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Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of long-term low- and high-dose ibuprofen on tumor growth and permeability were assessed in a glioma model in rats. The rats were treated with ibuprofen (24 mg/kg/day or 96 mg/kg/day) for 24 hours before implantation of C6 astrocytoma spheroids and then for 13 days following implantation. The wet and dry weight of the tumors and protein extravasation were measured by an Evans blue dye technique. Protein extravasation did not appear to be reduced by the treatments when assessed on the basis of tumor dry weight. The treatment significantly reduced the wet weight of the tumors in rats treated with high-dose and low-dose ibuprofen when compared to tumor wet weights in untreated rats. High-dose ibuprofen treatment significantly decreased the dry weight of the tumors compared to that of tumors in untreated control animals. It is hypothesized that the ibuprofen treatment regimen employed inhibits prostaglandin-associated angiogenesis induced by the C6 tumor cell growth and/or the implantation technique, thereby interfering with the ability of the tumors to grow.
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PMID:Effect of ibuprofen on tumor growth in the C6 spheroid implantation glioma model. 337 88

Cerebral edema produced by brain tumors is clinically and experimentally reduced by steroid therapy. Nonsteroid anti-inflammatory drugs (NSAID's) which have been used to treat non-neural inflammation and swelling have not been evaluated for their ability to affect edema produced by brain tumors. The authors have used the rat C6 glioma spheroid implantation model to compare the effects of two steroids (dexamethasone and methylprednisolone) and two NSAID's (ibuprofen and indomethacin) on protein extravasation caused by intracranial gliomas. Evans blue dye was used as a marker for serum albumin extravasation. The concentration of Evans blue dye was measured in the tumor and peritumoral and contralateral brain tissue 1 hour after intravenous injection. Extravasation of Evans blue dye within the tumor was decreased in all treatment groups when compared to placebo-injected control animals. The differences between the control specimens and those treated with dexamethasone, methylprednisolone, and indomethacin were highly significant (p less than 0.005). The Evans blue staining was also decreased in the peritumoral and contralateral brain. These results indicate that NSAID's compare favorably with steroids in diminishing tumor-induced protein extravasation. It is suggested that NSAID's may prove to be beneficial in clinical instances used either in conjunction with steroid therapy or alone when steroids are contraindicated.
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PMID:Effects of steroids and nonsteroid anti-inflammatory agents on vascular permeability in a rat glioma model. 372 82

The need for a large animal tumor model in experimental neuro-oncology led us to re-evaluate and to modify the transplantable canine glioma of Wodinsky and Walker. Successive passages of the original tumor brei were made in purebred beagles, from beagle to mongrel, and between various mongrel strains until an intracerebral injection of 0.1 cc on Days 1 to 3 of life produced a 93% incidence of tumor take in all breeds. The mean survival was 13.5 +/- 1.9 days after injection (range, 10 to 19 days) in 10 litters. The tumor was invariably fatal and possessed many of the histological characteristics of human glioblastoma (i.e., capillary proliferation, pseudopallisading, frequent mitotic figures, and multinucleated giant cells). The animals were large enough to be scanned on the Pfizer 450 scanner, and the tumors were visualized in vivo as typical "ring" lesions after the injection of contrast agent. Intravital staining with Evans blue outlined the areas of contrast enhancement observed in the same tumors by computed tomography. The apparent defect in the blood-brain barrier could be explained in part by the absence of endothelial tight junctions on electron microscopy. Stability in the histology and activity of the tumor could be demonstrated after more than 14 months of storage at -70 degrees C. The transplantable canine glioma model has many advantages including low cost, reproducible morphology, a short survival time, and relative safety for the investigator. The large size of the animal preparation allows the use of complex surgical instrumentation and radiographic study, as well as repeated sampling of cerebrospinal and other fluids.
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PMID:Transplantable canine glioma model for use in experimental neuro-oncology. 629 Sep 29

A model was developed for in vivo study of the human glioma-derived D-54 MG cell line in the brains of immunosuppressed Fischer 344 rats. The rats were injected with horse anti-rat thymocyte serum before and after intracerebral inoculation with 5 or 10 microliters of a D-54 MG tumor cell suspension. Reproducible mortality distributions were obtained, with deaths occurring 18 to 34 days after intracerebral inoculation. Tumors grew as well circumscribed intracerebral masses with sheets of anaplastic cells, areas of necrosis bordered by concentrated nuclei, and minimal lymphocytic infiltration. Cytogenetic analysis revealed the same general chromosome distribution and markers in the heterotransplanted glioma cells as in the cultured line. Blood-brain barrier disruption was demonstrated by intracerebral tumor staining after intravenous injection of Evans blue dye. The in vivo growth of D-54 MG in immunosuppressed rats provides a reliable experimental model for the study of chemotherapy, immunodiagnosis, and immunotherapy of a human glioma-derived tumor in an animal sufficiently large to evaluate intracarotid or intratumoral injection of therapeutic agents.
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PMID:Intracerebral transplantation of a human glioma line in immunosuppressed rats. 669 2

The tumorigenicity of neonatally administered N-ethyl-N-nitrosourea (ENU) was studied in four different inbred strain rats, that is Wistar/Furth (WF), Long-Evans (LE), F1 of Wistar/Furth and Long-Evans (F1) and Fischer 344 (F344) rats. All strains developed tumors of the nervous system with high incidence (97-100%) during 6 months of observation. The incidence of tumor of the central nervous system, including the brain (82-88%) and the spinal cord (53-76%), was high in all strains, but that of the peripheral nervous system, including the cranial nerve (21-89%) and the spinal root (13-93%), differed by strain. The peripheral nervous system of WF and F344 rats had a low susceptibility to the tumorigenic effect of ENU, but that of LE rats had a high susceptibility. Many brain tumors were induced in the temporal and frontal cortex and subcortex in all strains of rats. Spinal cord tumors were observed at all levels of the white matter of the spinal cord without any predilection site. Spinal root tumors were located in lumbosacral plexuses in WF and F344 rats, but in LE and F1 rats cervical and thoracic root tumors were also observed. Histological examination revealed that most of the brain and spinal cord tumors were oligodendroglioma, but in F344 rats about half of the brain tumors were mixed glioma. Epidermoid cysts of the lumbar spinal cord were observed only in F344 rats. Tumors of the peripheral nervous system were so-called anaplastic schwannoma.
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PMID:Strain differences of tumorigenic effect of neonatally administered N-ethyl-N-nitrosourea in rats. 711 58

Experimental brain tumours were produced in cats by stereotactic implantation of 4 million suspended cells of a rat glioma clone into the internal capsule. Three weeks after implantation a spherical tumour developed with a diameter of up to 10 mm which was surrounded by vasogenic white matter oedema. In untreated animals water content in the peritumoural white matter increased form 69.1 +/- 0.9 to 80.0 +/0 0.8 ml/100 g w. w., and regional blood flow reciprocally decreased from 32.2 +/- 5.6 to 18.9 +/- 0.05 ml/100 g/min. A single injection of a crystalline suspension of 10 mg/kg dexamethasone given intramuscularly one week before the animals were killed, led to a significant amelioration of brain oedema. Peritumoural white matter water content decreased to 73.0 +/- 0.5 ml/100 g w w. and blood flow rose to 35.7 +/- 2.8 ml/100 g/min. These changes were accompanied by parallel shifts of electrolyte content buy did not correlate with EEG activity, as assessed by Fourier frequency analysis. Corticosteroids did not prevent extravasation of peroxidase or Evans blue across the tumour vessels. The beneficial effect, therefore, is attributed to either an acceleration of resorption or an inhibition of the spread of oedema from tumour into the peritumoural brain tissue.
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PMID:Corticosteroid therapy of experimental tumour oedema. 732 60

To clarify the altered response of calcium antagonists on pathological vessels, we investigated the effect of intracarotid infusion of nifedipine on the blood-brain barrier (BBB) permeability using a rat glioma model. Animals were treated with 0, 0.1, 1, 5, and 10 micrograms/kg/min of intracarotid continuous infusion of nifedipine. 2% Evans blue (EB, 2 ml/kg) was injected intravenously immediately after nifedipine infusion. BBB and blood-tumor barrier (BTB) permeability were evaluated by direct visual and histological observation. During the entire experiment, systemic parameters such as arterial blood pressure and blood analysis were not changed significantly. There was a dose-dependent increase of EB permeability selectively in the tumor tissue without affecting the normal brain. These results indicate that tumor vessels may show an altered response to calcium antagonists. Intracarotid administration of calcium antagonists contribute to a selective enhancement of drug delivery to malignant brain tumors without affecting the normal brain.
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PMID:Selective increase in blood-tumor barrier permeability by calcium antagonists in transplanted rat brain tumors. 752 26

Histamine will alter blood flow and permeability in systemic and cerebral vessels. We reported that intracarotid infusion of histamine selectively increased the blood flow in experimental brain tumours and caused extravassation of Evans blue within tumours. In this study, the effects of histamine on tumour and brain capillary permeability were quantified using autoradiography. RG2 glioma cells were implanted in female Wistar rats. Seven days after implantation, either low doses of histamine (1 or 10 micrograms kg-1 min-1) or saline as a control was infused through the carotid artery of rats. Regional permeability was measured by autoradiography using [14C] aminoisobutyric acid, and the unidirectional transfer constant, Ki (microliters g-1 min-1), was calculated. Intracarotid infusion of 10 micrograms kg-1 min-1 histamine resulted in significant increase in brain tumour permeability, compared to controls. The permeability, Ki, for the 10 micrograms kg-1 min-1 histamine group, the 1 micrograms kg-1 min-1 histamine group, and the control group was 18.8 +/- 4.6 (p < 0.05), 14.9 +/- 5.2, 13.9 +/- 3.7 microliters g-1 min-1, respectively. There was no significant change in blood brain permeability in other brain regions. The effect of increased permeability by 10 micrograms kg-1 min-1 histamine was suppressed by the H2-blocker, cimetidine. This suggests that the effect of histamine on tumour capillaries is mediated by H2-receptors. Intracarotid histamine infusion selectively increases permeability in brain tumours.
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PMID:Intracarotid histamine infusion increases blood tumour permeability in RG2 glioma. 791 97

We studied the effect of intracarotid administration of histamine on the blood-tumor barrier permeability and also on the blood-brain barrier permeability in transplanted rat C6 glioma. There was no definite Evans blue (EB) extravasation either in normal or tumor tissue after intracarotid saline infusion. In contrast, histamine at doses of 1 and 10 micrograms/kg/min produced slight to moderate EB extravasation in the tumor without any significant extravasation in the normal brain tissue. Intravenously administered H1 and H2 receptor antagonists (5 mg/kg each) reduced the histamine (10 micrograms/kg/min) induced extravasation of EB in the tumor tissue. These results indicated that brain tumor vessels responded to histamine in a different fashion from normal brain capillaries. Histamine could thus be utilized for selective drug delivery to brain tumors without affecting normal brain tissue.
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PMID:Effect of histamine on the blood-tumor barrier in transplanted rat brain tumors. 797 2

Both horseradish peroxidase (HRP) and Evans blue dye (EBD) have been used previously to characterize the status of the blood-brain barrier (BBB) within brain tissue transplants and host brain tissue. We investigated the possibility that a differential permeability of the vasculature to these two markers can account for discrepancies in the literature concerning the presence of an intact BBB within the grafted tissues. Intravascular injection of both HRP and EBD was used to evaluate the status of the BBB within intracerebral tissue transplants. Simultaneous injection of HRP and EBD in rats with adrenal medulla transplants or C-6 glioma tumors demonstrated a lack of a BBB within these grafts. Both markers produced consistent results within each tissue type, although HRP was generally a more sensitive marker. In contrast to the lack of a BBB in the C-6 gliomas or adrenal medulla transplants, 1-week-old fetal striatal transplants had a BBB essentially intact to both HRP and EBD. Any reported discrepancies in the characterization of the BBB are not likely due to differences between the properties of HRP or EBD. Fetal striatal transplants appear to have an intact BBB at 1 week following transplantation.
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PMID:Permeability of the blood-brain barrier within rat intrastriatal transplants assessed by simultaneous systemic injection of horseradish peroxidase and Evans blue dye. 803 64


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