{"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":"Temporal profiles of Ca2+/calmodulin-dependent and -independent nitric oxide synthase activity in the rat brain microvessels following cerebral ischemia.","authors":"T Nagafuji, M Sugiyama, T Matsui","doi":"10.1007/978-3-7091-9334-1_76","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_76","url":null,"abstract":"<p><p>The present study was aimed at determining chronological alterations of Ca2+/calmodulin (CaM)-dependent and -independent nitric oxide synthase (NOS) activities in brain microvessels (MV) isolated from the affected hemisphere following an occlusion of the middle cerebral artery (MCAo) in rats. It was shown that significant enhancements of Ca2+/CaM-independent NOS activity to 922% and 920% of control level were manifested at 4 h and 24 h, respectively, which returned to the control level at 48 h after MCAo. Regarding Ca2+/CaM-dependent NOS, on the other hand, it was shown that the activity was invariably increased to 374% and 743% of control level at 48 h and 1 week following MCAo, respectively. Thus, the present study provided the first evidence that two distinct types of NOS activities were increased with different temporal patterns after MCAo. These heterogeneous alterations of NOS activities may be of critical importance for the induction of brain damage following cerebral ischemia.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"285-8"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18534025","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":"Selective increase in blood-tumor barrier permeability by calcium antagonists in transplanted rat brain tumors.","authors":"K Matsukado, T Nomura, K Ikezaki, M Fukui","doi":"10.1007/978-3-7091-9334-1_109","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_109","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"403-5"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18534028","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 G Go, F Zuiderveen, L De Ley, J G Ter Haar, L Parente, E Solito, W M Molenaar
{"title":"Effect of steroids on brain lipocortin immunoreactivity.","authors":"K G Go, F Zuiderveen, L De Ley, J G Ter Haar, L Parente, E Solito, 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":"In vivo differentiation of edematous changes after stroke in spontaneously hypertensive rats using diffusion weighted MRI.","authors":"M Takahashi, B Fritz-Zieroth, T Chikugo, H Ogawa","doi":"10.1007/978-3-7091-9334-1_60","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_60","url":null,"abstract":"<p><p>Apparent diffusion coefficients (ADCs) of tissue water were determined in chronic brain lesions of a rat stroke model, the stroke-prone spontaneously hypertensive rat, and compared with histology. ADCs increased in the order normal < edema < gliosis < cyst. The differences between individual groups were statistically significant. The increase in ADC is thought to mainly reflect a relative increase in the extracellular space in brain tissue. ADC may be a new parameter for tissue characterization.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"224-7"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18970434","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}
H Kobayashi, H Ide, T Kodera, Y Handa, M Kabuto, T Kubota, M Maeda
{"title":"Effect of mannitol on focal cerebral ischemia evaluated by magnetic resonance imaging.","authors":"H Kobayashi, H Ide, T Kodera, Y Handa, M Kabuto, T Kubota, M Maeda","doi":"10.1007/978-3-7091-9334-1_61","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_61","url":null,"abstract":"<p><p>We have evaluated the effect of mannitol on focal cerebral ischemia using T2-weighted magnetic resonance (MR) imaging and intravoxel incoherent motion (IVIM) MR imaging. The left middle cerebral artery (MCA) was exposed via the transorbital approach in 20 adult cats and occluded just proximal to the origin of the perforating arteries. Seven cats in treatment group received mannitol (0.5 g/kg i.v.) at 0, 6, 12 and 18 hours after MCA occlusion. The other 13 cats received saline and served as controls. Sequential MR coronal images were obtained at 2, 4, 6, and 24 hours after MCA occlusion using a GE Signa (1.5 tesla) system. IVIM MR imaging demonstrated ischemic cerebral injury as a sharply demarcated area at 2 hours after MCA occlusion in control group, while T2-weighted MR imaging failed to show clear evidence of the injury until 2-6 hours. At 24 hours after MCA occlusion, the infarcted area in the mannitol treatment group was 36.9 +/- 7.7% (S.E.M) of the left hemisphere, as compared to 57.3 +/- 5.3% in control group (p < 0.05). Mannitol has beneficial effect on ischemic injury.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"228-30"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18970435","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":"Histochemical demonstration of free radicals (H2O2) in ischemic brain edema and protective effects of human recombinant superoxide dismutase on ischemic neuronal damage.","authors":"H Morooka, N Hirotsune, T Wani, T Ohmoto","doi":"10.1007/978-3-7091-9334-1_82","DOIUrl":"https://doi.org/10.1007/978-3-7091-9334-1_82","url":null,"abstract":"<p><p>A new histofluorescence method by HPAA (p-hydroxyphenyl acetic acid) for free radicals in the brain tissue was devised to study neuronal damage induced by ischemia. Cerebral ischemia was produced in rats by injection of plastic microspheres and arachidonic acid (AA) into the right carotid artery. The concentration of malondialdehyde (MDA; free radical) in cerebral cortex of aminotriazol (an H2O2-dependent inhibitor of catalase) treated rats 2 h after stroke was 6.33 times the level before infarction, while the concentration of MDA in h-r SOD (free radical-scavenging enzyme) treated rats 2 h after stroke was significantly lower than in untreated rats. The histochemical findings demonstrated marked H2O2 production around blood vessels occluded by microspheres in the cerebral cortex of the aminotriazole treated rats 2 h after stroke together with disruption of the BBB. Light microscopical findings demonstrated extensive edematous changes in the aminotriazole treated rats 2 h after stroke, while pathological damage in SOD treated rat brains was absent or minimal. We conclude that free radicals are formed during ischemia, and that AA appears to be a major source of activated oxygen radicals. The findings indicate that SOD is protective against ischemia-induced neuronal damage.</p>","PeriodicalId":75393,"journal":{"name":"Acta neurochirurgica. Supplementum","volume":"60 ","pages":"307-9"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18971565","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":"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}
M Maeda, T Takachi, M Nakai, A J Krieger, H N Sapru
{"title":"Medullary cardiovascular center and acute brain swelling.","authors":"M Maeda, T Takachi, M Nakai, A J Krieger, 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, B S Carson, 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}