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.

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.

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.

A fluid percussion model of experimental brain injury in the rat

1987 ◽  
Vol 67 (1) ◽  
pp. 110-119 ◽  
Author(s):  
C. Edward Dixon ◽  
Bruce G. Lyeth ◽  
John T. Povlishock ◽  
Robert L. Findling ◽  
Robert J. Hamm ◽  
...  
Keyword(s):  
Brain Injury ◽  
Head Injury ◽  
Human Head ◽  
Systemic Hypertension ◽  
Content Type ◽  
Glucose Levels ◽  
Fluid Percussion ◽  
Fluid Percussion Injury ◽  
Locomotor Deficits ◽  
Necrotic Change

✓ Fluid percussion models produce brain injury by rapidly injecting fluid volumes into the cranial cavity. The authors have systematically examined the effects of varying magnitudes of fluid percussion injury in the rat on neurological, systemic physiological, and histopathological changes. Acute neurological experiments showed that fluid percussion injury in 53 rats produced either irreversible apnea and death or transient apnea (lasting 54 seconds or less) and reversible suppression of postural and nonpostural function (lasting 60 minutes or less). As the magnitude if injury increased, the mortality rate and the duration of suppression of somatomotor reflexes increased. Unlike other rat models in which concussive brain injury is produced by impact, convulsions were observed in only 13% of survivors. Transient apnea was probably not associated with a significant hypoxic insult to animals that survived. Ten rats that sustained a moderate magnitude of injury (2.9 atm) exhibited chronic locomotor deficits that persisted for 4 to 8 days. Systemic physiological experiments in 20 rats demonstrated that all levels of injury studied produced acute systemic hypertension, bradycardia, and increased plasma glucose levels. Hypertension with subsequent hypotension resulted from higher magnitudes of injury. The durations of hypertension and suppression of amplitude on electroencephalography were related to the magnitudes of injury. While low levels of injury produced no significant histopathological alterations, higher magnitudes produced subarachnoid and intraparenchymal hemorrhage and, with increasing survival, necrotic change and cavitation. These data demonstrate that fluid percussion injury in the rat reproduces many of the features of head injury observed in other models and species. Thus, this animal model could represent a useful experimental approach to studies of pathological changes similar to those seen in human head injury.

Regional metabolism in experimental brain tumors in cats: relationship with acid/base, water, and electrolyte homeostasis

1992 ◽  
Vol 77 (6) ◽  
pp. 917-926 ◽  
Author(s):  
Yoshikazu Okada ◽  
Otmar Kloiber ◽  
Konstantin A. Hossmann
Keyword(s):  
Brain Tumors ◽  
Tumor Tissue ◽  
Atp Depletion ◽  
Resonance Spectroscopy ◽  
Peritumoral Edema ◽  
Metabolic Pattern ◽  
Tissue Ph ◽  
Content Type ◽  
Experimental Brain Tumors ◽  
Fine Print

✓ Experimental brain tumors were produced in cats by xenotransplantation of the rat glioma clone F98 into the white matter of the left hemisphere. One to 4 weeks after implantation, local adenosine triphosphate (ATP), glucose, lactate, and tissue pH were measured via imaging techniques in cryostat sections passing through the center of the tumor and correlated with changes in water and electrolyte content. The tumors exhibited a heterogeneous metabolic pattern, with a tendency for ATP to decrease and lactate to increase during tumor development. Tissue pH was above 7.5 in tumors with high ATP content but it sharply declined at low ATP levels. In peritumoral edema, ATP also decreased and lactate increased but, in contrast to tumor tissue, pH became more alkaline. Metabolic changes were associated with edema formation, as evidenced by the rise in water and sodium content. There was a distinct difference between tumor tissue and peritumoral edema: in tumor tissue, pH declined with increasing water content, whereas in peritumoral edema it increased. These observations are interpreted as follows: 1) in tumor tissue, “lactacidosis” and ATP depletion are attributed to disturbances in blood flow, resulting in metabolic failure and the intracellular “cytotoxic” accumulation of water; 2) in peritumoral edema, “lactalkalosis” is the result of an efflux of (alkaline) lactate salts from the tumor into the expanded extracellular compartment, and the decrease in ATP is the volumetric effect of extracellular “vasogenic” edema fluid and not the result of cellular energy failure. These findings are of importance for the interpretation of volume-selective magnetic resonance spectroscopy and may contribute to the establishment of spectroscopic criteria for the evaluation of therapeutical interventions.

Loss of forebrain cholinergic neurons following fluid-percussion injury: implications for cognitive impairment in closed head injury

1995 ◽  
Vol 83 (3) ◽  
pp. 496-502 ◽  
Author(s):  
Richard H. Schmidt ◽  
M. Sean Grady
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Head Injury ◽  
Cholinergic Neurons ◽  
Nucleus Basalis ◽  
Neuron Loss ◽  
Content Type ◽  
Fluid Percussion ◽  
Concussive Injury ◽  
Fine Print

✓ Disturbances in memory, concentration, and problem solving are common after even mild to moderate traumatic brain injury. Because these functions are mediated in part by forebrain cholinergic and catecholaminergic innervation, in this study the authors sought to determine if experimental concussive injury produces detectable morphological damage to these systems. Fluid-percussion head injury, sufficient to cause a 13- to 14-minute loss of righting reflex, was produced in rats that had been anesthetized with halothane. Injury was delivered either at midline or 2 mm off midline and compared with appropriate sham-injured controls. After 11 to 15 days, the rat brains were stained in serial sections for choline acetyltransferase, tyrosine hydroxylase, dopamine β-hydroxylase, acetylcholinesterase, and nicotinamide adenine dinucleotide phosphate diaphorase. Cell counts were determined for the entire population of ventrobasal forebrain cholinergic cells. Midline injury produced a bilateral loss of cholinergic neurons averaging 36% in area Ch1 (medial septal nucleus), 45% in Ch2 (nucleus of the diagonal band of Broca), and 41% in Ch4 (nucleus basalis of Meynart), (p ≤ 0.05). Lateralized injury resulted in cholinergic neuron loss of similar magnitude ipsilaterally (p ≤ 0.05), but a smaller contralateral loss of between 11% and 28%. No loss of neurons was detected in the pontomesencephalic cholinergic groups Ch5 and Ch6. There was no visible effect of head injury on forebrain dopamine or noradrenergic innervation. A significant and apparently selective loss of ventrobasal forebrain cholinergic neurons following brief concussive injury in rats is demonstrated in this study. This type of injury is known to produce significant disturbance in cognitive tasks linked to neocortical and hippocampal cholinergic function. It remains to be determined how this neuron loss occurs, whether it can be prevented with neuroprotective agents, how it affects innervation in target tissues, and whether it occurs in human victims of traumatic brain injury.

Acid-base balance and arterial and CSF lactate levels following human head injury

1974 ◽  
Vol 40 (5) ◽  
pp. 617-625 ◽  
Author(s):  
Lionel R. King ◽  
Robert L. McLaurin ◽  
Harvey C. Knowles
Keyword(s):  
Metabolic Acidosis ◽  
Head Injury ◽  
Human Head ◽  
Respiratory Alkalosis ◽  
Acid Base Balance ◽  
Acid Base ◽  
Content Type ◽  
Base Balance ◽  
Csf Lactate ◽  
Lactate Levels

✓ Sequential arterial and cerebrospinal fluid (CSF) lactate, pH, pCO2, HCO3−, and pO2 levels were determined for 4 days in 17 patients immediately following uncomplicated head injury. Lactate was initially markedly elevated in both fluids and decreased by the third day after injury. There was mild arterial metabolic acidosis and respiratory alkalosis on admission; the alkalosis continued. Arterial pO2 was below normal at all times. The CSF showed a normal pO2, and metabolic acidosis related to lactate accumulation. Blood and CSF pCO2 and HCO3− levels equilibrated well, probably because of the time factor; CSF and arterial pO2 levels were not significantly related. The clinical implications of CSF lacticacidosis after head injury are discussed.

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