuscitated. In the trauma-induced animals, the SI increased dramatically immediately after impact. By 15 minutes permeability decreased exponentially and by 30 minutes it was equal to that of control animals. When trauma was coupled with secondary insult, the SI enhancement was lower after the trauma, consistent with reduced blood pressure and blood flow. However, the SI increased dramatically on reperfusion and was equal to that of control by 60 minutes after the combined insult. In conclusion, the authors suggest that closed head injury is associated with a rapid and transient BBB opening that begins at the time of the trauma and lasts no more than 30 minutes. It has also been shown that addition of posttraumatic secondary insult-hypoxia and hypotension-prolongs the time of BBB breakdown after closed head injury. The authors further conclude that MR imaging is an excellent technique to follow (time resolution 1-1.5 minutes) the evolution of trauma-induced BBB damage noninvasively from as early as a few minutes up to hours or even longer after the trauma occurs.

Animals↗
PubMed1995

Cerebrovascular carbon dioxide reactivity assessed by intracranial pressure dynamics in severely head injured patients.

Appropriate management of intracranial pressure (ICP) in severely head injured patients depends in part on the cerebral vessel reactivity to PCO2; loss of CO2 reactivity has been associated with poor outcome. This study describes a new method for evaluating vascular reactivity in head-injured patients by determining the sensitivity of ICP change to alterations in PCO2. This method was combined with measurements of the pressure volume index (PVI), which allowed calculation of blood volume change necessary to alter ICP. The objective of this study was to investigate the ICP response and the blood volume change corresponding to alterations in PCO2 and to examine the correlation of responsivity and outcome as measured on the Glasgow Outcome Scale. The PVI and ICP at different end-tidal PCO2 levels produced by mild hypo- and hyperventilation were obtained in 49 patients with Glasgow Coma Scale scores of less than 8 and over a wide range of PCO2 (25 to 40 mm Hg) in eight patients. Given the assumption that the PVI remained constant during alteration of PaCO2, the estimated blood volume change per torr change of PCO2 was calculated by the following equation: BVR = PVI x delta log(ICP)/delta PCO2, where BVR = blood volume reactivity. The data in this study showed that PVI remained stable with changes in PCO2, thus validating the assumption used in the blood volume estimates. Moreover, the response of ICP to PCO2 alterations followed an exponential curve that could be described in terms of the responsivity indices to capnic stimuli. It was found that responsivity to hypocapnia was reduced by 50% compared to responsivity to hypercapnia measured within 24 hours of injury (p < 0.01). The sensitivity of ICP to estimated blood volume changes in patients with a PVI of less than 15 ml was extremely high with only 4 ml of blood required to raise ICP by 10 mm Hg. The authors conclude from these data that, following traumatic injury, the resistance vessels are in a state of persistent vasoconstriction, possibly due to vasospasm or compression. Furthermore, BVR correlates with outcome on the Glasgow Coma Scale, indicating that assessment of cerebrovascular response within the first 24 hours of injury may be of prognostic value.

Adolescent↗
PubMed1994

Traumatic brain edema: an overview.

This article provides a brief summary of concepts describing the formation and resolution of traumatic brain edema. Recent laboratory and clinical data are reviewed targeted toward resolving the contribution of edema to the swelling process. These data, indicate that blood volume is reduced in areas of ischemia following traumatic injury and edema volume is increased. Thus, edema is the major contributor to the swelling process in diffuse injury. As clinical MRI studies have not revealed barrier compromise in the presence of swelling, it is considered that other forms of edema, primarily ischemic and neurotoxic, make a substantial contribution to the edema volume.

Animals↗
PubMed1994

The cause of acute brain swelling after the closed head injury in rats.

The major component of acute brain swelling was determined using a new closed head injury (CHI) model in rats. Twenty seven Sprague-Dawley rats were separated into four groups (Sham, CHI, CHI combined with hypotension and CHI combined with hypoxia and hypotension). Hypoxia (pO2 of 40 mmHg) and hypotension (mean arterial blood pressure of 30 to 40 mmHg) were induced immediately after head injury and were maintained for 30 minutes. These experiments were terminated at two hours after CHI by transcalvarial freezing with liquid nitrogen. Blood pressure, intracranial pressure (ICP) and physiological parameters were monitored. Regional cerebral blood volume and water content were measured quantitatively. Rats with CHI, and with CHI and hypotension, had mild increase in ICP. Otherwise, rats with CHI, hypoxia and hypotension showed a significant increase in ICP (36.2 +/- 5.6 mmHg). Water content showed an increase of 1.6% in the estimated total brain and 2.4% in the cerebral cortex in those rats. Cerebral blood volume decreased by 61.4% in the total brain and 57.3% in the cortex. There was a reduction in the cerebral hematocrit of 2.4% in the total brain and 4.7% in the cortex. The main component of brain swelling in this head injury model was brain edema. Cerebral blood volume and hematocrit were reduced in the remarkable edematous brain.

Animals↗
PubMed1994

Quantitative analysis of blood-brain barrier damage in two models of experimental head injury in the rat.

The integrity of the blood-brain barrier was studied in a new model of closed head injury, and in an established model of fluid percussion injury, in the rat. Brain injury in this new model is induced by impact and acceleration of the protected rat skull. Severe hypertension is not a characteristic of this new model as compared to the tremendous surge following direct dural percussion. This is important because of the well known sensitivity of the cerebral microvasculature for acute hypertension. Using a radioactive tracer technique the dysfunction of the barrier was quantified. It is shown that the BBB is temporarily damaged due to trauma, subsequent arterial pressure surge, as seen in the percussed animals, deteriorates the dysfunction of the barrier even further. This study indicates that vascular damage is a key event following head injury. Yet the concomitant basic pathophysiological sequelae of different models must be considered when studying barrier damage and cerebral edema following brain injury. Time window studies of the barrier indicate that the barrier seals within a few hours following severe concussive head injury, and in the absence of a hypertensive surge.

Animals↗
PubMed1994

Brain edema resolution by CSF pathways and brain vasculature in cats.

Brain edema is a major contributor to the brain swelling process and raised intracranial pressure, yet the specific pathways involved in clearance of brain edema (fluid and proteins) and their relative contribution to the resolution process remain unknown. The objective of this study was to document the temporal course of edema resolution from brain to cerebrospinal fluid (CSF) and by the brain vasculature. Radioiodinated (125I) cat serum albumin (RICSA) was infused continuously into the white matter of anesthetized adult cats for 8 h, and ventriculocisternal perfusion was used to monitor the RICSA activity in CSF at 15-min intervals and to compare with the blood taken at 15-min intervals. The RICSA that cleared from the brain in 8 h measured 29.8% of the amount infused. Of the amount of RICSA leaving the brain, we found that the CSF compartment accounted for 87.14% of the cleared RICSA volume, while only 10.96% of RICSA was found in the blood during the 8-h experiment. The amount of RICSA remaining in the brain when the animal was killed equaled 71.2 +/- 15.9% (mean +/- SD) of the RICSA infused. We conclude that vascular clearance during the acute stage of resolution is minimal and that clearance of RICSA occurs predominantly via the CSF pathways.

Animals↗
PubMed1994

A new model of diffuse brain injury in rats. Part I: Pathophysiology and biomechanics.

This report describes the development of an experimental head injury model capable of producing diffuse brain injury in the rodent. A total of 161 anesthetized adult rats were injured utilizing a simple weight-drop device consisting of a segmented brass weight free-falling through a Plexiglas guide tube. Skull fracture was prevented by cementing a small stainless-steel disc on the calvaria. Two groups of rats were tested: Group 1, consisting of 54 rats, to establish fracture threshold; and Group 2, consisting of 107 animals, to determine the primary cause of death at severe injury levels. Data from Group 1 animals showed that a 450-gm weight falling from a 2-m height (0.9 kg-m) resulted in a mortality rate of 44% with a low incidence (12.5%) of skull fracture. Impact was followed by apnea, convulsions, and moderate hypertension. The surviving rats developed decortication flexion deformity of the forelimbs, with behavioral depression and loss of muscle tone. Data from Group 2 animals suggested that the cause of death was due to central respiratory depression; the mortality rate decreased markedly in animals mechanically ventilated during the impact. Analysis of mathematical models showed that this mass-height combination resulted in a brain acceleration of 900 G and a brain compression gradient of 0.28 mm. It is concluded that this simple model is capable of producing a graded brain injury in the rodent without a massive hypertensive surge or excessive brain-stem damage.

Animals↗
PubMed1994

A new model of diffuse brain injury in rats. Part II: Morphological characterization.

A new model producing diffuse brain injury, without focal brain lesions, has been developed in rats. This has been achieved by allowing a weight of 450 gm to fall onto a metallic disc fixed to the intact skull of the animal which is supported by a foam bed. Two levels of injury were examined by adjusting the height of the falling weight to either 1 m or 2 m. Two groups of animals were studied. Group 1 animals were separated into three subgroups: 10 received a 1-m weight drop, 58 received a 2-m weight drop, and 13 served as controls; all were allowed to breathe spontaneously. Group 2 animals were separated into the same subgroups: four received a 1-m weight drop, six received a 2-m weight drop, and four served as controls; all of these were mechanically ventilated during the procedure. In Group 1, morphological studies using light and electron microscopy were performed at 1, 6, 24, or 72 hours, or 10 days after insult; all Group 2 rats were studied at 24 hours after injury. Results from Group 1 animals showed that no mortality occurred with the 1-m level injury, while 59% mortality was seen with the 2-m level injury. On the other hand, no mortality occurred in Group 2 animals regardless of the level of trauma induced. However, the morphological changes observed in both groups were similar. Gross pathological examination did not reveal any supratentorial focal brain lesion regardless of the severity of the trauma. Petechial hemorrhages were noticed in the brain stem at the 2-m level injury. Microscopically, the model produced a graded widespread injury of the neurons, axons, and microvasculature. Neuronal injury was mainly observed bilaterally in the cerebral cortex. Brain edema, in the form of pericapillary astrocytic swelling, was also noted in these areas of the cerebral cortex and in the brain stem. Most importantly, the trauma resulted in a massive diffuse axonal injury that primarily involved the corpus callosum, internal capsule, optic tracts, cerebral and cerebellar peduncles, and the long tracts in the brain stem. It is concluded that this model would be suitable for studying neuronal, axonal, and vascular changes associated with diffuse brain injury.

Animals↗
PubMed1994

Temporal profile of outcomes in severe head injury.

The authors present data describing the temporal progress of 786 severely head-injured patients from discharge to 12 months postinjury. Changes in outcome over time are characterized and the effects on these changes of patient age, Glasgow Coma Scale score, pupillary response, and type of injury are investigated. The feasibility of using these factors and the outcome at 3 months postinjury to predict the outcome at 6 months post-trauma is explored via logistic regression analysis. The data indicate that a significant proportion of patients improve continuously during the first 6 months after injury; outcome tends to stabilize thereafter, which suggests that the response at this time may be the appropriate end point for clinical trials in severe head injury. Dichotomized outcomes are predictable with approximately 94% accuracy at 6 months postinjury; therefore, missing outcomes may safely be replaced by the corresponding predicted outcomes. The findings also indicate striking improvement over time in patients who are in a vegetative state at discharge, suggesting that decisions regarding withdrawal of supportive care should be postponed until 6 months after injury in these patients.

Adolescent↗
PubMed1993

Traumatic brain tissue acidosis: experimental and clinical studies.

We have been focusing on potential metabolic derangement associated with severe head injury and a clinical trail directed toward treating brain tissue acidosis is currently underway. More specifically, we based this study on the hypothesis that following brain trauma brain tissue acidosis develops which may contribute to the prolongation of coma and neurologic deficit. Tromethamine (THAM), a safe and low toxicity agent which buffers in major part by causing a hypocapnic alkalosis, was selected for trial. Patients admitted with GCS < 8 were randomized into one of three arms: control: THAM plus hyperventilation; hyperventilation alone. Each regimen was maintained for 5 days post injury. Our analysis of 3 and 6 months Glasgow outcome score showed that prophylactic hyperventilation retards recovery, and the use of THAM overcomes the apparent deleterious effects of hyperventilation. One explanation is that the reduced ICP instability observed in THAM treated patients may account for this improvement. Is THAM effective in buffering traumatized brain tissue? What factors account for improvement in ICP stability? We addressed these questions in experimental studies utilizing MR spectroscopy to measure brain lactate production and tissue pH in fluid percussed anaesthetized cats. The protocol was designed to match our clinical trial, and brain injured animals were randomized into control, THAM, and hyperventilated groups. We observed that brain lactate production increased with trauma and remained above control at 8 hrs post injury. Lactate production in THAM treated animals was not elevated. Highest lactate production was associated with injured animals treated with sustained hyperventilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗