大鼠脑血管痉挛时血及脑组织NO,内皮素改变和银杏叶制剂？…

目的 探讨ＮＯ、内皮素（ＥＴ）与蛛网膜下腔出血（ＳＡＨ）后脑血管痉挛（ＣＶＳ）的关系和银杏叶制剂（ＧＢＥ）的防治作用。方法 对假手术组、单纯 和ＧＢＥ处理组大鼠检测２４小时内局部脑血流量、血及脑组织ＮＯ、ＥＴ含量,并测基底动脉管径及行海马病理检查。结果 ＳＡＨ造成局部脑血流量持续下降,并有基底动脉痉挛,海马ＣＡ１区神经元明显受损;血ＮＯ减少、ＥＴ增多,脑组织ＮＯ、ＥＴ均增加;ＧＢＥ使上述改变均减轻     

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目的 探讨血中的一氧化氮等自由基在急性胰腺炎（ＡＰ）及并发全身炎症反应综合征（ＳＩＲＳ）发病中的作用。方法 ３９例ＡＰ病人按有无并发ＳＩＲＳ分为有ＳＩＲＳ组及无ＳＩＲＳ组,另取５０例健康正常人作为对照组,检测血浆一氧化氮（Ｐ－ＮＯ）、血浆维生素Ｃ（Ｐ－ＶＣ）、血浆维生素Ｅ（Ｐ－ＶＥ）、血浆β－胡萝卜素（Ｐ－β－ＣＡＲ）、全血还原型谷光甙肽（ＷＢ－ＧＳＨ）的含量以及红细胞超氧化物歧化酶（Ｅ－ＳＯＤ）、红细胞过氧化氢酶（Ｅ－ＣＡＴ）的活性变化。结果 有ＳＩＲＳ的ＡＰ组较无ＳＩＲＳ的ＡＰ组Ｐ－ＮＯ的含量明显增加,而Ｐ－ＶＣ、Ｐ－ＶＥ、Ｐ－β－ＣＡＲ、ＷＢ－ＧＳＨ的含量及Ｅ－ＳＯＤ、Ｅ－ＣＡＴ的活性明显减少（Ｐ〈０．００１）;病人组与正常对照组比较得出相同的结果（Ｐ〈０．００１）。结论 体内自由基释放－清除机制和氧化机     

梗阻性黄疸兔血浆内毒素和内皮素1含量与血流动力学改变的关系

研究梗阻性黄疸内毒素血症对血管内皮细胞产生内皮素１（ＥＴ－１）的作用及ＥＴ－１与梗阻性黄应时血流动力学改变的关系。方法用肝总管结扎法建立梗阻性黄疸（ＯＪ）兔模型,偶氮显色法定量测定血内毒素含量,特异性放射免疫分析法测定血浆ＥＴ－１,生理记录仪和电磁血流计测定心率（ＨＲ）、平均动脉压（ＭＡＰ）、心输出量（ＣＯ）、肝动脉血流量（ＨＡＢＦ）、门静脉血流量（ＰＶＢＦ）、门静脉压力（ＰＶＰ）及内脏血管阻力（ＳＡＲ）。结果ＯＪ组血浆内毒素含量明显高于正常对照（ＮＣ）组;血浆ＥＴ－１低于ＮＣ组。ＯＪ组血浆内毒素与血浆ＥＴ－１含量呈负相关;ＯＪ组血浆ＥＴ－１含量与ＭＡＰ、ＨＡＢＦ、ＰＶＢＦ及ＳＡＲ呈正相关。结论梗阻性黄疽时血浆ＥＴ－１水平降低,内毒素血症不能刺激血管内皮细胞产生ＥＴ－１,血浆ＥＴ－１水平下降在系统血流动力学改变中起一定的作用。     

乙型肝炎表面抗原阳性对肾移植存活率的影响

乙型肝炎表面抗原阳性对肾移植存活率的影响黄英伟，陈统清ＩＮＦＬＵＥＮＣＥＯＦＨＢＳｓＡＧＰＯＳＩＴＩＶＥＯＮＳＵＲ－ＶＩＶＡＬＲＡＴＥＯＦＲＥＮＡＬＴＲＡＮＳＰＬＡＮＴＡＴＩＯＮ．ＨｕａｎｇＹｉｎｇｗｅｉ；ＣｈｅｎＴｏｎｇｑｉｎｇ．（ＦｉｒｓｔＰｅｏ...     

蝮蛇抗栓酶治疗肾病综合征高粘血症近期疗效观察

蝮蛇抗栓酶治疗肾病综合征高粘血症近期疗效观察徐刚，钱桐荪，徐学康ＯＢＳＥＲＶＡＴＩＯＮＯＮＳＨＯＲＴＴＩＭＥＥＦＦＥＣＴＯＦＦＵＳＨＥＫＡＮＧＳＨＵＡＮＭＥＩＩＮＴＲＥＡＴＩＮＧＢＬＯＯＤＨＹＰＥＲＶＩＳＣＯＳＩＴＹＯＦＮＥＰＨＲＯＴＩＣＳＹＮＤＲＯ...     

猪原位肝移植术中内皮素和血流动力学关系的研究

目的 探讨猪原位肝移植（ＯＬＴｘ）术中血浆内皮素（ＥＴ）与血流动力学的关系。方法 观察静脉转流组（ＶＶＢ）和无静脉转流组（ＮＶＶＢ）各６例猪ＯＬＴｘ术中ＥＴ水平和血流动力学指标改变及其相互关系。结果 复灌后ＮＶＶＢ组的ＥＴ水平比ＶＶＢ组高。血浆ＥＴ水平与ＭＡＰ、ＳＶＲ、ＰＶＰ、ＰＡＷＰ呈正相关,与ＣＯ、ＳＶ呈负相关关系。结论 ＥＴ参与猪ＯＬＴｘ术中血流动力学紊乱的病理过程,ＶＶＢ可降低ＯＬＴｘ术中血浆ＥＴ水平,有助于血流动力学稳定。     

在正常和多囊性卵巢综合征卵巢编码胰岛素样生长因子（IGF－I，II），IGF及胰岛素受体和IGF结合蛋白1－6的其基因表达及基因产物的定位

在正常和多囊性卵巢综合征卵巢编码胰岛素样生长因子（ＩＧＦ－Ｉ，ＩＩ），ＩＧＦ及胰岛素受体和ＩＧＦ结合蛋白１－６的其基因表达及基因产物的定位ＡＬＢＥＲＴＥＬ－ＲＯＥＩＹ，ＸＩＡＯＨＯＵＣＨＥＮ，ＶＥＲＯＮＩＣＡＪ．ＲＯＢＥＲＴＳＳＨＵＮＩＣＨＩＳＨＩＭ...     

内皮素及NO在严重烧伤早期胃肠粘膜缺血中的作用

目的　采用３０ ％ Ｔ Ｂ Ｓ Ａ 烧伤小型猪模型,系统观察内皮素及一氧化氮（ Ｅ Ｔ／ Ｎ Ｏ） 在胃肠缺血中的作用,并通过应用 Ｎ Ｏ 供体 Ｃ８７３７５４ 对胃肠缺血防治机制进行探讨。方法　小型猪１８只,随机分为对照组（ Ｃ 组） 、烧伤组（ Ｂ 组） 及 Ｎ Ｏ 供体组（ Ｎ 组） 。 Ｃ 组只手术不致伤,其余各组伤后按 Ｐａｒｋｌａｎｄ 公式进行复苏。 Ｎ 组在复苏同时给予 Ｃ８７３７５４（００１２５ ｍｇ·ｋｇ － １ ·ｍｉｎ － １） 。结果　烧伤后 Ｂ 组在肠道血流量下降的同时,门脉血及肠道组织中的 Ｅ Ｔ 含量迅速升高,于伤后１ｈ 达到峰值,伤后７２ｈ 未能恢复到伤前水平;而同时 Ｎ Ｏ 含量呈相反变化,二者呈显著负相关。 Ｎ 组能使肠道血流量在伤后２４ｈ 内恢复较快,同时发现能升高门脉血及肠道组织内 Ｎ Ｏ 含量。 Ｎ Ｏ Ｓｄ Ｎ Ａ Ｄ Ｐ Ｈ 染色也发现肠组织内密度明显较 Ｂ 组增加。结论　①胃肠道血流量下降与 Ｅ Ｔ／ Ｎ Ｏ 变化有关。② Ｎ Ｏ 供体能通过释放 Ｎ Ｏ,有效地改善胃肠组织血流灌注,对防治胃肠缺血有积极意义。     

肿瘤合并膜性肾病一附三例报道及近20年文献复习

肿瘤合并膜性肾病一附三例报道及近２０年文献复习陈广平，郭慕依ＴＵＭＯＲＡＳＳＯＣＩＡＴＥＤＷＩＴＨＭＥＭＢＲＡＮＯＵＳＮＥＰＨＲＯＰＡＴＨＹＣｈｅｎＧｕａｎｇｐｉｎｇ；ＧｕｏＭｕｙｉ．（ＤｅｐａｒｔｍｅｎｔｏｆＰａｔｈｏｌｏｇｙ，ＳｈａｎｇｈａｉＭｅ...     

对于严重股骨骨质溶解应用带骨水泥的CHARNLEY翻修关节成形术

对于严重股骨骨质溶解应用带骨水泥的ＣＨＡＲＮＬＥＹ翻修关节成形术ＣＥＭＥＮＴＥＤＣＨＡＲＮＬＥＹＲＥＶＩＳＩＯＮＡＲＴＨＲＯＰＬＡＳＴＹＦＯＲＳＥＶＥＲＥＦＥＭＯＲＡＬＯＳＴＥＯＬＹＳＩＳＶＶＲＡＵＴ，ＰＤＳＩＮＥＹ，ＢＭＷＲＯＢＬＥＷＳＫＩ我们对１...     

Therapeutic effects of intracarotid infusion of spermine/nitric oxide complex on cerebral vasospasm

BACKGROUND: Vasospasm is one of the underlying causes of morbidity and mortality in subarachnoid haemorrhage (SAH). The therapeutic effects of intracarotid infusion of spermine/nitric oxide complex (SPER/NO) on cerebral vasospasm in an experimental model of SAH were investigated. METHOD: Twenty-four adult male New Zealand white rabbits (2.6-3.4 kg in weight) were randomly divided into four groups (n=6), as follows: (I) control group (without SAH and drug), (II) SAH alone group (with SAH, without drug), (III) SAH placebo group (with SAH and saline), and (IV) SAH-SPER/NO group (with SAH and SPER/NO). The fresh autologous non-heparinized blood was injected into the cisterna magna to induce a SAH, after 24 hour SAH, the substance (saline or SPER/NO) was delivered to animals. All rabbits were scarified at 48-hours of induced SAH. The basilar artery with surrounding tissue was removed from the cranium and processed for paraffin embedding. Histopathological and stereological examinations of the basilar artery were done. FINDINGS: In the SPER/NO treated group of rabbits, the histopathological changes were less severe than in the SAH-alone and SAH-placebo groups. Regarding the intracarotid pressure, there was a statistically significant difference between SAH-alone and SAH-SPER/NO groups and also between SAH-SPER/NO and control groups (p<0.05). The mean cross sectional area of basilar arteries was 0.26 mm(2) in the control, whereas in SAH alone, placebo and SAH-SPER/NO groups were 0.13, 0.15 and 0.20 mm(2), respectively. INTERPRETATION: It is well known that NO is a critical substance involved in cerebral vascular dynamics. Present results indicate that treatment of vasospasm with SPER/NO in SAH may be promising. However, further studies should be done on this substance to clarify its effect on vasospasm before using the drug in clinical situations.     

Neuroprotective effect of recombinant human erythropoietin in experimental subarachnoid hemorrhage

BACKGROUND: Acute cerebral vasoconstriction and subsequent brain ischemia, often occurring in the early phase of subarachnoid hemorrhage (SAH), are critical problems in the management of patients affected by ruptured intracranial aneurysms. It is known that nitric oxide (NO) decreases during SAH with impairment of cerebrovascular relaxation, and glutamate is mainly involved in the consequent brain ischemic damage. Recently, erythropoietin (EPO) has shown to exert a neuroprotective effect during cerebral ischemia by enhancing the NO system activity. In the present study the effect of systemic administration of recombinant human erythropoietin (rHuEPO) has been investigated in a rabbit model of SAH. METHODS: Thirty-two rabbits were assigned to four groups: 1) Control; 2) SAH; 3) SAH plus placebo; 4) SAH plus rHuEPO. Experimental SAH was induced by injecting autologous blood into the cisterna magna. rHuEPO, at a dose of 1000 IU/kg, and placebo were given 5 minutes after SAH. Administration was repeated three times during 24 hours. The animals were killed 24 hours after SAH by a perfusion-fixation method. Luminal cross-sections of the basilar artery were measured by computer-assisted morphometric analysis. Ischemic injury was histologically evaluated by analysis of the frequency of ischemia-induced damaged cortical neurons. RESULTS: Administration of rHuEPO significantly reversed the vasoconstriction of the basilar artery in Group 4 compared with the other groups (p<0.05). Histological examination showed a significant reduction in total damaged neurons count in Group 4 compared with the other groups (p<0.01). CONCLUSIONS: These results suggest that rHuEPO is effective in attenuating acute cerebral vasoconstriction and ischemic brain injury following experimental SAH.     

SAH大鼠抗脑血管细胞增殖研究

目的 探讨大鼠SAH后脑血管细胞增殖变化,观察大鼠SAH后早期阻断VEGF的作用是否能减轻脑血管细胞增殖. 方法 72只Sprague-Dawley大鼠随机分为3组,假手术组枕大池注入NS,模型组采用枕大池二次注血法制作SAH模型,干预组在制作SAH模型的同时通过枕大池注入抗VEGF多克隆抗体.于SAH（或NS）后1、3、5、7天时处死动物,分离脑干（包含基底动脉）做形态学和PCNA免疫组化检查,观测三组大鼠基底动脉的形态学改变、基底动脉壁PCNA表达. 结果 在SAH后第1天基底动脉即出现明显血管痉挛,第3、5天达到高峰,第7天逐渐缓解.SAH模型组大鼠基底动脉壁PCNA表达第1天即开始升高,第3、5天达到顶峰,第7天后逐渐下降;NS假手术组基底动脉壁PCNA呈阴性表达;抗VEGF抗体干预组基底动脉壁PCNA呈低水平表达.枕大池注射抗VEGF抗体能缓解SAH后脑血管肌内膜增殖,减轻脑血管壁的增厚程度. 结论 VEGF介导的血管内膜增殖反应和脑血管壁增厚可能在脑血管痉挛的发生发展过程中起促进作用,SAH后早期应用VEGF拮抗剂能缓解脑血管细胞增殖.     

不同时间浅低温对蛛网膜下腔出血犬脑血管痉挛的影响

目的 探讨不同时间浅低温对蛛网膜下腔出血犬脑血管痉挛的影响.方法 成年健康犬30只,雌雄不拘,体重14～20 kg,采用枕骨大孔二次注血法制备犬蛛网膜下腔出血模型.随机分为5组(n=6),人工脑脊液组(ACSF组):枕骨大孔处注入ACSF 0.5 ml/ks;蛛网膜下腔出血组(SAH组):制备蛛网膜下腔出血模型,维持直肠温度38～39℃;不同时间浅低温组(H_(1～3)组):在第2次注血后分别立即实施8、16和32 h浅低温(33.5℃),随后复温至38～39℃.于第1次注血或注入ACSF前和第2次注血或注入ACSF 5、12和19 d时行整体功能分级(OPC),并采用ELISA法和硝酸还原酶法分别测定血浆和脑脊液内皮素-1(ET-1)和一氧化氮(NO)代谢产物NO_2~-/NO_3~-的浓度,采用CT血管造影动态测量脑基底动脉直径.结果 与ACSF组比较,SAH组和H_1,2组OPC分级升高,血浆和脑脊液ET-1浓度升高,NO_2~-/NO_3~-浓度降低,基底动脉直径减小(P＜0.05),H_3组上述指标差异无统计学意义(P＞0.05);与SAH组比较,H_2,3组OPC分级降低,血浆和脑脊液ET-1浓度降低,NO_2~-/NO_3~-浓度升高,基底动脉直径增大(P＜0.05),H_1组各时点上述指标差异无统计学意义(P＞0.05);与H_2组比较,H_3组血浆和脑脊液ET-1浓度降低,NO_2~-/NO_3~-浓度升高,基底动脉直径增大(P＜0.05).结论 浅低温16～32 h可缓解蛛网膜下腔出血犬脑血管痉挛,且随浅低温时间延长该作用增强,其机制可能与降低全身和脑组织ET-1水平,升高NO水平,调节脑血管收缩-舒张平衡有关.     

Dynamic expression of the suppressor of cytokine signaling-3 and cytokines in the cerebral basilar artery of rats with subarachnoid hemorrhage,and the effect of acetylcholine

Background

There are complex interactions between acetylcholine (ACh), the suppressor of cytokine signaling-3 (SOCS-3), and cytokines, however, little is known about their dynamic expression or their effects on cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH). Therefore, we aimed to describe and clarify the dynamic expression of SOCS-3 and cytokines after SAH, as well as the relationships between the levels of SOCS-3, cytokines, and ACh.

Methods

The rat model of single cisterna magna injection was used to mimic acute SAH. The degree of CVS was indicated by lumen diameter and artery wall thickness under H&E staining. A semi-quantitative immunohistochemical analysis method was used to clarify the role of SOCS-3 in the CVS after SAH. We also measured the content of IL-6 and IL-10 in cerebrospinal fluid.

Results

We found that SOCS-3 expression levels increased rapidly within 12 h after SAH, more slowly after 12 h, and did not reach a peak within 48 h. Interleukin 6 (IL-6) levels rapidly increased within 24 h after SAH, reached a peak 24 h after SAH, and decreased slightly at 48 h. IL-10 levels increased during the first 6 h after SAH, after which this increase tapered off. ACh treatment reduced IL-6 levels and resulted in elevated levels of SOCS-3, but had no effect on IL-10 expression. Furthermore, ACh treatment relieved basilar arterial vasospasm, whereas mecamylamine pretreatment counteracted the activity of ACh.

Conclusions

Taken together, these data indicate that SOCS-3 was involved in vasospasm via an IL-6- and IL-10-related mechanism, and that CVS following SAH could be reversed by the intraventricular injection of ACh.     

Elevated level of endothelin-1 in cerebrospinal fluid and lack of nitric oxide in basilar arterial plasma associated with cerebral vasospasm after subarachnoid haemorrhage in rabbits

Background  The role of endothelin-1 (ET-1) and nitric oxide (NO) as two important mediators in the development of cerebral vasospasm (CVS) after subarachnoid haemorrhage (SAH) is controversial. The objective of this study was to determine whether local levels of ET-1 and NO in cerebral arterial plasma and/or in cerebrospinal fluid (CSF) are associated with the occurrence of CVS after SAH. Methods  CVS was induced using the one-haemorrhage rabbit model and confirmed by digital subtraction angiography of the rabbits’ basilar artery on day 5. Prior to sacrifice, local CSF and basilar arterial plasma samples were obtained by a transclival approach to the basilar artery. Systemic arterial plasma samples were obtained. ET-1 levels were determined by immunometric technique (pg/ml ± SEM) and total nitrate/nitrite level spectrophotometrically (μmol/l ± SEM). Findings  Angiographic CVS was documented after SAH induction (n = 12, P < 0.05). The ET-1 level in CSF was significantly elevated by 27.3% to 0.84 ± 0.08 pg/ml in SAH animals (n = 7) in comparison to controls (0.66 ± 0.04 pg/ml, n = 7, P < 0.05). There was no significant difference in ET-1 levels in systemic and basilar arterial plasma samples of SAH animals compared to controls. A significant lack of local NO metabolites was documented in basilar arterial plasma after SAH (36.8 ± 3.1 μmol/l, n = 6) compared to controls (61.8 ± 6.2 μmol/l, n = 6, P < 0.01). Conclusion  This study demonstrates that an elevated ET-1 level in CSF and local lack of NO in the basilar arterial plasma samples are associated with CVS after experimental SAH.     

不同剂量人组织激肽释放酶对兔症状性脑血管痉挛的影响

目的 探讨不同剂量人组织激肽释放酶(HTK)对兔症状性脑血管痉挛的影响.方法 双侧颈总动脉结扎后2周无神经功能障碍的日本大耳白兔40只,体重2.0～2.5 kg,随机分为5组(n=8):对照组(C组)、症状性脑血管痉挛组(V组)和低、中、高剂量HTK组(L组、M组和H组).采用枕大池二次注血法建立兔症状性脑血管痉挛模型,V组于第1次枕大池注血后耳缘静脉注射生理盐水5 ml/d,L组、M组和H组每天分别耳缘静脉注射HTK 0.002 5、0.005 0、0.010 0 PNAU/kg,连续14 d0于枕大池注血前1 d(T_1)及注血后每天评价神经功能并记录进食量,于T_1及枕大池第1次注血后5、7、14 d(T_(2～4))时采用三维CT血管造影测定基底动脉直径,第15天时取基底动脉观察病理学结果.结果 与C组比较,V组低进食量和神经功能障碍发生率升高(P＜0.05);与V组比较,L组、M组和H组低进食量与神经功能障碍发生率降低,T_3时基底动脉直径增加,H组T_4时基底动脉直径增加(P＜0.05);与T_1时比较,V组T_(2,3)时基底动脉直径缩短(P＜0.05),L组、M组和H组T_(2,3)时基底动脉直径差异无统计学意义(P＞0.05),T_4时基底动脉直径增加(P＜0.05);与L组和M组比较,H组T_4时基底动脉直径增加(P＜0.05).结论 耳缘静脉注射HTK(0.002 5～0.010 0 PNAU/kg,连续14 d)可改善兔症状性脑血管痉挛,其效应呈剂量依赖性.     

Study the effects of zonisamide on fine structure of rabbit basilar artery and hippocampus in rabbit subarachnoid hemorrhage model

Background

In this study, we investigated the effect of a novel antiepileptic drug, zonisamide (ZNS), on the basilar artery and hippocampus in a rabbit subarachnoid hemorrhage (SAH) model.

Methods

Three groups of New Zealand white rabbits were used: a sham (non-SAH) group, an SAH?+?saline group, and SAH?+?drug treatment group that received ZNS. In the treatment group, the subjects were given ZNS for 3 days after the SAH. Hippocampal sections were evaluated for neural tissue degeneration. Basilar artery lumen areas and arterial wall thickness were also measured in all groups.

Results

The mean luminal area of the SAH?+?ZNS was significantly greater than the SAH?+?saline group. In addition, the arterial wall thickness of SAH?+?ZNS group was significantly thinner than the SAH?+?saline group. The neuronal degeneration scores of the hippocampal CA1 regions in the SAH?+?ZNS group were significantly lower than the SAH?+?saline treatment animals.

Conclusions

These results indicate that ZNS has a vasodilatatory effect on the basilar artery and a neuronal protective effect in the CA1 region of the hippocampus in a rabbit SAH model.     

蛛网膜下腔出血后脑血管痉挛与c-myc、c-fos、c-jun表达的关系

目的 通过采用兔基底动脉穿刺建立的蛛网膜下腔出血（SAH）模型，系统研究蛛网膜下腔出血后脑血管痉挛发生（CVS）的情况，脑血管痉挛的病理损害。方法应用逆转录-聚合酶链反应（RT-PCR）及免疫组织化学的方法分别检测受累动脉c-myc、c-fos、c-jun mRNA及c-myc、c-fos，c-jun蛋白表达情况。结果 SAH后CVS发生过程中，在8h后相继出现c-myc、c-fos、c-jun mRNA的明显表达，c-myc、c-fos、c-jun的蛋白表达落后于基因表达，免疫组织化学显示c-myc、c-fos、c-jun主要表达在血管内皮细胞及平滑肌细胞。基因与蛋白表达均具有明显的时间依赖性，并与病理损害程度相平行。结论 揭示SAH后CVS的发生可能与细胞凋亡的发生有关，为防治SAH后CVS提供了一个研究方向。