奥力保克防治蛛网膜下腔出血后脑血管痉挛的临床观察

目的探讨奥力保克对蛛网膜下腔出血（SAH）后脑血管痉挛（CVS）的治疗作用。方法将42例蛛网膜下腔出血住院患者随机分成两组,奥力保克组（20例）和对照组（22例）。两组均于发病48 h内接受治疗,对照组用脱水、止血等常规疗法;奥力保克组在常规疗法基础上加用奥力保克5.0 mg,3次/d,口服,共3-4周。结果1个月内,奥力保克组的CVS发生率、死亡率明显低于对照组（P〈0.05）,再出血发生率两组比较无明显差异（P〉0.05）。结论奥力保克防治SAH后CVS疗效确切,并能促进神经功能的尽快恢复,且无增加再出血的危险。     

蛛网膜下腔出血对皮质神经元超微结构的影响

目的探讨蛛网膜下腔出血(SAH)对皮质神经元超微结构的影响。方法将25只大耳白兔随机分为5组:A组(空白对照组)、B组、C组、D组、E组(实验组)。以脑池内血液注入法制作SAH模型。对A组动物脑枕大池内注入生理盐水,对B、C、D、E组动物注入自体鲜血。分别于术后1d(B组)、3d(C组)、5d(D组)及7d(E组)处死实验组动物及对照组动物,立即取颞叶的大脑皮质分别行光镜和电镜,观察,了解其形态学及细胞超微结构的变化。结果B组的神经元大部分保持完好,部分细胞有轻度的水肿。C组、D组、E组的神经元有明显的破坏,出现超微结构的改变,核固缩、浓染。实验组动物均有皮质细胞密度的减少,B组皮质细胞密度低于C组、D组、E组(P<0.05)。结论SAH可引起迟发性神经元死亡。     

仿真3D-CT血管内镜对脑动脉瘤的诊断价值及临床意义

目的:评价应用仿真3D-CT血管内镜对以蛛网膜下腔出血(SAH)为首发症状的脑动脉瘤的诊断价值。方法:自发性SAH患者46例,均行多层面螺旋CT三维血管造影(3D-MSCTA)和数字减影血管造影(DSA)检查,31例接受手术治疗。3D-MSCTA采用遮盖容积重建(SVR)、多层面重建(MPR)和仿真3D-CT血管内镜(Fly-around、Fly-through)三种后处理技术。所得3D-MSCTA图像和DSA图像采用双盲法进行评价。结果:46例患者经Fly-around成像检出37例共有脑动脉瘤39个,经DSA和(或)手术证实均准确(真阳性),漏检1个动脉瘤(假阴性)。另9例SVR、Fly-around和DSA均未检出动脉瘤(真阴性)。敏感性为98%,特异性100%,准确性98%。用SVR成像共检出上述39个动脉瘤中的37个。DSA检出37例38个动脉瘤。SVR、Fly-around、DSA三者检出率分别为93%、98%、95%。它们之间的差异无统计学意义。Fly-through图像显示动脉瘤内附壁血栓形成6个。结论:仿真3D-CT血管内镜诊断脑动脉瘤敏感性高、准确性高,对疑诊脑动脉瘤者可首选3D-MSCTA检查,且应把仿真3D-CT血管内镜列为常规检查;仿真3D-CT血管内镜能显示动脉瘤腔内血栓形成。     

Mechanisms of apoptosis induced by purine nucleosides in astrocytes

Astrocytes release adenine-based and guanine-based purines under physiological and, particularly, pathological conditions. Thus, the aim of this study was to determine if adenosine induced apoptosis in cultured rat astrocytes. Further, if guanosine, which increases the extracellular concentration of adenosine, also induced apoptosis determined using the TUNEL and Annexin V assays. Adenosine induced apoptosis in a concentration-dependent manner up to 100 microM. Inosine, hypoxanthine, guanine, and guanosine did not. Guanosine or adenosine (100 microM) added to the culture medium was metabolized, with 35% or 15%, respectively, remaining after 2-3 h. Guanosine evoked the extracellular accumulation of adenosine, and particularly of adenine-based nucleotides. Cotreatment with EHNA and guanosine increased the extracellular accumulation of adenosine and induced apoptosis. Inhibition of the nucleoside transporters using NBTI (100 microM) or propentophylline (100 microM) significantly decreased but did not abolish the apoptosis induced by guanosine + EHNA or adenosine + EHNA, respectively. Apoptosis produced by either guanosine + EHNA or adenosine + EHNA was unaffected by A(1) or A(2) adenosine receptor antagonists, but was significantly reduced by MRS 1523, a selective A(3) adenosine receptor antagonist. Adenosine + EHNA, not guanosine + EHNA, significantly increased the intracellular concentration of S-adenosyl-L-homocysteine (SAH) and greatly reduced the ratio of S-adenosyl-L-methioine to SAH, which is associated with apoptosis. These data demonstrate that adenosine mediates apoptosis of astrocytes both, via activation of A(3) adenosine receptors and by modulating SAH hydrolase activity. Guanosine induces apoptosis by accumulating extracellular adenosine, which then acts solely via A(3) adenosine receptors.     

Early cerebral hyperglycolysis after subarachnoid haemorrhage correlates with favourable outcome

Summary.  Background: Intracerebral microdialysis (MD) was applied in patients with severe subarachnoid haemorrhage treated in a neurosurgical intensive care unit in order to explore their cerebral energy metabolism.  Method: Brain MD fluid levels of glucose, lactate and pyruvate were measured for 3 to 12 days in 20 patients and 2,635 hourly samples were analysed. The MD data were related to computerized tomography and clinical outcome, assessed by the Glasgow Outcome Scale.  Findings: The study showed that most patients who made a good recovery had a specific curve pattern when plotting the studied metabolites over time, characterised by a distinct decrease in MD-glucose and a parallel increase in both MD-lactate and pyruvate. Patients who had an unfavourable outcome lacked this distinct curve pattern and exhibited more irregular changes, including increased levels of both MD-glucose and lactate and low MD-pyruvate levels.  Interpretation: This exploratory study suggests that accumulation of interstitial lactate and pyruvate, together with decreasing levels of glucose is a favourable prognostic pattern presumably reflecting increased glucose metabolism. Such hyperglycolysis may be elicited in patients with recovery potential to cope with an extreme metabolic demand set in motion by a brain insult to restore brain cell homeostasis and integrity. Published online October 31, 2002 Acknowledgments  The authors are grateful to Ms Karin Wettervik and Ms Monica Edberg for technical help. The study was supported by the Faculty of Medicine, Uppsala University, the Swedish MRC (proj no. 7888), The Selander Foundation, The ?hlén Foundation and The King Gustaf V and Queen Victoria's Foundation. Correspondence: Dr. Lennart Persson, Department of Neurosurgery, Uppsala University Hospital, SE-751 85, UPPSALA, Sweden.     

蛛网膜下腔出血后血浆和脑脊液ET、CGRP变化与脑血管痉挛的关系

目的：观察伴和不伴脑血管痉挛蛛网膜下腔出血患者血浆与脑脊液中ET和CGRP浓度的变化。方法：根据是否合并脑血管痉挛，将53例蛛网膜下腔出血患者分为有症状脑血管痉挛组、无症状脑血管痉挛组和非痉挛组。72h、1W、2W、3W和4W时分别抽血和采取脑脊液，对照组为无神经系统疾病、免疫系统疾病与免疫相关疾病的外科手术病人，分别测定血浆和脑脊液中ET和CGRP含量。结果：出血后。3组患者血浆和脑脊液ET逐渐增加，1-2W时达最高，随后含量又逐步降低，而血浆和脑脊液CGRP逐渐降低，1-2W时降到最低，随后含量又逐步升高：1W、2W、3W时痉挛组血浆和脑脊液中CGRP含量较非痉挛组明显降低，而ET含量较非痉挛组明显增高。结论：蛛网膜下腔出血后血浆和脑脊液ET升高与CGRP含量降低可能是引起脑血管痉挛的重要因素。     

尼莫同治疗重型颅脑损伤合并蛛网膜下腔出血临床疗效评价

目的 评价尼莫同治疗重型颅脑损伤合并外伤性蛛网膜下腔出血的临床疗效.方法 将60例合并外伤性蛛网膜下腔出血的重型颅脑损伤患者随机分为尼莫同组和对照组,尼莫同组予以尼莫同40mg 24h微泵维持匀速静脉注射,疗程10d,后改为尼莫同片60mg,每天4次.疗程15d.对照组除未给予尼莫同外其他治疗相同.记录两组入院后10d GCS评分及监测7d的颅内压变化,行统计学分析;治疗后6个月时对两组GOS评分及脑积水、脑梗死等并发症的发生率进行比较,行统计学分析.结果 尼莫同组GCS评分从治疗第4天始明显高于对照组(P＜0.05);尼莫同组颅内压在前3d略高于对照组,但不存在统计学差异(P>0.05),自治疗后第4天始则明显低于对照组(P＜0.05);尼莫同组脑梗死、脑积水发生例数明显少于对照组,迟发性出血例数略多于对照组,但两组无统计学差异(P>0.05);治疗后6个月GOS评分尼莫同组明显优于对照组,两组存在统计学差异(P<0.01).结论 尼莫同对重型颅脑损伤合并外伤性蛛网膜下腔出血有明显的治疗作用.     

Effect of acute betaine administration on hepatic metabolism of S-amino acids in rats and mice

Alterations of hepatic glutathione level by betaine were observed previously. In this study effects of betaine administration (1000 mg/kg, i.p.) on S-amino acid metabolism in rats and mice were investigated. Hepatic glutathione level decreased rapidly followed by marked elevation in 24 hr. Concentrations of S-adenosylmethionine, S-adenosylhomocysteine, and methionine were increased whereas cystathionine decreased significantly, suggesting that homocysteine generated in the methionine cycle is preferentially remethylated to methionine rather than being utilized for synthesis of cysteine. Hepatic cysteine concentration declined immediately, but plasma cysteine increased. Effect of betaine on hepatic cysteine uptake was estimated from the difference in cysteine concentration in major blood vessels connected to liver. Cysteine concentration either in the portal vein or abdominal aorta was not altered, however, a significant increase was noted in the hepatic vein, indicating that hepatic uptake of cysteine was decreased by betaine treatment. Activities of glutamate cysteine ligase, cystathionine beta-synthase, and cystathionine gamma-lyase were elevated in 24 hr. Pretreatment with propargylglycine, an irreversible inhibitor of cystathionine gamma-lyase, did not abolish the betaine-induced reduction of hepatic glutathione in 4 hr, however, the elevation at t=24 hr was blocked completely. In conclusion the present results indicate that betaine administration induces time-dependent changes on hepatic metabolism of S-amino acids. Betaine enhances metabolic reactions in the methionine cycle, but inhibits cystathionine synthesis and cysteine uptake, leading to a decrease in supply of cysteine for glutathione synthesis. Reduction in glutathione is subsequently reversed due to induction of cysteine synthesis and glutamate cysteine ligase activity.     

巴曲酶鞘内注射防治犬蛛网膜下腔出血后迟发性脑血管痉挛的实验研究

目的　探讨巴曲酶鞘内注射防治蛛网膜下腔出血后迟发性脑血管痉挛 (SAH DCVS)及其所致脑水肿的作用。方法　“枕大池二次注血法”建立犬SAH DCVS动物模型 ,采用DSA等方法动态观察了巴曲酶鞘内注射对犬SAH DCVS的脑血管口径大小的影响 ,干湿法测定脑组织含水量变化。结果　巴曲酶组在枕大池注血后 7d脑血管口径显著大于单纯注血组 (P <0 .0 1 ) ,而脑组织含水量则显著低于单纯注血组 (P <0 .0 1 )。结论　巴曲酶可以防治SAH DCVS及其所致的脑水肿