{"title":"Excitatory amino acid release from contused brain tissue into surrounding brain areas.","authors":"H Tanaka, Y Katayama, T Kawamata, T Tsubokawa","doi":"10.1007/978-3-7091-9334-1_144","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_144","url":null,"abstract":"<p><p>The EAA release from contused brain tissue and its effect on the extracellular EAA levels in brain areas surrounding the contusion were investigated with microdialysis technique in the rat. A significant increase in extracellular EAA levels was observed in the contused brain tissue. The EAA increase was significantly greater in the contused brain tissue than in the isolated but non-contused brain tissue. It was further demonstrated that EAAs were released from non-contused brain areas 1-2 mm distant from contused brain tissue. No such EAA release from surrounding brain areas was demonstrated when the cavity was filled with isolated but non-contused brain tissue. The increase in EAAs was attenuated by KYN administered through microdialysis, suggesting that the EAA release from the surrounding brain areas appears to be a consequence that is secondary to the EAA release from the contused brain tissue. Such a diffusion-reaction process is probably mediated by the neurotransmitter actions of EAAs. The results of the present study are of clinical importance, since surgical removal of contused brain tissue and administration of EAA antagonists may serve to protect the surrounding brain areas from EAA neurotoxicity.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"524-7"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18971573","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A Nishino, M Suzuki, T Yoshimoto, H Otani, H Nagura
{"title":"A novel aspect of thrombin in the tissue reaction following central nervous system injury.","authors":"A Nishino, M Suzuki, T Yoshimoto, H Otani, H Nagura","doi":"10.1007/978-3-7091-9334-1_22","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_22","url":null,"abstract":"<p><p>Thrombin and two different types of control solutions (buffer and albumin) were continuously infused into the rat caudoputamen by an osmotic minipump. Routine histological studies with immunohistochemistry using antibodies for BrdU, GFAP, vimentin and laminin were carried out to assess infiltration of inflammatory cells, formation of edema, cell proliferation, and reactivity of astrocytes and mesenchymal cells. The number of inflammatory cells, number of BrdU positive cells, area and number of vimentin positive astrocytes, and the area of GFAP-positive reactive astrocytes were quantitatively analyzed. In the thrombin group, pale tissue foci due to spongiosis were observed together with infiltration of inflammatory cells, proliferation of mesenchymal cells, and increase of vimentin positive astrocytes which was significantly different from the control groups. The results suggest that thrombin plays an important role in inflammation, brain edema and reactive gliosis following CNS injury.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"86-8"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18971919","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M Suzuki, O Motohashi, A Nishino, K Umezawa, N Shida, T Yoshimoto
{"title":"Differences in wound healing pattern between mature and immature brain behavior of extravasated serum protein.","authors":"M Suzuki, O Motohashi, A Nishino, K Umezawa, N Shida, T Yoshimoto","doi":"10.1007/978-3-7091-9334-1_118","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_118","url":null,"abstract":"<p><p>To clarify the fate of extravasated serum protein and tissue reaction following blood brain-barrier breakdown in mature and immature brain, we produced cryogenic injury in the cortices of adult and post natal day 2 rats, and immunohistochemical examination with GFAP, vimentin and albumin, endogenous tracer of serum proteins, antibodies. Mature and immature brain showed the same histological changes by day 3. However, fibrotic scar, cyst formation and GFAP, vimentin-positive astrocytosis were main features in mature brain, fusion of adjoining cortical plate without scar and astrocytosis was typical in the immature brain. In adult rats, presence of albumin was observed near the lesion on day 1, evidently extending to the contralateral hemisphere on day 7 and localized again around scar and cyst on day 14. In the P2 rats, albumin was present in both hemispheres on day 1, but was localized to molecular layer periventricular region and choroid plexus on day 7. No albumin was detected on day 14. These results suggest that rapid spreading and clearance of extravasted serum proteins may take place in the immature brain and this may be deeply involved in the characteristic wound healing pattern.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"434-6"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18971244","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
K Otsubo, Y Katayama, F Kashiwagi, H Muramatsu, A Terashi
{"title":"Comparison of the effects of glycerol, mannitol, and urea on ischemic hippocampal damage in gerbils.","authors":"K Otsubo, Y Katayama, F Kashiwagi, H Muramatsu, A Terashi","doi":"10.1007/978-3-7091-9334-1_86","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_86","url":null,"abstract":"<p><p>The effects of glycerol and mannitol, as well as urea, on delayed neuronal death (DND) in the gerbil hippocampus were investigated. 20% solution of glycerol, mannitol and urea were prepared, and 6.5 ml/kg of each agent, or saline, was administered to male Mongolian gerbils intraperitoneally 30 min before ischemia. The animals were subjected to transient forebrain ischemia for 5 min. Seven days after the ischemic insult, the brains were fixed and stained for histopathological analysis. The number of normal neurons (neuronal density, ND) in a 1 mm linear length of hippocampal CA1 region was counted. ND of sham-operated group (n = 6) was 275.3 +/- 16.7 (mean +/- SD). ND in the saline-treated group (n = 6) was 14.8 +/- 5.0. ND of groups treated with glycerol (n = 6), mannitol (n = 6) and urea (n = 4) was 68.2 +/- 56.7 (p < 0.01), 52.8 +/- 54.4 (p < 0.01) and 12.0 +/- 2.5 (NS), respectively. The present study demonstrates that glycerol and mannitol have some protective effects against DND in the gerbil hippocampus, whereas urea has no effect.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"321-4"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18971570","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Combined treatment with nicardipine, phenobarbital, and methylprednisolone ameliorates vasogenic brain edema.","authors":"S Z Lin, T L Chiou, Y H Chiang, W S Song","doi":"10.1007/978-3-7091-9334-1_145","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_145","url":null,"abstract":"<p><p>Free radicals formed around the edematous areas of the brain can cause lipoperoxidation of the cellular membrane, followed by calcium influx into the cell through calcium channels. These secondary insults may aggravate vasogenic brain edema. Since phenobarbital is a free radical scavenger, methylprednisolone has an antilipoperoxidation effect; and nicardipine is a calcium channel blocker, we hypothesized that combined treatment with phenobarbital, methylprednisolone, and nicardipine would be beneficial in vasogenic brain edema. This hypothesis was tested in Sprague-Dawley rats with a transdural cold-injury on the right parietal cortex. The animals were randomly divided into two groups. Animals in the treatment group were injected intraperitoneally with phenobarbital (4 mg/kg), methylprednisolone (50 mg/kg), and nicardipine (10 micrograms/kg) at 5 min and 8 hours after the cold-injury. The control animals were injected with saline. These animals were sacrificed 24 hours after the injury. The extent of brain edema was assessed by measuring the water content, the inulin distribution volume, and the distribution area of Evans blue in the brain. Our results showed that the water content of the edematous hemisphere was similar in the control and the treatment groups. However, Evans blue distribution area and inulin distribution volume of the treatment group were less than those of the control group by 12% and 31%, respectively. In conclusion, the combined treatment with phenobarbital, methylprednisolone and nicardipine is beneficial in vasogenic brain edema.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"528-30"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18971574","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Quantitation of peritumoural oedema and the effect of steroids using NMR-relaxation time imaging and blood-brain barrier analysis.","authors":"C Andersen, J Astrup, C Gyldensted","doi":"10.1007/978-3-7091-9334-1_112","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_112","url":null,"abstract":"<p><p>A new method of in vivo quantitation of peritumoural brain oedema using NMR relaxation time imaging (T1-maps) and Gd-DTPA-enhanced Blood-Tumour-Barrier (BTB) analysis is presented. The method is based on image pixel histogram analysis and a fast imaging method combined with arterial [Gd-DTPA]-measurement. The method was applied in 26 brain tumour patients, studied prior to--and 1, 3 and 7 days after initiation of dexamethasone. Oedema resorption rate following dexamethasone treatment was almost equal in glioblastomas and metastases, mean T1 being reduced by ca. 12% in 7 days. In meningiomas no significant changes in peritumoural oedema could be detected. Simultaneous BTB-analysis was obtained in 4 patients showing correlation between oedema resorption in vivo and reduction of BTB transport rate constant Ki after 7 days of steroid treatment. This method is a powerful tool in quantitation and monitoring of brain oedema in vivo, as both steroid influence on oedema resorption and on BTB-defect can be monitored simultaneously.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"413-5"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/978-3-7091-9334-1_112","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18971916","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
P C Warnke, F J Hans, A Korst, C Mall, C B Ostertag
{"title":"Simultaneous measurement of bidirectional capillary permeability, vascular volume, extracellular space, and rCBF in experimental gliomas and surrounding edema.","authors":"P C Warnke, F J Hans, A Korst, C Mall, C B Ostertag","doi":"10.1007/978-3-7091-9334-1_91","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_91","url":null,"abstract":"<p><p>Measurements of bidirectional capillary permeability in the ASV tumor model revealed a heterogeneous distribution of transport rates for the small water-soluble molecules which are believed to be the driving force in perifocal edema formation. Mean K1 values were 8.1 +/- 5.5 microliters/g/min in whole tumor and 18.89 +/- 12.3 microliters/g/min in highly permeable areas. Tumor blood flow ranged between normal white matter and cortex, whereas the plasma vascular space in the tumors was increased as compared to the normal brain. The size of the extracellular space was depending on the regional capillary permeability, underlining the vasogenic nature of peritumoral edema which was capable of being studied using in vivo methods.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"341-3"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18972100","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Proton MR spectroscopy of experimental brain tumors in vivo.","authors":"M L Gyngell, T Els, M Hoehn-Berlage, K A Hossmann","doi":"10.1007/978-3-7091-9334-1_94","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_94","url":null,"abstract":"<p><p>F98 gliomas, E367 neuroblastomas, and RN6 Schwannomas in rat brain were studied non-invasively in vivo by localized proton MR spectroscopy (MRS). The spectra obtained from homotopic brain contralateral to the tumors were qualitatively indistinguishable from those of normal rat brain in vivo and showed resonance lines assigned to N-acetylaspartate, glutamate, total creatine (creatine and phosphocreatine), choline, glucose, and myo-inositol. The tumor spectra displayed marked differences compared to those obtained from contralateral brain. There were increases in choline, myo-inositol and lipids, which are presumably associated with increased membrane turnover. The presence of lactate indicated anaerobic glycolysis. Other differences included the absence of signals from NAA resulting from the destruction or displacement of neuronal tissue by the tumor. There was also a loss of total creatine. Although the spectra of all three tumor types were distinct from contralateral brain, there were no obvious differences between the different tumor types.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"350-2"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18972103","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
F Kashiwagi, Y Katayama, H Igarashi, S Iida, H Muramatsu, A Terashi
{"title":"Effect of a new calcium antagonist (SM-6586) on experimental cerebral ischemia.","authors":"F Kashiwagi, Y Katayama, H Igarashi, S Iida, H Muramatsu, A Terashi","doi":"10.1007/978-3-7091-9334-1_77","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_77","url":null,"abstract":"<p><p>SM-6586 (SM) is a new derivative of dihydropyridine with potent calcium blocking activity and inhibitory activity of the Na+/H+ and Na+/Ca++ exchange transport. The effect of SM on survival rate, brain edema and metabolites was evaluated using two different models in spontaneously hypertensive rat (SHR). Global ischemia was induced by bilateral common carotid artery ligation (BLCL) and focal ischemia was induced by middle cerebral artery occlusion. The survival rate after BLCL was higher in the SM-treated group. The brain water content was lower, the ATP level was higher and lactate level was lower in the SM-treated group compared to the control group. In focal ischemia models, the SM-treated group showed a reduction of T1 relaxation time. The brain water content was significantly decreased in the SM-treated group. These results indicate that SM was effective in ameliorating the ischemic insult in global and focal cerebral ischemia models.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"289-92"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18972222","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
T Winkler, H S Sharma, E Stålberg, Y Olsson, F Nyberg
{"title":"Naloxone reduces alterations in evoked potentials and edema in trauma to the rat spinal cord.","authors":"T Winkler, H S Sharma, E Stålberg, Y Olsson, F Nyberg","doi":"10.1007/978-3-7091-9334-1_140","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_140","url":null,"abstract":"<p><p>The influence of naloxone (an opioid receptor antagonist) on spinal cord conduction and edema formation as a result of trauma to the cord was investigated in a rat model. The spinal cord injury (SCI) was inflicted in urethane anesthetized animals by a longitudinal incision into the right dorsal horn of the T10-11 segments, about 2 mm deep and 5 mm long. Spinal cord evoked potentials (SCEP) were recorded epidurally from the T9 (rostral) and T12 (caudal) segments after stimulation of the ipsilateral tibial and sural nerves at the ankle. The edema was measured by determining water content of the cord at s h after injury. In rats not given naloxone SCI resulted in an immediate long-lasting depression of the rostral maximal negative peak (MNP) amplitude (about 60%) and a significant increase in the latency of the rostral maximal positive peak (MPP). Pretreatment with naloxone inhibited the immediate post-injury decrease of the rostral MNP and some of the increase of MPP latency. The water content in the traumatized spinal cord was reduced by 3% in naloxone treated animals compared with untreated injured controls. Our results indicate that endogenous opioid peptides participate in changes of spinal cord conduction after trauma and influence edema formation probably via multiple opioid receptors.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"511-5"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18972231","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}