The entry of glycerol into brain tissue

Waterhouse, John; Coxon, R. V.

doi:10.1016/0022-510x(70)90157-7

Cited by 37 publications

(17 citation statements)

References 9 publications

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“…(Figure 1). The mean_+STD, the white matter:serum glycerol ratio (0.30+_0.31) and the grey matter:serum glycerol ratio (0.33_+0.29) were similar to those found by Waterhouse and Coxon [15] in healthy rabbits 7 h after continuous glycerol infusion (mean = 0.42).…”

Section: Glycerol Kineticssupporting

confidence: 84%

“…Glycerol entered the CSF more readily in infected animals than in healthy animals as previously reported by Waterhouse and Coxon [15]. In contrast, glycerol brain tissue:serum ratios in animals suffering from meningitis were almost equal to those in non-meningitic animals [15]. This implies that (a) despite a pronounced disturbance of the blood CSF barrier the blood brain barrier appears less affected in early bacterial meningitis, and (b) the long diffusional distances and the bulk flow of the interstitial fluid of the brain tissue towards the subarachnoid space prevents equilibration between brain tissue and CSF.…”

Section: Discussionsupporting

confidence: 64%

“…To minimize interfering variables, infected animals were not treated with an antibiotic agent. Glycerol entered the CSF more readily in infected animals than in healthy animals as previously reported by Waterhouse and Coxon [15]. In contrast, glycerol brain tissue:serum ratios in animals suffering from meningitis were almost equal to those in non-meningitic animals [15].…”

Section: Discussionsupporting

confidence: 57%

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Glycerol does not reduce neuronal damage in experimental Streptococcus pneumoniae meningitis in rabbits

et al. 1998

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To study the effect of high-dose glycerol therapy on inflammation and neuronal destruction in a model of experimental pneumococcal meningitis, 14 New Zealand White rabbits were infected intracisternally with Streptococcus pneumoniae type 3. Sixteen hours after infection, 7 animals received intravenous glycerol therapy (1 g kg(-1) bolus and 0.5 g kg (1)h(-1) maintenance dose) and 7 animals served as untreated controls.After 8 h of therapy, the glycerol CSF:serum ratio exceeded the previously observed values in rabbits with an intact blood-CSF barrier (0.72+/-0.25 vs. 0.35), i.e. glycerol crossed the blood-CSF barrier more readily in animals altered by meningitis than in healthy animals. In contrast, the brain tissue:serum ratio of glycerol (grey matter 0.33+/-0.29, white matter 0.30+/-0.31) was substantially lower than the CSF:serum ratio (p=0.03 and p=0.047). There was no significant effect of glycerol on intracranial pressure, brain water content and neuron-specific enolase release into the CSF. Glycerol significantly increased the density of neuronal apoptosis in the dentate gyrus of the hippocampal formation. Therefore, glycerol does not appear to be beneficial in experimental pneumococcal meningitis.

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Section: Glycerol Kineticssupporting

confidence: 84%

Section: Discussionsupporting

confidence: 64%

Section: Discussionsupporting

confidence: 57%

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Glycerol does not reduce neuronal damage in experimental Streptococcus pneumoniae meningitis in rabbits

et al. 1998

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“…However, animal experiments suggest that glycerol readily enters even intact brain tissue. 4 Other than a potential adverse rebound effect, glycerol may also be beneficial for ischemic brain tissue: first, by offering an alternative source of energy for neuronal tissue which can metabolize glycerol if glucose is lacking 5 ; second, by redistribution of cerebral blood flow with increase in regional cerebral blood flow and regional cerebral blood volume in ischemic brain secondary to reduction in focal cerebral edema, 6 though no reduction of healthy brain volume was observed in MRI studies 7 ; and third, glycerol may modulate the leukocyte-endothelium interaction by preventing leukocytes from interfering with the blood cell and plasma flow, thus improving cerebral blood flow. 8 In conclusion, glycerol can reduce ICP in stroke patients though its main mechanism does not consist of creating a sustained osmotic gradient.…”

Section: Discussionmentioning

confidence: 99%

Neurochemical Monitoring of Glycerol Therapy in Patients With Ischemic Brain Edema

Berger

Sakowitz

Kiening

et al. 2005

Stroke

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Background and Purpose-Osmotic agents such as glycerol are used to treat brain edema in stroke patients. We investigated the pharmacokinetics of glycerol in brain tissue by cerebral microdialysis. Methods-Patients experiencing large middle cerebral artery infarction were included in this prospective study. O smotic agents are used in acute cerebral ischemia to treat brain edema, particularly in space-occupying stroke where the mass effect may cause further clinical deterioration. Other than mannitol, glycerol is commonly used to treat increased intracranial pressure (ICP). 1 However, a potential rebound effect with increasing ICP following glycerol administration may restrict its use in treating brain edema.We studied the pharmacokinetics of glycerol in brain tissue using cerebral microdialysis in patients requiring ICP treatment with intravenous glycerol. Additionally, we investigated potential effects of glycerol therapy on glutamate, lactate, and pyruvate concentration in cerebral microdialysate. We administered glycerol if standard therapy with 15 g mannitol had only insufficient effects and either spontaneous ICP increase Ͼ20 mm Hg persisted Ͼ10 minutes or pupillary functions were disturbed. Then 25 g of glycerol (250 mL 10% Glycerosteril, Fresenius Kabi) were infused through a central venous catheter over 15 minutes. The following variables were assessed before and every 10 minutes until 80 minutes after drug application: ICP and serum osmolarity and microdialysate concentrations of glycerol, glutamate, pyruvate, and lactate, which were analyzed enzyme-photometrically (CMA 600 Autoanalyser). To account for varying baseline values of glycerol, ICP, and osmolarity, we calculated relative changes at all subsequent time points. Patients and MethodsWe used the Wilcoxon signed rank test to detect differences between each time point and baseline values. Statistical analyses were performed with StatView statistical software. A PϽ0.05 was considered statistically significant. Data are presented as meanϮSEM. ResultsA total of 16 episodes with ICP crises in 7 patients (3 female, 4 male) experiencing large middle cerebral artery infarction were included in this study. Their mean age was 51.7 with a range between 35 and 65 years.Cerebral glycerol concentrations rose immediately after intravenous glycerol administration from 73.9Ϯ17.0 mol/L by a maximum of 350% within 20 minutes. Subsequently, glycerol decreased gradually to a nonsignificantly different level at 60 minutes after the infusion had ended. Conversely, ICP (baseline 25Ϯ2.4 mm Hg) rapidly decreased by almost 50% and remained significantly lower for 50 minutes with a short rebound at 40 minutes. In contrast, serum osmolarity (baseline 305Ϯ5.6 mOsm/L) increased only briefly by Ϸ3% (Figure 1).

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“…Of the two immediate products of lipolysis (FFA and glycerol), glycerol seemed the more attractive because although its rate of transport across the blood-brain barrier appears to be quite limited (3), evidence has been presented for its metabolism by the brain (4-6), and because its entry into metabolic pathways depends upon glycerol kinase, an enzyme not widely distributed ( 7 ) . Therefore, the finding of increased activity of this enzyme in a potential control site would suggest that glycerol could act as a metabolic signal.…”

mentioning

confidence: 99%

The Metabolism of Glycerol by Hypothalamic and Pituitary Tissues in Vitro in the Rat

Goodner

Ogilvie

Koerker

1973

Experimental Biology and Medicine

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Specific chemical signals for hypothalamic regulation of appetite, and other metabolic events have been difficult to identlify in vivo.Evidence for glucoreceptors is most convincing, but lipid, amino acid, hormonal and temperature receptors have also been postulated (1). On the premise that chemoreceptor function might be reflected in the metabolic pathways of the neurons in the receptor area, we have undertaken a search for biochemical differences between areas within the hypothalamus and other parts of the central nervous system.Because some evidence suggests the participation of a signal from adipose tissue in long-term regulation of appetite (2) (the lipostatic theory), we have examined the possibility that free glycerol might be such a signal. Of the two immediate products of lipolysis (FFA and glycerol), glycerol seemed the more attractive because although its rate of transport across the blood-brain barrier appears to be quite limited (3), evidence has been presented for its metabolism by the brain (4-6), and because its entry into metabolic pathways depends upon glycerol kinase, an enzyme not widely distributed ( 7 ) . Therefore, the finding of increased activity of this enzyme in a potential control site would suggest that glycerol could act as a metabolic signal.Methods. Tissues for incubation with glycerol in vitro were obtained from female rats weighing 180-200 g, sacrificed by decapitation after an 18-hr fast. The brain, anterior This investigation was supported by Research Grant 1 R 0 1 AM10866 land Training Grant 2. 4 5331 03 from the National Institute of Arthritis and Metabolic Diseases, National Institutes of Health.pituitary (AP); and other tissues were quickly removed and placed in iced buffer solution. The chilled brain was placed on its cortical surface and sliced into four 0.5 mm frontal sections between the landmarks of the optic chiasm (anteriorly) and the anterior margin of the pons (posteriorly). These sections were laid flat on a chilled plastic plate in cold buffer, Krebs Ringer phosphate (KR P ) , and further dissected into specific segments with fine scissors under a 2 0 x dissecting microscope. The margins used to define hypothalamus were the lateral sulcus between the hypothalamus and the cortex and the superior limit of the third ventricle. The margin between cortical grey and white tissue was easily identified at 20x magnification. The tissue segments were weighed to the nearest 0.1 mg on a torsion balance and minced into uniformly sized fragments using fine scissors. The tissue fragments were quantitatively transferred to micro-incubation vessels (8). Fragments were prepared to be about 0.5 mm in greatest thickness. Control tissues such as liver, kidney, and muscle were similarly minced.Incubations and analyses were done as previously described (9). The medium volume was 0.50 ml. The buffer was KRP (pH 7.4) containing 1 .O mg/ml glucose, glycerol-1,3-14C a t a final concentration of 3.0 pCi/ml and 0.3 pmole/ml. The sealed flasks were incubated for 1 to 2 hr in room air at 37". ...

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The entry of glycerol into brain tissue

Cited by 37 publications

References 9 publications

Glycerol does not reduce neuronal damage in experimental Streptococcus pneumoniae meningitis in rabbits

Glycerol does not reduce neuronal damage in experimental Streptococcus pneumoniae meningitis in rabbits

Neurochemical Monitoring of Glycerol Therapy in Patients With Ischemic Brain Edema

The Metabolism of Glycerol by Hypothalamic and Pituitary Tissues in Vitro in the Rat

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