A simple gravimetric technique for measurement of cerebral edema

Marmarou, Anthony; Pöll, W.; Shulman, Kenneth I.; Bhagavan, H. N.

doi:10.3171/jns.1978.49.4.0530

Cited by 261 publications

(109 citation statements)

References 6 publications

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“…Water content of each specimen was measured gravimetrically using a density gradient of bromobenzene-kerosene precalibrated with K 2 SO 4 as previously described. 20 The cortical samples were placed into the fluid column, and the equilibration point was measured within 2 minutes. The specific gravity of the tissue was calculated and results were expressed as percentage of water content.…”

Section: Methodsmentioning

confidence: 99%

Mild hypothermia delays the onset of coma and prevents brain edema and extracellular brain glutamate accumulation in rats with acute liver failure

et al. 2000

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Mild hypothermia is effective in the prevention of brain edema associated with cerebral ischemia and traumatic brain injury. Brain edema is also a serious complication of acute liver failure (ALF). To assess the effectiveness of hypothermia in ALF, groups of rats were subjected to hepatic devascularization (portacaval anastomosis, followed 48 hours later by hepatic artery ligation), and body temperatures were maintained at either 35ЊC (hypothermic) or 37ЊC (normothermic). A major cause of death in patients with acute liver failure (ALF) is brain herniation resulting from raised intracranial pressure caused by a progressive increase in brain water content. 1 It has been estimated that up to 40% of patients with ALF die while on the waiting list for liver transplantation, 2 in whom, in almost all cases, death results from brain herniation. Despite several decades of investigation, the pathophysiological mechanisms responsible for the central nervous system consequences of ALF have not been fully elucidated. However, ammonia remains a prime candidate. Hyperammonemia is a consistent finding in experimental animal models of ALF resulting from hepatectomy, 3 hepatic devascularization, 4,5 or toxic liver injury 6 , and, in these cases, brain edema is invariably observed. In ALF, brain ammonia may reach millimolar concentrations, 7 and exposure of various in vitro brain preparations to millimolar concentrations of ammonia results in significant cell swelling. 8,9 Hyperammonemia is a feature of Reye' s Syndrome 10 and congenital urea cycle enzymopathies, 11 conditions in which cerebral edema is also consistently observed.Previous studies showed that hypothermia extended the survival time and prevented the development of brain edema in rats with ALF. 12 Furthermore, mild hypothermia (33°C-35°C) has been shown to be neuroprotective in experimental models of traumatic 13 and ischemic brain injury. 14 In the case of the latter, it was suggested that the beneficial effects of hypothermia were the result of inhibition of the release of neurotransmitters, rather than of an effect on cerebral energy metabolism. 15 The goals of the present investigation, therefore, were to study the effect of hypothermia on the development of hepatic encephalopathy and brain edema in relation to blood and cerebrospinal fluid (CSF) ammonia levels, and to extracellular glutamate and glutamine concentrations in rats with ALF caused by hepatic devascularization. MATERIALS AND METHODSO-phthaldialaldehyde reagent solution, 2-mercaptoethanol, Trisacetate, Ringer' s solution constituents, and amino acid standards were purchased from Sigma Chemical Co. (St. Louis, MO). Sodium phosphate (monobasic), methanol (high-performance liquid chromatography [HPLC]-grade), and tetrahydrofuran (HPLC-grade) were obtained from Anachemia (Montreal, Quebec, Canada). Doubledistilled deionized water was used for preparation of standard amino acid solutions and buffers. The mobile phase used for HPLC was filtered through 0.45-mm-pore-size membrane filters (Millipore Corp., B...

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Section: Methodsmentioning

confidence: 99%

Mild hypothermia delays the onset of coma and prevents brain edema and extracellular brain glutamate accumulation in rats with acute liver failure

et al. 2000

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“…Water content of the brain (percentage) was measured gravimetrically using a density gradient of bromobenzenekerosene precalibrated with K2SO4 as previously described [18]. Eight measurements were made per animal, and values were arithmetically averaged.…”

Section: Brain Water Measurementmentioning

confidence: 99%

Selective alterations of brain osmolytes in acute liver failure: protective effect of mild hypothermia

et al. 2004

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Zwingmann, C. et al., 2004. Selective alterations of brain osmolytes in acute liver failure: protective effect of mild hypothermia. Brain Research, 999(1), ABSTRACTThe principal cause of mortality in patients with acute liver failure (ALF) is brain herniation resulting from intracranial hypertension caused by a progressive increase of brain water. In the present study, ex vivo highresolution 1 H-NMR spectroscopy was used to investigate the effects of ALF, with or without superimposed hypothermia, on brain organic osmolyte concentrations in relation to the severity of encephalopathy and brain edema in rats with ALF due to hepatic devascularization. In normothermic ALF rats, glutamine concentrations in frontal cortex increased more than fourfold at precoma stages, i.e. prior to the onset of severe encephalopathy, but showed no further increase at coma stages. In parallel with glutamine accumulation, the brain organic osmolytes myo-inositol and taurine were significantly decreased in frontal cortex to 63% and 67% of control values, respectively, at precoma stages (p<0.01), and to 58% and 67%, respectively, at coma stages of encephalopathy (p<0.01). Hypothermia, which prevented brain edema and encephalopathy in ALF rats, significantly attenuated the depletion of myo-inositol and taurine. Brain glutamine concentrations, on the other hand, did not respond to hypothermia. These findings demonstrate that experimental ALF results in selective changes in brain organic osmolytes as a function of the degree of encephalopathy which are associated with brain edema, and provides a further rationale for the continued use of hypothermia in the management of this condition.

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“…Tissue specific gravity of the two hemispheres was measured on 40-to 50-mg samples taken from the injured zone and from the contralateral hemisphere by linear gra dient columns using a kerosene and bromobenzene mix ture, as described by Nelson et al (1971) and improved by Marmarou et al (1978) …”

Section: Specific Gravity Determinationmentioning

confidence: 99%

Head Injury Induces Increased Prostaglandin Synthesis in Rat Brain

Shohami

Shapira

Sidi

et al. 1987

J Cereb Blood Flow Metab

123

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Summary: Head injury was induced in the left hemi sphere of rats, The rats were killed at various time in tervals after trauma (immediately, 15 min, 1 and 18 h, and 4 and 10 days), and the rates of synthesis and release of prostaglandin PGE2, 6-keto-PGF I", and thromboxane TXB2 from cortical slices of both hemispheres were studied. The rate of synthesis of PGE2 after 18 h was six and four times higher than control in the contused and contralateral hemispheres, respectively. By 10 days post trauma, both hemispheres had normal rate of PGE2 re lease. TXB2 and 6-keto-PGFI" synthetases were affected already 15 min after the injury, and a similarly elevated rate of synthesis was found in both hemispheres. The maximal effect was detected after 1 or 18 h with return to

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A simple gravimetric technique for measurement of cerebral edema

Cited by 261 publications

References 6 publications

Mild hypothermia delays the onset of coma and prevents brain edema and extracellular brain glutamate accumulation in rats with acute liver failure

Mild hypothermia delays the onset of coma and prevents brain edema and extracellular brain glutamate accumulation in rats with acute liver failure

Selective alterations of brain osmolytes in acute liver failure: protective effect of mild hypothermia

Head Injury Induces Increased Prostaglandin Synthesis in Rat Brain

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