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肿瘤坏死因子及中性粒细胞在脊髓继发性损伤中的作用 总被引:2,自引:0,他引:2
目的 探讨炎性反应对脊髓损伤细胞凋亡的影响及其作用机制。方法 健康Wistar大鼠48只。随机分为2组,实验组与对照组。采用Allen法挫伤大鼠T10节段脊髓,于术后1、8h和1、2、3、7d取材。检测肿瘤坏死因子(TNF)与髓过氧化物酶水平的变化。结果 实验组肿瘤坏死因子与髓过氧化物酶水平均明显升高(P〈0.01)。结论 中性粒细胞及TNF-α参与了脊髓继发性损伤,并可能是触发迟发性神经元凋亡的重要因素之一。 相似文献
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目的:通过大鼠肝右叶血供干预分别建立肝细胞凋亡和坏死动物模型,为进一步的磁共振成像实验奠定基础。方法:选取体重为250-300克的SD大鼠90只,随机分为A、B、C三组,每组30只,分别行肝右叶门静脉和肝动脉结扎术、门静脉结扎术及假手术,各组在术后3 h及1、3、7和14 d分别处死6只大鼠,取肝脏标本送病理及电镜检查。结果: A组30只大鼠肝右叶发生凝固性坏死,光镜及电镜下均呈典型的坏死改变,TUNEL染色呈阴性;B组30只大鼠肝右叶发生小灶性凋亡,光镜下可见肝细胞核固缩改变,电镜下见肝组织核边集和凋亡小体,TUNEL染色呈阳性改变。术后3 h 即可见凋亡细胞,24 h时凋亡细胞数最多,7 d后肝组织开始发生小灶性坏死;C组30只大鼠肝右叶未发生凋亡和坏死的病理改变。结论:大鼠肝右叶门静脉和肝动脉双结扎可建立胆脏凝固性坏死模型,单纯肝右叶门静脉结扎能构建肝细胞小灶性凋亡模型。 相似文献
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股骨头缺血性坏死的CT诊断 总被引:3,自引:0,他引:3
本文报告了19例股骨头缺血性坏死的CT及多平面重建和三维CT成像表现,并探讨其对术前病变评估的价值,在显示Ⅱ期病变时CT明显优于平片,多平面重建有利于发现股骨头塌陷、关节间隙改变和髋臼改变,三维CT可作为一种补充检查手段。 相似文献
5.
当归或三七对兔甘油致急性肾衰的保护作用及其机制研究 总被引:14,自引:1,他引:13
目的:用甘油复制兔急性肾小管坏死(ATN)模型,观察当归、三七对ATN的保护作用,并初步探讨其机制。方法:40只健康新西兰白色家兔,等分为四组:当归组、三七组、对照组、正常组。当归、三七、对照三组均用50%甘油等渗盐水15ml/kg注入兔双后肤皮下,复制ATN模型,当归组于注射甘油后即刻,第3小时,第6小时,肌注当归注射液50mg/kg,三七组于相同时点肌注三七皂甙50mg/kg,正常组则于兔双后肢皮下注射生理盐水15ml/kg,并于相同时点注射5%葡萄糖注射液。于实验第24小时取血液、尿液和肾脏,检测血清尿素氮、肌酐、尿液总渗透压、尿总氨基酸、肾组织MDA、SOD、GSH—PX、ATP酶、Ca2^ 、肾组织病理形态学检查。结果:各组与正常组比,肌酐、尿素氮明显升高,说明模型复制成功。当归、三七纪元l例死亡,对照组死士率为30%,血清肌酐、尿素氮、丙二醛、尿总氨基酸、滤过钠排泄分数和肾组织钙含量均明显低于对照组(P<0.01),而肾组织ATP酶、SOD、GSH-PX活性均高于对照组(P<0.01),病理形态学变化轻于对照组。以上指标,当归与三七组无显著差异(P>0.05)。结论:当归、三七对甘油所致的ATN有明显保护作用,二者效果无差异,其机制可能与二者均有改善微循环、血液流变学、抑制脂质过氧化反应、保护肾脏抗氧化酶和ATP酶活性及减轻肾组织钙超载有关。 相似文献
6.
Summary Flurothyl-induced status epilepticus was studied by light and electron microscopy (LM, EM) to determine the time course and structural features of neuronal necrosis in the vulnerable brain regions in epilepsy. The cerebral cortex, hippocampus and thalamus were examined after closely spaced recovery periods of up to 1 week. The results showed that acidophilic neurons appeared simultaneously in neurons of the neocortex, hippocampus and thalamus, and that this occurred within 1 h following the end of the epilepsy. The corresponding features of acidophilic neurons by EM were mitochondrial flocculent densities and large discontinuities in cell and nuclear membranes. Dark neurons were ubiquitous during the epilepsy, but recovered almost universally. A few dark neuronal forms persisted and underwent cytorrhexis after 12-h recovery or longer. Axon-sparing dendritic lesions characteristic of excitotoxic neuronal death were found in the neuropil of the neocortex, and in both vulnerable CA1 and resistant CA3 neurons of the hippocampus. Other than acute edema, glial changes were absent. The findings support an excitotoxic mechanism in epilepsy-induced selective neuronal necrosis also in brain regions outside the hippocampus, and contrast with previous reports in ischemia and hypoglycemia in that neuronal necrosis occurs virtually immediately after an epileptic insult. No maturation of cell damage, as described in ischemia, was seen. Furthermore, even exceedingly dark neuronal forms and massive dendritic swelling must be considered sub-lethal or prelethal cellular changes. Lethal cellular changes include acidophilia by LM, cell membrane breaks, and mitochondrial flocculent densities by EM.Supported by the Alberta Hertage Foundation for Medical Research, the Swedish Society of Medicine, the Swedish Medical Research Council, the Magnus Bergvall Foundation, and the Research Funds of the Karolinska Institute. 相似文献
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Ultrastructural confirmation of neuronal protection by melatonin against the neurotoxin 6-hydroxydopamine cell damage 总被引:9,自引:0,他引:9
6-Hydroxydopamine (6-OHDA) is a neurotoxin used in the induction of experimental Parkinson's disease in both animals and cultured neuronal cells. Biochemical and molecular approaches showed previously that low doses of 6-OHDA induced apoptosis in PC12 cells, while high doses of this neurotoxin induced necrosis. Melatonin has been shown to protect against the neuronal programmed cell death induced by 6-OHDA, although it was not able to prevent the massive necrotic cellular death occurring after the addition of high doses of the neurotoxin. In the present work, we demonstrate by ultrastructural analysis that although low doses of 6-OHDA induced apoptosis in PC12 cells, it also damaged the non-apoptotic cells, morphologically corresponding this damage to incipient and reversible necrotic lesions. When the doses of the neurotoxin increase, there are still apoptotic cells, although most of the cells show necrotic irreversible lesions. We also found that melatonin partially prevents the incipient necrotic lesions caused by low doses of 6-OHDA. The fact that melatonin was shown in previous work to prevent apoptosis caused by low doses of 6-OHDA, but not necrosis induced by high doses of the neurotoxin, seemed to indicate that this agent is only able to protect against apoptosis. However, our present results, melatonin preventing also the incipient necrotic neuronal lesions, suggest that this hormone may provide a general protection against cell death, suggesting that higher doses should be tried in order to prevent the necrotic cell death induced by high doses of the neurotoxin. 相似文献
9.
M. Melikoglu S. Apaydin V. Hamuryudan S. Yurdakul N. Uygun H. Aki G. Ozbay Dr. H. Yazici 《Clinical rheumatology》1996,15(5):498-500
Summary A patient with end stage renal disease developed ischaemic skin necrosis and digital gangrene. He had diffuse arterial calcification associated with hyperparathyroidism secondary to renal failure. The patient received inappropriate cyclophosphamide therapy as he had been misdiagnosed as having an inflammatory vasculitis. This clinical picture, previously named calciphylaxis should come into the differential diagnosis of systemic vasculitis in a uraemic patient with hyperparathyroidism. 相似文献
10.
Summary A study of nine cases of post-traumatic avascular necrosis of the head of the humerus is presented with a review of 60 cases previously published. Onset of symptoms begins between one and two years after fracture. Pain and stiffness are the principal features. The clinical picture eventually stabilises with decreasing pain and variable loss of movement. The chief radiological changes are sclerosis and a snow-cap appearance of the head or a characteristic spanner-shaped deformity. The possible causative factors are listed and the importance of associated vascular damage emphasised. Conservative treatment is usually adequate but prosthetic replacement of the head may be indicated.
Résumé Les auteurs analysent 60 cas de nécrose post-traumatique de la tête humérale publiés dans la littérature, auxquels ils ajoutent neuf cas personnels.Ils soulignent le rôle des facteurs combinés dans la pathogénie parmi lesquels le facteur vasculaire est le plus important. Après 1 à 2 ans de latence, les manifestations cliniques apparaissent et vont évoluer lentement vers une certaine stabilisation, en particulier des phénomènes douloureux, souvent intenses au début, mais au prix d'une raideur résiduelle quasi constante. La radiologie reconnaît deux types principaux d'image:condensation en calotte de neige;déformation en clé anglaise de la tête humérale;la glène restant très longtemps indemne.Le traitement, le plus souvent médical, devrait peut-être ressortir de la chirurgie par prothèse type Neer, qui pourrait dans les types les plus graves, être placée préventivement.相似文献