Acta neurochirurgica. Supplementum最新文献

{"title":"The effect of alkalizing agents on experimental focal cerebral ischemia.","authors":"H. Kuyama, T. Kitaoka, K. Fujita, S. Nagao","doi":"10.3995/JSTROKE.16.173","DOIUrl":"https://doi.org/10.3995/JSTROKE.16.173","url":null,"abstract":"We investigated the immediate effect of tris (hydroxymethyl) aminomethane (THAM) and NaHCO3 on focal cerebral ischemia produced by occlusion of the left middle cerebral artery (MCA) in cats. The animals were divided into three groups. In the control group, physiological saline was infused continuously. The THAM and NaHCO3 groups received continuous administration of 0.3 mol THAM and 7% NaHCO3, respectively, to normalize arterial pH. Local CBF measured in the marginal and suprasylvian gyri decreased less than 30 ml/100 g/min after the MCA occlusion and there were no significant differences among the three groups. Extracellular pH of the marginal gyrus (peri-infarct zone) decreased from 7.21 to 6.86 in the control group. However, extracellular pH did not show significant changes in the THAM and NaHCO3 groups. Intracellular pH of the infarct area decreased from 7.23 to 6.13 in the control group within 6 hours after occlusion. THAM had a tendency to normalize intracellular pH compared with that in the control and NaHCO3 groups. THAM significantly (p < 0.05) decreased water content of the gray matter in the marginal gyrus at 6 hours after occlusion and the infarct size compared with those in the control and NaHCO3 groups. Therefore, normalization of systemic and perifocal acidosis with THAM is effective for reducing cortical edema and infarct size in the early stage of focal cerebral ischemia probably due to the improvement of intracellular acidosis.","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"40 1 1","pages":"325-8"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83362813","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":"The effect of leukotriene C4 on the permeability of brain capillary endothelial cell monolayer.","authors":"T Nagashima,&nbsp;W Shigin,&nbsp;A Mizoguchi,&nbsp;M Arakawa,&nbsp;M Yamaguchi,&nbsp;N Tamaki","doi":"10.1007/978-3-7091-9334-1_14","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_14","url":null,"abstract":"<p><p>The role of leukotrienes as mediator of brain edema is still controversial. Recently, the ability of gamma-GTP to act as enzymatic barrier and to inactivate leukotrienes in normal brain capillaries was pointed out. A hypothesis tested in our experiments was that Leukotriene C4 (LTC4) increases permeability of a cerebral capillary endothelial monolayer which lacks gamma-GTP activity. Brain capillary endothelial cells were obtained of 10 rats from cerebral cortex by an enzymatic isolation procedure. The cells have an intact function, however, lack gamma-GTP activity. The endothelial cells were cultured on an optically clear collagen membrane mounted on a plastic frame. Effects of bradykinin (1 x 10(-5) M) and LTC4 (1 x 10(-7) M, 1 x 10(-6) M, 5 x 10(-6) M, 1 x 10(-5) M) were tested on permeability of the endothelial cell monolayer by measuring leakage of 14C-sucrose. The effect of LTC4 and bradykinin on intracellular calcium was studied by laser scanning confocal microscopy. LTC4 did not increase permeability of the brain capillary endothelial cell monolayer which lacked gamma-GTP activity. LTC4 did neither increase the concentration of intracellular calcium. Differences of LTC4 receptor function in normal brain capillaries and tumor capillaries remain to be studied.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"55-7"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18972106","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":"Do N-methyl-D-aspartate antagonists have disproportionately greater effects on brain swelling than on ischemic damage in focal cerebral infarction?","authors":"C K Park,&nbsp;J McCulloch,&nbsp;D S Jung,&nbsp;J K Kang,&nbsp;C R Choi","doi":"10.1007/978-3-7091-9334-1_74","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_74","url":null,"abstract":"<p><p>Using a frozen section technique, we have assessed the effects of N-methyl-D-aspartate (NMDA) antagonist upon brain swelling caused by ischemic brain edema in a rat model of focal cerebral infarction. Although pretreatment with the competitive NMDA antagonist, D-CPPene or the noncompetitive NMDA antagonist, CNS 1102 reduced both the volumes of infarction and ischemic edema in the cerebral hemisphere, mean reduction in brain edema was proportionately similar to decrease in infarct volume in the same animals (correlation coefficient, r = 0.82, p < 0.001). There was, therefore, no evidence of disproportionately greater effects with NMDA antagonist upon brain edema.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"279-81"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18972219","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":"Role of serotonin and prostaglandins in brain edema induced by heat stress. An experimental study in the young rat.","authors":"H S Sharma,&nbsp;J Westman,&nbsp;F Nyberg,&nbsp;J Cervos-Navarro,&nbsp;P K Dey","doi":"10.1007/978-3-7091-9334-1_17","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_17","url":null,"abstract":"<p><p>The possibility that serotonin and prostaglandins participate in edema formation following heat stress (HS) was examined in young rats. Exposure of conscious young animals (8-9 weeks old) to heat at 38 degrees C in a biological oxygen demand (BOD) incubator (relative humidity 50-55%; wind velocity 20-25 cm/s) for 4 h resulted in marked increase in the whole brain water content (about 3%) as compared to animals kept at room temperature (21 degrees C). A marked extravasation of Evans blue and 131I-sodium occurred in the brain of heat exposed animals as compared to normal animals. Morphological examination using electron microscopy of selected brain regions of heat stressed animals showed profound cell changes. Thus perivascular edema, swollen neuronal and glial cells, membrane damage, vesiculation of myelin, axonal swelling and synaptic damage was frequent in this group of untreated animals. Pretreatment with ketanserin (a selective serotonin2 receptor antagonist) or indomethacin (an inhibitor of prostaglandin synthesis) markedly reduced edema formation after 4 h HS in young animals. These heat stressed animals had considerably less extravasation of protein tracers as compared to the untreated group. Cell changes and edema at the ultrastructural level were mainly absent. Our results suggest that serotonin and prostaglandins are involved in heat stress induced breakdown of the BBB permeability, edema formation, and cell damage.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"65-70"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18973998","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":"Evaluation of BBB damage in an UV irradiation model by endogenous protein tracers.","authors":"J V Lafuente,&nbsp;J Cervós-Navarro,&nbsp;E Gutierrez Argandoña","doi":"10.1007/978-3-7091-9334-1_37","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_37","url":null,"abstract":"<p><p>Autologous serum proteins have proved to be suitable tracer to evaluate vascular permeability. The dynamic behaviour of anti-HRP immunoglobulins was studied in ultraviolet (UV) irradiation induced brain edema. Cerebral cortex of 36 anaesthetized adult rats was irradiated following a 2 x 2 mm parietal craniotomy. Immunization was carried out by 3 subcutaneous injections of 10 mg HRP in 0.5 ml complete freund adjuvant (CFA), 6, 4 and 2 weeks before the injury. Control animals were immunized only with CFA; further control animals were operated and irradiated without any previous immunization. After survival times ranging from 30 min to 24 hours, postoperation animals were transcardially perfused with 4% fresh paraformaldehyde solution in phosphate buffered saline. After postfixation at 4 degrees C, 20 microns vibratome sections were prepared for incubation with a solution of 0.05% HRP, washed and developed by the DAB reaction. The reactions showed a remarkable exsudation and spreading of anti-HRP antibodies in the edematous brain. The antigen-antibody reaction was conspicuous in animals with shorter survival periods in the necrotic area and near the lesion (1-2 mm). After a longer survival time extravasation involved the whole hemisphere. In animals with the longest survival period labeled serum proteins were found even in the white matter of the hemisphere contralateral to the injury. Endogenous tracer of BBB function is useful to study the spreading of brain edema in a delayed time after the edematous lesion.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"139-41"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18975711","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":"Regional cerebral blood flow trends in head injured patients with focal contusions and cerebral edema.","authors":"M J Alexander,&nbsp;N A Martin,&nbsp;R Khanna,&nbsp;M Caron,&nbsp;D P Becker","doi":"10.1007/978-3-7091-9334-1_131","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_131","url":null,"abstract":"<p><p>Focal contusions following head injury may be associated with focal or diffuse cerebral edema. Early global hyperemia and perifocal hyperemia may play a role in cerebral edema, although causal relationships have yet to be clearly been defined. We studied 27 patients with head injury (admission GCS 3-12) resulting in focal contusions (without evidence of subarachnoid, intraventricular or intraparenchymal hemorrhage by CT). Patients were studied with ICP monitors, head CTs, and intravenous 133Xenon regional cerebral perfusion studies serially over several days post injury. Low cortical blood flow and a low mean CBF15 flow were evident on the day of the injury. Additionally, F1 analysis indicated significantly (p < 0.05) greater cortical blood flow in the surrounding brain (mean 60 cc/100 g/min) compared to the contusion area (mean 43 cc/100 g/min) on the day of trauma. Mean regional CBF remained below normal in the contused areas (CBF15 < 35 cc/100 g/min), however the cortical flow increased in the first few days post-injury (peak F1 = 95 cc/100 g/min on day 3) then decreased to sub-normal levels. The mean CBF in the surrounding brain was low on the day of injury (CBF15 = 29 cc/100 g/min), although higher than the contused area, and increased to a peak of 45 cc/1009/min on day 3 posttrauma. Cortical flow in the surrounding brain, however, exhibited a different trend. The mean F1 was low on the day of trauma and significantly higher one day after trauma (mean 105 cc/100 g/min). Only 15 of the 27 patients with focal contusions had evidence of cerebral edema. Eleven of these exhibited focal edema and 4 exhibited diffuse edema. Focal edema developed over the first few days posttrauma as seen in followup CT, whereas patients with diffuse edema exhibited edema on the admission CT. Initial oligemia in the contused areas was associated with a subsequent hyperemic rim about the contusion. Focal hyperemia was associated with focal edema in 41% of the patients, whereas diffuse edema appeared to be independent of the hyperemic response in contusions.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"479-81"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18975726","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":"Effect of steroids on brain lipocortin immunoreactivity.","authors":"K G Go,&nbsp;F Zuiderveen,&nbsp;L De Ley,&nbsp;J G Ter Haar,&nbsp;L Parente,&nbsp;E Solito,&nbsp;W M Molenaar","doi":"10.1007/978-3-7091-9334-1_26","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_26","url":null,"abstract":"<p><p>LCT-1, LCT-2 and LCT-5 were assessed in uninjured rats and rats subjected to a cortical freezing injury or middle cerebral artery (MCA) occlusion. Apart from animals receiving no treatment, other uninjured or injured animals received methylprednisolone (2 or 30 mg/kg) or the 21-aminosteroid U-74389F (10 mg/kg) one day and 2 hours before killing. The animals were killed by decapitation 1 hour after the freezing injury or the MCA occlusion and the area containing the lesion was removed and frozen in Freon. Frozen sections were treated with rabbit polyclonal anti-LCT antibody; binding of antibody was visualized by horseradish peroxidase-conjugated swine antirabbit antibody. Without steroid pretreatment, in the uninjured brain LCT immunoreactivity was absent in the greater part of the brain, except in sporadic microglia. In steroid-pretreated animals and in the freezing lesion of both pretreated and untreated animals there was extensive immunostaining; in the freezing lesion it may be due to passage of systemic LCT across the impaired blood-brain barrier in the lesion. The cellular elements showing immunostaining were meningeal cells, neurons, ependyma, choroid plexus, oligodendroglia and capillary endothelium. It implies that also in the brain the steroid effect is consistent with LCT formation.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"101-3"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18970423","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":"Medullary cardiovascular center and acute brain swelling.","authors":"M Maeda,&nbsp;T Takachi,&nbsp;M Nakai,&nbsp;A J Krieger,&nbsp;H N Sapru","doi":"10.1007/978-3-7091-9334-1_45","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_45","url":null,"abstract":"<p><p>Acute brain swelling is reported to be due to acute vasodilatation of cerebral vessels. One of the causes of acute brain swelling may be disturbance of central control mechanisms of cerebral vessels. It has been reported that the anatomical location of the area which controls cerebral circulation is related to the area which controls systemic circulation. However, the role of the cardiovascular center on cerebral circulation has not been clear. The present study was, therefore, undertaken to examine the effects of chemical stimulation of the medullary cardiovascular center [nucleus tractus solitarius (NTS), ventrolateral depressor area (VLDA), and ventrolateral pressor area (VLPA)] on cerebral circulation. In anesthetized, paralyzed and artificially ventilated rats, the neurons in the NTS, VLDA, and VLPA were chemically stimulated and the cerebral blood flow (CBF) was determined using labeled microspheres. The CBF decreased significantly and the cerebrovascular resistance (CVR) increased significantly by chemical stimulation of the NTS, VLDA, and VLPA. These results suggest that the neurons within the NTS, VLDA, and VLPA control cerebral vessels vasoconstrictively. There is a possibility that the dysfunction of the NTS, VLDA, and VLPA may cause acute brain swelling.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"168-70"},"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_45","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18971640","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":"The effects of topical dexamethasone on experimental brain tumors and peritumoral brain edema.","authors":"Y Ikeda,&nbsp;B S Carson,&nbsp;D M Long","doi":"10.1007/978-3-7091-9334-1_107","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_107","url":null,"abstract":"<p><p>To determine if topical dexamethasone administered to brain tumor beds would not only control peritumoral edema and suppress tumor growth but also prevent systemic steroid complications, we studied experimental brain tumors produced in 102 rabbits by implanted VX2 carcinoma cells. We separated 58 animals into three groups: 1) untreated rabbits (n = 15), 2) systemic dexamethasone-treated (4 mg/kg/day) rabbits (n = 18), and 3) topical dexamethasone-treated (2.5 microliters/h, osmotic pump) rabbits (n = 25). We administered systemic or topical dexamethasone from the third day or from the seventh day after tumor implantation, and sacrificed the animals on the 13th day. We compared survival in these three groups with that of another 44 rabbits, beginning treatment on the seventh day. We measured brain water content in the white matter of the sacrificed rabbits by the specific gravity method. We measured the length and width of the brain tumors of all the rabbits and estimated tumor volume. Systemic and topical dexamethasone administered from the third day produced statistically significant inhibition of tumor volume as well as a mean reduction in peritumoral brain edema in most tested sites. Systemic and topical dexamethasone treatment resulted in a statistically significant increase in survival relative to the untreated group. These results suggest that topical dexamethasone is efficacious in a brain tumor model and its administration to brain tumor beds constitutes a new therapeutic modality.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"397-9"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18971912","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":"Sequential change of brain edema by semiquantitative measurement on MRI in patients with hypertensive intracerebral hemorrhage.","authors":"S Suga,&nbsp;S Sato,&nbsp;K Yunoki,&nbsp;B Mihara","doi":"10.1007/978-3-7091-9334-1_156","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_156","url":null,"abstract":"<p><p>The progression of brain edema in seven patients with hypertensive intracerebral hemorrhage (ICH) was evaluated. Five were of putaminal and two were of thalamic hemorrhage. The hematoma volume in the patients was 4 approximately 40 ml (18.9 +/- 8.0 ml). Sequential MRI (SE: 2000/40) was performed at one, two and four weeks after onset. The edema volume (EV) was calculated as 1/2.(long diameter).(short diameter).(thickness) of the high intensity area (HIA) on MRI. In comparison with the EV at one week after onset, the EV at two weeks was increased and the EV at four weeks returned to the same level of that at one week (132.3 +/- 26.1%, 100 +/- 10.6%, respectively). In contrast, the consciousness level and motor weakness of the patients had already improved at two weeks after onset. Our results demonstrate that progression of brain edema after small or medium size ICH may not bring about a deterioration of the clinical course. Moreover, progression of brain edema to the cerebral cortex and ventricle as indicated by MRI suggested an absorption pathway for the edema fluid, and implying that brain edema following ICH could play a part in the healing process after ICH.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"564-7"},"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_156","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18972111","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}