Experimental head injury in the rat

1977 ◽  
Vol 47 (2) ◽  
pp. 241-251 ◽  
Author(s):  
Bengt Nilsson ◽  
Urban Pontén ◽  
Gerhard Voigt
Keyword(s):  
Blood Flow ◽  
Energy Metabolism ◽  
Head Injury ◽  
Impact Velocity ◽  
Albino Rat ◽  
Functional Disturbance ◽  
Content Type ◽  
Cerebral Energy Metabolism ◽  
Impact Acceleration ◽  
Fine Print

✓ Impact acceleration was used to elicit cerebral concussion in the albino rat. The pathophysiological response and morphological damage from the concussion were studied in groups of animals. The animals were grouped according to impact velocity (6–11 m/sec), and the threshold and different degrees of the concussive response were established. The concept of concussion as primarily a neuronal, functional disturbance was confirmed. However, this reaction was readily influenced by respiratory and circulatory changes, and morphological damage. Defined reactions could be elicited in groups of animals according to impact velocity. Thus, the model appeared well standardized for further studies of concussion pathophysiology, expressed in terms of cerebral energy metabolism and blood flow.

Cerebral blood flow and metabolism in severely head-injured children

1989 ◽  
Vol 71 (1) ◽  
pp. 63-71 ◽  
Author(s):  
J. Paul Muizelaar ◽  
Anthony Marmarou ◽  
Antonio A. F. DeSalles ◽  
John D. Ward ◽  
Richard S. Zimmerman ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Head Injury ◽  
Severe Head Injury ◽  
Cerebral Blood Volume ◽  
Closed Head Injury ◽  
Volume Index ◽  
Content Type ◽  
Gcs Score ◽  
Fine Print

✓ The literature suggests that in children with severe head injury, cerebral hyperemia is common and related to high intracranial pressure (ICP). However, there are very few data on cerebral blood flow (CBF) after severe head injury in children. This paper presents 72 measurements of cerebral blood flow (“CBF15”), using the 133Xe inhalation method, with multiple detectors over both hemispheres in 32 children aged 3 to 18 years (mean 13.6 years) with severe closed head injury (average Glasgow Coma Scale (GCS) score 5.4). In 25 of the children, these were combined with measurements of arteriojugular venous oxygen difference (AVDO2) and of cerebral metabolic rate of oxygen (CMRO2). In 30 patients, the first measurement was taken approximately 12 hours postinjury. In 18 patients, an indication of brain stiffness was obtained by withdrawal and injection of ventricular cerebrospinal fluid and calculation of the pressure-volume index (PVI) of Marmarou. The CBF and CMRO2 data were correlated with the GCS score, outcome, ICP, and PVI. Early after injury, CBF tended to be lower with lower GCS scores, but this was not statistically significant. This trend was reversed 24 hours postinjury, as significantly more hyperemic values were recorded the lower the GCS score, with the exception of the most severely injured patients (GCS score 3). In contrast, mean CMRO2 correlated positively with the GCS score and outcome throughout the course, but large standard deviations preclude making predictions based on CMRO2 measurements in individual patients. Early after injury, there was mild uncoupling between CBF and CMRO2 (CBF above metabolic demands, low AVDO2) and, after 24 hours, flow and metabolism were completely uncoupled with an extremely low AVDO2. Consistently reduced flow was found in only four patients; 28 patients (88%) showed hyperemia at some point in their course. This very high percentage of patients with hyperemia, combined with the lowest values of AVDO2 found in the literature, indicates that hyperemia or luxury perfusion is more prevalent in this group of patients. The three patients with consistently the highest CBF had consistently the lowest PVI: thus, the patients with the most severe hyperemia also had the stiffest brains. Nevertheless, and in contrast to previous reports, no correlation could be established between the course of ICP or PVI and the occurrence of hyperemia, nor was there a correlation between the levels of CBF and ICP at the time of the measurements. The authors argue that this lack of correlation is due to: 1) a definition of hyperemia that is too generous, and 2) the lack of a systematic relationship between CBF and cerebral blood volume. The implications of these findings for therapeutic modes of controlling ICP in children, such as hyperventilation and the use of mannitol, are discussed.

Temporal changes in intracranial pressure in a modified experimental model of closed head injury

1998 ◽  
Vol 89 (5) ◽  
pp. 796-806 ◽  
Author(s):  
Koen Engelborghs ◽  
Jan Verlooy ◽  
Jos Van Reempts ◽  
Bruno Van Deuren ◽  
Mies Van de Ven ◽  
...  
Keyword(s):  
Head Injury ◽  
Intracranial Pressure ◽  
Experimental Model ◽  
Closed Head Injury ◽  
Content Type ◽  
Closed Head ◽  
Impact Acceleration ◽  
The Moment ◽  
The Impact ◽  
Fine Print

Object. The authors describe an experimental model of closed head injury in rodents that was modified from one developed by Marmarou and colleagues. This modification allows dual control of the dynamic process of impact compared with impulse loading that occurs at the moment of primary brain injury. The principal element in this weight-drop model is an adjustable table that supports the rat at the moment of impact from weights positioned at different heights (accelerations). The aim was to obtain reproducible pathological intracranial pressure (ICPs) while maximally reducing the incidence of mortality and skull fractures. Methods. Intracranial pressure was investigated in different experimental settings, including two different rat strains and various impact-acceleration conditions and posttrauma survival times. Identical impact-acceleration injuries produced a considerably higher mortality rate in Wistar rats than in Sprague—Dawley rats (50% and 0%, respectively). Gradually increasing severity of impact-acceleration conditions resulted in findings of a significant correlation between the degree of traumatic challenge and increased ICP at 4 hours (p < 0.001, R2 = 0.73). When the impact-acceleration ratio was changed to result in a more severe head injury, the ICP at 4, 24, and 72 hours was significantly elevated in comparison with that seen in sham-injured rats (4 hours: 19.7 ± 2.8 mm Hg, p = 0.004; 24 hours: 21.8 ± 1.1 mm Hg, p = 0.002; 72 hours: 11.9 ± 2.5 mm Hg, p = 0.009). Comparison of the rise in ICP between moderate and severe impact-acceleration injury at 4 and 24 hours revealed a significantly higher value after severe injury (4 hours: p = 0.008; 24 hours: p = 0.004). Continuous recordings showed that ICP mounted very rapidly to peak values, which declined gradually toward a pathological level dependent on the severity of the primary insult. Histological examination after severe trauma revealed evidence of irreversible neuronal necrosis, diffuse axonal injury, petechial bleeding, glial swelling, and perivascular edema. Conclusions. This modified closed head injury model mimics several clinical features of traumatic injury and produces reliable, predictable, and reproducible ICP elevations with concomitant morphological alterations.

Changes in cerebral blood flow during PaCO2 variations in patients with severe closed head injury: comparison between the Fick and transcranial Doppler methods

1998 ◽  
Vol 88 (6) ◽  
pp. 996-1001 ◽  
Author(s):  
Aram Ter Minassian ◽  
Eliane Melon ◽  
Caroline Leguerinel ◽  
Carlo Alberto Lodi ◽  
Françis Bonnet ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Head Injury ◽  
Transcranial Doppler ◽  
Closed Head Injury ◽  
High Group ◽  
Content Type ◽  
Closed Head ◽  
Fine Print ◽  
Group 1

Object. The aim of this study was to reassess whether middle cerebral artery blood flow velocity (MCAv) variations measured by transcranial Doppler ultrasonography during acute PaCO2 manipulation adequately reflect cerebral blood flow (CBF) changes in patients with severe closed head injury. Methods. The study was performed by comparing MCAv variations to changes in CBF as assessed by measurements of the difference in the arteriovenous content in oxygen (AVDO2). The authors initiated 35 CO2 challenges in 12 patients with severe closed head injury during the acute stage. By simultaneous recording of systemic and cerebral hemodynamic parameters, 105 AVDO2 measurements were obtained. Patients were stratified into two groups, “high” and “low,” with respect to whether their resting values of MCAv were greater than 100 cm/second during moderate hyperventilation. Four patients displayed an elevated MCAv, which was related to vasospasm in three cases and to hyperemia in one case. The PaCO2 and intracranial pressure levels were not different between the two groups. The slope of the regression line between 1 divided by the change in (Δ)AVDO2 and ΔMCAv was not different from identity in the low group (1/ΔAVDO2 = 1.08 × ΔMCAv − 0.07, r = 0.93, p < 0.001) and significantly differed (p < 0.05) from the slope of the high group (1/ΔAVDO2 = 1.46 × ΔMCAv − 0.4, r = 0.83, p < 0.001). Conclusions. In patients with severe closed head injury, MCAv variations adequately reflect CBF changes as assessed by AVDO2 measurements in the absence of a baseline increase in MCAv. These observations indicate that both moderate variations in PaCO2 and variations in cerebral perfusion pressure do not act noticeably on the diameter of the MCA. The divergence from the expected relationship in the high group seems to be due to the heterogeneity of CO2-induced changes in cerebrovascular resistance between differing arterial territories.

Dynamic autoregulatory response after severe head injury

2002 ◽  
Vol 97 (5) ◽  
pp. 1054-1061 ◽  
Author(s):  
Roman Hlatky ◽  
Yu Furuya ◽  
Alex B. Valadka ◽  
Jorge Gonzalez ◽  
Ari Chacko ◽  
...  
Keyword(s):  
Blood Flow ◽  
Head Injury ◽  
Severe Head Injury ◽  
Content Type ◽  
Factors Affecting ◽  
Physiological Variables ◽  
End Tidal ◽  
A Prospective Study ◽  
Pressure Autoregulation ◽  
Fine Print

Object. The purpose of this study was to evaluate the extent and timing of impairment of cerebral pressure autoregulation after severe head injury. Methods. In a prospective study of 122 patients with severe head trauma (median Glasgow Coma Scale Score 6), dynamic tests of pressure autoregulation were performed every 12 hours during the first 5 days postinjury and daily during the next 5 days. The autoregulatory index ([ARI] normal value 5 ± 1.1) was calculated for each test. The changes in the ARI over time were examined and compared with other physiological variables. The ARI averaged 2.8 ± 1.9 during the first 12 hours postinjury, and continued to decrease to a nadir of 1.7 ± 1.1 at 36 to 48 hours postinjury. At this nadir, in 87% of the patients the value was less than 2.8. This continued deterioration in the ARI during the first 36 to 48 hours postinjury occurred despite an increase in cerebral blood flow ([CBF], p < 0.05) and in middle cerebral artery blood flow velocity ([BFV], p < 0.001), and could not be explained by changes in cerebral perfusion pressure, end-tidal CO2, or cerebral metabolic rate of O2. A marked decrease in cerebrovascular resistance ([CVR], p < 0.001) accompanied this deterioration in the ARI. Patients with a relatively higher BFV on Day 1 had a lower CVR (p < 0.05) and more impaired pressure autoregulation than those with a lower BFV. Conclusions. The inability of cerebral vessels to regulate CBF normally may play a role in the vulnerability of the injured brain to secondary ischemic insults. These studies indicate that this vulnerability continues and even increases beyond the first 24 hours postinjury. Local factors affecting cerebrovascular tone may be responsible for these findings.

Cerebral circulation after head injury

1983 ◽  
Vol 59 (3) ◽  
pp. 439-446 ◽  
Author(s):  
Jørn Overgaard ◽  
William A. Tweed
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Head Injury ◽  
Neurological Outcome ◽  
Cerebral Perfusion ◽  
Boundary Zone ◽  
Content Type ◽  
Poor Neurological Outcome ◽  
Gcs Score ◽  
Fine Print

✓ A considerable body of evidence suggests that posttraumatic disturbances of the cerebral circulation contribute to poor neurological outcome after blunt head injury, especially when regional cerebral blood flow (rCBF) falls to the ischemic range (below 17 ml/100 gm/min). Cerebral infarction concentrated in the arterial boundary regions has been described in patients who died. Since arterial boundary zones are the cortical areas most susceptible to cerebral ischemia, the authors have investigated the relationship between neurological outcome and the anatomic pattern of rCBF values in the acute phase. The bolus-injection xenon-133 washout technique was used to measure rCBF in 35 regions of the hemisphere during the 1st week after head injury. Eighty-eight hemispheres were studied in 80 patients whose Glasgow Coma Scale (GCS) score was less than 8 on admission to the neurosurgical department. A characteristic pattern of rCBF was found in patients who later died of neurological complications, or who survived in a persistent vegetative state, with low flows in regions conforming to the arterial boundary zones. These patients also had lower average global cerebral blood flow (CBF), GCS scores, and cerebral perfusion pressure compared with those who recovered, with or without neurological deficits; the latter group had an rCBF pattern similar to that of normal individuals. There was little change in the GCS score between the time of hospital admission and CBF measurement, suggesting that the major neurological injury had occurred prior to admission. It was not possible to determine whether boundary-zone ischemia preceded neurological deterioration, but the rCBF pattern of boundary-zone flow deprivation was clearly related to poor neurological outcome. These observations suggest that elevated intracranial pressure and arterial hypotension were important etiological factors. Measures to protect regional cerebral perfusion should be instituted as early as possible after injury, preferably before the patient reaches the hospital.

Cerebral energy metabolism following fluid-percussion brain injury in cats

1988 ◽  
Vol 68 (4) ◽  
pp. 594-600 ◽  
Author(s):  
Andreas W. Unterberg ◽  
Bruce J. Andersen ◽  
Geoff D. Clarke ◽  
Anthony Marmarou
Keyword(s):  
Brain Injury ◽  
Energy Metabolism ◽  
Glucose Consumption ◽  
Tissue Ph ◽  
Content Type ◽  
Cerebral Energy Metabolism ◽  
Fluid Percussion ◽  
Metabolic Perturbation ◽  
Fine Print ◽  
Observation Period

✓ Clinical and experimental evidence suggests that head injury can cause alterations of cerebral energy metabolism. However, the etiology of this metabolic perturbation is not known. The objective of this study was to determine the effect of fluid-percussion trauma on cerebral energy metabolism. Seven ventilated, chloralose-anesthetized cats were subjected to a 3.2-atm fluid-percussion brain injury. Before and for 8 hours after trauma, continuous phosphorus-31 magnetic resonance spectrography was obtained to noninvasively monitor tissue pH, phosphocreatine (PCr), and inorganic phosphate (Pi) levels. Measurement of cerebral blood flow (CBF) by the radioactive microsphere technique and calculation of oxygen and glucose consumption (CMRO2 and CMRGl) were also performed before trauma as well as 30 minutes and 1,2,4, and 8 hours after trauma. The data showed a moderate decrease in tissue pH from 7.04 to 6.89 at 30 minutes following trauma with return to control levels by 3 hours posttrauma. During the 8-hour observation period, CBF, CMRO2, and CMRGl remained at control levels. Tissue PCr and Pi levels were also unchanged. Fluid-percussion trauma at the 3.2-atm level in ventilated cats causes a moderate and transient decrease in tissue pH that returns to control levels after trauma. No other metabolic changes are seen later than 30 minutes posttrauma. This indicates that a mild metabolic disturbance occurs after trauma in the ventilated animal and quickly returns to normal.

Cerebral blood flow as a predictor of outcome following traumatic brain injury

1997 ◽  
Vol 86 (4) ◽  
pp. 633-641 ◽  
Author(s):  
Daniel F. Kelly ◽  
Neil A. Martin ◽  
Rouzbeh Kordestani ◽  
George Counelis ◽  
David A. Hovda ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Head Injury ◽  
Intracranial Hypertension ◽  
Maximum Flow ◽  
Necessary Condition ◽  
Content Type ◽  
Group 3 ◽  
Severe Degree ◽  
Fine Print

✓ As part of a prospective study of the cerebrovascular effects of head injury, 54 moderate and severely injured patients underwent 184 133Xe—cerebral blood flow (CBF) studies to determine the relationship between the period of maximum blood flow and outcome. The lowest blood flows were observed on the day of injury (Day 0) and the highest CBFs were documented on postinjury Days 1 to 5. Patients were divided into three groups based on CBF values obtained during this period of maximum flow: Group 1 (seven patients), CBF less than 33 ml/100 g/minute on all determinations; Group 2 (13 patients), CBF both less than and greater than or equal to 33 ml/100 g/minute; and Group 3 (34 patients), CBF greater than or equal to 33 ml/100 g/minute on all measurements. For Groups 1, 2, and 3, mean CBF during Days 1 to 5 postinjury was 25.7 ± 4, 36.5 ± 4.2, and 49.4 ± 9.3 ml/100 g/minute, respectively, and PaCO2 at the time of the CBF study was 31.4 ± 6, 32.7 ± 2.9, and 33.4 ± 4.7 mm Hg, respectively. There were significant differences across Groups 1, 2, and 3 regarding mean age, percentage of individuals younger than 35 years of age (42.9%, 23.1%, and 76.5%, respectively), incidence of patients requiring evacuation of intradural hematomas (57.1%, 38.5%, and 17.6%, respectively) and incidence of abnormal pupils (57.1%, 61.5%, and 32.4%, respectively). Favorable neurological outcome at 6 months postinjury in Groups 1, 2, and 3 was 0%, 46.2%, and 58.8%, respectively (p < 0.05). Further analysis of patients in Group 3 revealed that of 14 with poor outcomes, six had one or more episodes of hyperemia-associated intracranial hypertension (simultaneous CBF > 55 ml/100 g/minute and ICP > 20 mm Hg). These six patients were unique in having the highest CBFs for postinjury Days 1 to 5 (mean 59.8 ml/100 g/minute) and the most severe degree of intracranial hypertension and reduced cerebral perfusion pressure (p < 0.0001). These results indicate that a phasic elevation in CBF acutely after head injury is a necessary condition for achieving functional recovery. It is postulated that for the majority of patients, this rise in blood flow results from an increase in metabolic demands in the setting of intact vasoreactivity. In a minority of individuals, however, the constellation of supranormal CBF, severe intracranial hypertension, and poor outcome indicates a state of grossly impaired vasoreactivity with uncoupling between blood flow and metabolism.

Effect of stable xenon inhalation on intracranial pressure during measurement of cerebral blood flow in head injury

1994 ◽  
Vol 81 (6) ◽  
pp. 822-828 ◽  
Author(s):  
Jan Plougmann ◽  
Jens Astrup ◽  
Jens Pedersen ◽  
Carsten Gyldensted
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Head Injury ◽  
Intracranial Pressure ◽  
Content Type ◽  
Head Injured ◽  
Stable Xenon ◽  
The Mean ◽  
Injured Patients ◽  
Fine Print

✓ Xenon-enhanced computerized tomography (CT) is well suited for measurements of cerebral blood flow (CBF) in head-injured patients. Previous studies indicated divergent results on whether inhalation of xenon may cause a clinically relevant increase in intracranial pressure (ICP). The authors employed Xe-enhanced CT/CBF measurements to study the effect of 20 minutes of inhalation of 33% xenon in oxygen on ICP, cerebral perfusion pressure (CPP), and arteriovenous oxygen difference (AVDO2) in 13 patients 3 days (mean 1 to 5 days) after severe head injury (Glasgow Coma Scale score ≤ 7). The patients were moderately hyperventilated (mean PaCO2 4.3 kPa or 32.3 mm Hg). Six patients were studied before and during additional hyperventilation. All 13 patients reacted with an increase in ICP and 11 with a decrease in CPP. The mean ICP increment was 6.9 ± 7.7 (range 2 to 17 mm Hg). The mean CPP decrement was −9.7 ± −14.6 (range 17 to 47 mm Hg). The time course of the ICP changes indicated that ICP increased rapidly during the first 5 to 6 minutes, then declined to a plateau (peak-plateau type in four of 13 patients), remained at a plateau (plateau type in six of 13), or continued to increase in three of 13, indicating individual variance in xenon reactivity. Additional hyperventilation had no effect on the xenon-induced increments in ICP but these occurred at lower ICP and higher CPP baseline levels. The AVDO2 values, an index of flow in relation to metabolism, indicated a complex effect of xenon on CBF as well as on metabolism. This study indicates that xenon inhalation for Xe-CT CBF measurements in head-injured patients according to our protocol causes clinically significant increments in ICP and decrements in CPP. It is suggested that the effect of xenon is analogous to anesthesia induction. Individual variations were observed indicating possible individual tolerance, possible influence of type and extent of the cerebral injury, disturbances in cerebrovascular reactivity, and possible influence of medication. These effects of xenon suggest that hyperventilation should be ensured in patients with evidence of reduced compliance or high ICP. On the other hand, inhalation of stable xenon is not believed to pose a risk because no signs of cerebral oligemia or ischemia were indicated in the AVDO2 values.

Hyperemia following traumatic brain injury: relationship to intracranial hypertension and outcome

1996 ◽  
Vol 85 (5) ◽  
pp. 762-771 ◽  
Author(s):  
Daniel F. Kelly ◽  
Rouzbeh K. Kordestani ◽  
Neil A. Martin ◽  
Tien Nguyen ◽  
David A. Hovda ◽  
...  
Keyword(s):  
Blood Flow ◽  
Head Injury ◽  
Intracranial Hypertension ◽  
Favorable Outcome ◽  
Suppressive Therapy ◽  
Metabolic Demand ◽  
Content Type ◽  
Therapeutic Implications ◽  
Gcs Score ◽  
Fine Print

✓ The role of posttraumatic hyperemia in the development of raised intracranial pressure (ICP) has important pathophysiological and therapeutic implications. To determine the relationship between hyperemia (cerebral blood flow (CBF) > 55 ml/100 g/minute), intracranial hypertension (ICP > 20 mm Hg), and neurological outcome, 193 simultaneous measurements of ICP and CBF (xenon-133 method) were obtained in 59 patients with moderate and severe head injury. Hyperemia was associated with an increased incidence of simultaneous intracranial hypertension compared to nonhyperemic CBF measurements (32.2% vs. 21.6%, respectively; p < 0.059). However, in 78% of blood flow studies in which ICP was greater than 20 mm Hg, CBF was less than or equal to 55 ml/100 g/minute. At least one episode of hyperemia was documented in 34% of patients, all of whom had a Glasgow Coma Scale (GCS) score of 9 or below. In 12 individuals with hyperemia without simultaneous intracranial hypertension, ICP was greater than 20 mm Hg for an average of 11 ± 16 hours and favorable outcomes were seen in 75% of patients. In contrast, in eight individuals with hyperemia and at least one episode of hyperemia-associated intracranial hypertension, ICP was greater than 20 mm Hg for an average of 148 ± 84 hours (p < 0.001), and a favorable outcome was seen in only one patient (p < 0.001). Compared to the remainder of the cohort, patients with hyperemia-associated intracranial hypertension were distinctive in being the youngest, exhibiting the lowest GCS scores (all ≤ 6), and having the highest incidence of effaced basilar cisterns and intractable intracranial hypertension. In the majority of individuals with hyperemia-associated intracranial hypertension, their clinical profile suggests the occurrence of a severe initial insult with resultant gross impairment of metabolic vasoreactivity and pressure autoregulation. In a minority of these patients, however, high CBF may be coupled to a hypermetabolic state, given their responsiveness to metabolic suppressive therapy. In patients with hyperemia but without intracranial hypertension, elevated CBF is also likely to be a manifestation of appropriate coupling to increased metabolic demand consistent with a generally favorable outcome. This study supports the concept that there are multiple etiologies of both elevated blood flow and intracranial hypertension after head injury.

Effect of posttraumatic hypoventilation on cerebral energy metabolism

1988 ◽  
Vol 68 (4) ◽  
pp. 601-607 ◽  
Author(s):  
Bruce J. Andersen ◽  
Andreas W. Unterberg ◽  
Geoff D. Clarke ◽  
Anthony Marmarou
Keyword(s):  
Energy Metabolism ◽  
Head Injury ◽  
Human Head ◽  
Realistic Model ◽  
Resonance Spectroscopy ◽  
Cerebral Tissue ◽  
Tissue Ph ◽  
Content Type ◽  
Cerebral Energy Metabolism ◽  
Fluid Percussion

✓ Cerebral energy metabolism was studied in cats subjected to fluid-percussion brain trauma followed immediately by 30 minutes of controlled hypoventilation for the purpose of simulating a more realistic model of human head injury. The cerebral blood flow (CBF) and cerebral metabolic rates of oxygen (CMRO2) and glucose (CMRGl) were measured, with simultaneous phosphorus-31 magnetic resonance spectroscopy quantifications of cerebral tissue pH, phosphocreatine (PCr), and inorganic phosphate (Pi). Hypoventilation alone did not produce marked changes in CMRGl, tissue pH, or PCr:Pi ratios. When hypoventilation was combined with trauma, marked alterations in CBF, CMRGl, PCr:Pi ratio, and tissue pH were seen, indicating relative ischemia. The alterations of cerebral energy metabolism produced by combining trauma and hypoventilation are more severe than those caused by fluid-percussion trauma alone, and may provide a more realistic model of human head injury.

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