{"title":"The effect of alkalizing agents on experimental focal cerebral ischemia.","authors":"H Kuyama, T Kitaoka, K Fujita, S Nagao","doi":"10.1007/978-3-7091-9334-1_87","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_87","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","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":"18971571","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 von Berenberg, A Unterberg, G H Schneider, W R Lanksch
{"title":"Treatment of traumatic brain edema by multiple doses of mannitol.","authors":"P von Berenberg, A Unterberg, G H Schneider, W R Lanksch","doi":"10.1007/978-3-7091-9334-1_146","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_146","url":null,"abstract":"<p><p>Mannitol is frequently used to reduce elevated intracranial pressure often associated with brain edema. In cases of a damaged blood-brain barrier, however, mannitol might aggravate vasogenic cerebral edema, as has recently been stressed. The aim of this study was to investigate whether multiple doses of mannitol administered during development of vasogenic brain edema following a cryogenic cortical injury affect hemispheric swelling and edema. Sprague-Dawley rats were anesthetized with ketamine and xylazine. A cortical freezing lesion was applied to the right parietal region. A first series of eight rats received four doses of 20% mannitol (0.4 g/kg within 10 minutes) thirty minutes, 3, 6 and 9 hours after trauma. Twelve hours after cryogenic injury, the brains were removed for determination of hemispheric swelling and cerebral water content. Eight control rats were infused with saline only. In a second series nine rats received eight doses of 20% mannitol 30 minutes, 3, 6, 9, 12, 15, 18 and 21 hours after trauma. In this series, the brains were removed 24 hours after freezing. Again respective control animals were infused with saline only. Hemispheric swelling was 7.2 +/- 0.5% after four doses of mannitol compared to 7.6 +/- 0.5% in control animals (n.s.). Following eight doses of mannitol hemispheric swelling was 8.9 +/- 0.4% compared to 10.1 +/- 0.4% in control rats (p < 0.05). Accordingly, the water content of traumatized hemispheres was lower following repeated mannitol treatment (80.5 versus 80.8%). Water content in control hemispheres was not affected by mannitol. Taken together, these results indicate that multiple doses of mannitol do not aggravate total hemispheric swelling, nor global water content following induction of vasogenic edema.(ABSTRACT TRUNCATED AT 250 WORDS)</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"531-3"},"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_146","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18971575","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 Kuroiwa, M Ueki, Q Chen, H Suemasu, I Taniguchi, R Okeda
{"title":"Biomechanical characteristics of brain edema: the difference between vasogenic-type and cytotoxic-type edema.","authors":"T Kuroiwa, M Ueki, Q Chen, H Suemasu, I Taniguchi, R Okeda","doi":"10.1007/978-3-7091-9334-1_42","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_42","url":null,"abstract":"<p><p>Some of the basic biomechanical properties of edematous brain tissue have yet to be clarified. Therefore we measured regional tissue compliance and swelling isotropy/anisotropy in cat brain during development of vasogenic-type and cytotoxic-type edema. In vasogenic-type edema induced by cryogenic injury, the edematous white matter showed an increase of regional tissue compliance (indentation method), which paralleled the increase in the regional tissue water content (gravimetry). Swelling of the white matter due to edema was anisotropic, in which expansion transverse to the neuronal fibers caused by their dissociation was 91.1%, whereas longitudinal expansion was 2.3%. In cytotoxic-type edema induced by cerebral ischemia for 3 h, regional tissue compliance was decreased in the area suffering energy failure, which was visualized as an area of reduced succinic dehydrogenase activity. The ischemic gray matter showed isotropic swelling, and morphologically, prominent swelling of neuroglial cells. These marked differences in basic biomechanical properties between vasogenic-type and cytotoxic-type edema should be taken into account when analyzing the mechanism of edema-mediated tissue injury.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"158-61"},"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_42","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18971637","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}
S Kida, D W Ellison, P V Steart, F Iannotti, R O Weller
{"title":"Perivascular edema fluid pathway in astrocytic tumors.","authors":"S Kida, D W Ellison, P V Steart, F Iannotti, R O Weller","doi":"10.1007/978-3-7091-9334-1_104","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_104","url":null,"abstract":"<p><p>Perivascular spaces are anatomical routes for the bulk flow drainage of fluid from the gray matter to the subarachnoid space in normal rat brain. Perivascular cells are the resident scavengers in perivascular spaces. Following focal brain damage, perivascular cells upregulate MHC Class II antigens associated with uptake of edema fluid. Similar cells can be defined in damaged human brain. In the present investigation, the distribution of MHC Class II upregulated perivascular cells was measured in 30 astrocytic tumors and adjacent edematous tissues by immunocytochemistry using the following antibodies: HLA-DR (MHC Class II), PGM1 and MAC387 (macrophages). Perivascular cells were PGM1+/MAC387- and were located in perivascular spaces along blood vessels of all sizes. MHC Class II+ perivascular cells were distributed mainly in the tumors but in some cases (4 of 10 in astrocytomas, 4 of 10 in anaplastic astrocytomas, and 7 of 10 in glioblastomas) they were also found in adjacent edematous brain. The extensive MHC Class II expression on perivascular cells suggests that perivascular cells play a scavenging role in the perivascular spaces in human brain. The results of the present study indicate the similarity between perivascular spaces in human and rat brains and emphasize the significance of perivascular spaces as anatomical routes for edema fluid drainage from human brain tissue.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"384-6"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18971909","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 J Terzis, G Nowak, E Mueller, O Rentzsch, H Arnold
{"title":"Induced hyperthermia in brain tissue in vivo.","authors":"A J Terzis, G Nowak, E Mueller, O Rentzsch, H Arnold","doi":"10.1007/978-3-7091-9334-1_110","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_110","url":null,"abstract":"<p><p>Concerning hypothermia treatment, knowledge of time-temperature and of temperature distributions within tumor volumes is essential in order to obtain the maximal therapeutic effect. New techniques are being developed to overcome these difficulties. Two different heat sources, a contact Nd:YAG laser system and an automatically controlled high-frequency current system were investigated on 15 rabbits. Changes of the intracerebral temperature were registered at 4 different distances from the energy source. The intracerebral temperature was increased to 42.5 degrees C at a distance of 5 mm to the heat source and maintained at this level for a period of 60 min. The contact Nd:YAG laser system reached 42.5 degrees C at 3 W of output power. Using higher laser output power, brain tissue herniation (brain edema) through the burrhole was observed. The automatically controlled high-frequency current system reached 42.5 degrees C at 18.75 W of output current. A very small herniation of brain tissue could be observed using higher output current. Both heat sources presented an exponential decrease of the temperature profile depending on the distance. The tissue heat clearance was compensated for by intermittent laser or high-frequency current application. Both systems proved efficient for inducing hyperthermia as needed for antitumoral therapy.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"406-9"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18971914","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 Davis, A D Mendelow, R H Perry, I R Chambers, O F James
{"title":"The effect of age on cerebral oedema, cerebral infarction and neuroprotective potential in experimental occlusive stroke.","authors":"M Davis, A D Mendelow, R H Perry, I R Chambers, O F James","doi":"10.1007/978-3-7091-9334-1_75","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_75","url":null,"abstract":"<p><p>A model of occlusive stroke in the aging brain has been developed and used to evaluate the effects of age upon cerebral infarction, cerebral oedema and neuroprotective potential. Focal ischaemia following left middle cerebral artery occlusion has been compared in aged (30 month) and adult (< 17 month) rats, with histological assessment of infarct volume and analysis of specific gravity as an index of cerebral oedema. Aging was associated with a significant increase in cerebral infarct size. The mean infarct volume in aged rats was 40.5% +/- 2.6% of the hemisphere volume, compared to 30.9% +/- 0.7% in adults (p < 0.01). Pre-treatment with the competitive N-Methyl-D-Aspartate (NMDA) receptor antagonist 3-(2-Carboxy Piperazin-4-yl)Propyl-l-Phosphonate (D-CPP-ene) reduced infarct volumes in both age groups to 33.0% +/- 1.8% and 20.7% +/- 3.2% in aged and adult animals, respectively (p < 0.05). There was significantly less oedema of the cerebral cortex in D-CPP-ene pre-treated rats; mean cortical specific gravity 4 hours post-infarction was 1.0381 +/- 0.0013 in untreated aged rats and 1.0391 +/- 0.0014 in untreated adults, compared to 1.0458 +/- 0.0031 in treated aged rats and 1.0442 +/- 0.0014 in treated adults (p < 0.05). At 24 hours post-infarction, D-CPP-ene pre-treated aged rats had a mean cortical specific gravity of 1.0403 +/- 0.0006 compared to 1.0361 +/- 0.0014 in untreated aged animals (p < 0.05). This study has demonstrated an age-related increase in cerebral infarct size, but has shown that the aging brain is amenable to neuroprotection by NMDA receptor antagonism.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"282-4"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18972221","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}
L Schürer, S Corvin, F Röhrich, C Abels, A Baethmann
{"title":"Leukocyte/endothelial interactions and blood-brain barrier permeability in rats during cerebral superfusion with LTB4.","authors":"L Schürer, S Corvin, F Röhrich, C Abels, A Baethmann","doi":"10.1007/978-3-7091-9334-1_13","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_13","url":null,"abstract":"<p><p>The experimental study analyses the vasomotor response (change of diameter of pial arterioles and venules), and blood-brain barrier function of the pia-arachnoidea at the rat brain surface before, during and after cerebral superfusion with 1.5 or 15.0 nM LTB4 in mock CSF. Leukocyte dynamics were studied by assessment of their centerline velocity, of rolling along (\"roller\") and attachment to (\"sticker\") the venular wall of white blood cells intravitally stained by Rhodamin 6G. Superfusion of the brain with LTB4 at both dose levels led to dilation of arterioles to 130% (p < 0.001), while of venules to 117% (p < 0.001) of control. The centerline velocity of leukocytes increased from 0.7 to 0.9 mm/s, however, only after superfusion with LTB4 at the high dose level. LTB4 induced a dose-dependent rolling (p < 0.01) and sticking of leukocytes (p < 0.001). Yet, a delay of about 60 min between cerebral administration of LTB4 and the maximal response of leukocyte rolling and sticking was observed. Whereas the blood-brain barrier was not opened by cerebral superfusion with 1.5 or 15.0 nM LTB4, for i.v. Na(+)-fluorescein, barrier leakage was promptly induced by 30.0 nM. The present findings demonstrate that cerebral administration of LTB4 by superfusion of the exposed brain surface is eliciting a pronounced vasomotor response, whereas the induction of leukocyte/endothelial interactions is less impressive.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"51-4"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18972230","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":"Neuron-glial interaction during injury and edema of the CNS.","authors":"O S Kempski, C Volk","doi":"10.1007/978-3-7091-9334-1_2","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_2","url":null,"abstract":"<p><p>During injury and ischemia of the CNS mediator compounds are released or activated which cause secondary swelling and damage of nerve cells. Such mediators are glutamate, acidosis, free fatty acids, or high extracellular potassium. Glial homeostatic mechanisms are activated to prevent the secondary injury from these mediators. The glial clearance mechanisms have been studied in detail using in vitro systems allowing for a close control of the glial environment. Current evidence suggests glial swelling to occur together with glutamate uptake or in response to extracellular acidosis. Glial swelling, therefore, is rather the result of homeostatic mechanisms than an indication of glial demise.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"7-11"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18973999","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":"Pharmacological reduction of brain edema induced by intracarotid infusion of protamine sulphate: a comparison between a free radical scavenger and an AMPA receptor antagonist.","authors":"B B Johansson, I Westergren","doi":"10.1007/978-3-7091-9334-1_34","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_34","url":null,"abstract":"<p><p>The blood-brain barrier (BBB) of rats was opened by infusing 10 mg protamine sulphate (200 microliters in 30 s) into the right internal carotid artery. Ten minutes later, tirilazad, a 21-aminosteroid (3 mg/kg): NBQX, an AMPA receptor antagonist (5 mg/kg); or dixyrazine, a phenotiazine derivate (10 mg/kg), was administered intravenously and the rats were killed 2 h after protamine infusion. Brain specific gravity was determined in the frontal, parietal and occipital cortex and in the striatum. In separate experiments, serum albumin content was determined in the brain of rats by immunoelectrophoresis 2 h after protamine infusion with or without tirilazad pretreatment. Specific gravity was significantly higher in all of the studied brain regions in rats given tirilazad or NBQX than in those given vehicle or dixyrazine (p < 0.001). A combination of tirilazad and NBQX was significantly more efficient than either drug alone in reducing edema in the occipital cortex (p < 0.05) and more efficient than NBQX alone in the frontal and parietal cortex (p < 0.05). None of the drugs reduced the albumin content in CSF; in addition, tirilazad failed to reduce albumin extravasation in the brain and CSF when given before protamine infusion. We conclude that the anti-edematous effect of tirilazad and NBQX is related to cellular events within the brain and not to a reduction of leakage over the BBB.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"128-31"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18975708","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":"Early changes of blood-brain barrier and superoxide scavenging activity in rat cryogenic brain injury.","authors":"Y Ikeda, S Toda, M Wang, S Nakazawa","doi":"10.1007/978-3-7091-9334-1_36","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_36","url":null,"abstract":"<p><p>Cryogenic brain injury results in blood-brain barrier (BBB) disruption which may be mediated in part by oxygen free radicals. In this study, sequential changes of BBB and endogenous superoxide scavenging activity were investigated in brains subjected to cryogenic injury. 92 male Wistar rats were sacrificed at 15, 30 minutes, 1, 2, 3, 4, 6, 24 and 48 hours after the lesion. The extent of BBB disruption was determined by quantitative assessment of Evans blue (EB) uptake based on extraction from tissue using dimethylformamide. Determination of endogenous superoxide scavenging activity in the injured brain was performed by electron spin resonance spectrometry using a spin trapping agent. Superoxide scavenging activity was significantly decreased within one hour after the injury relative to normal rat brain (p < 0.05, student's t test) persisting for at least 6 hours. The EB content in the lesioned hemisphere was significantly increased within one hour after the injury relative to the normal rat brain (p < 0.01) and continued to increase for 24 hours. In conclusion, early changes of BBB and endogenous superoxide scavenging activity in rat cryogenic injured brain indicate that BBB may be an early target for oxygen free radicals in cryogenic brain injury.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"136-8"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18975710","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}