Glucose levels and outcome after subarachnoid hemorrhage

In a cohort of 337 patients with subarachnoid hemorrhage (SAH), we investigated the relationship between blood glucose levels, baseline characteristics, and outcome by means of Student's t-test and multivariate logistic regression. The mean glucose levels on admission and from day 1 to 10 were significantly higher in patients with poor condition on admission and in patients with poor outcome. In a multivariate analysis, glucose level on admission was not an independent predictor of outcome. Hyperglycemia may be a link in the association between poor condition on admission and poor outcome.     

大鼠脑出血后脑组织MMP-2、MMP-9 表达的实验研究

目的　探讨大鼠脑出血后不同时程脑组织中的基质金属蛋白酶 - 2 ( MMP- 2 )、基质金属蛋白酶 - 9( MMP- 9)的表达及其规律。方法　采用立体定向技术制作大鼠脑出血模型 ,在脑出血后不同时间分别断头取脑 ,免疫组化法测定脑组织 MMP- 2、MMP- 9的表达量。结果　 ( 1)与假手术对照组比较 ,脑出血后 6 h血肿周围可见到微血管内皮表达 MMP- 9( P<0 .0 1) ,48h达高峰 ,至 5～ 7d后下降 ,但仍高于假手术对照组 ( P<0 .0 1) ,2周时降至零表达 ;12～ 2 4h中性粒细胞亦表达 MMP- 9;( 2 ) MMP- 2的表达要迟于 MMP- 9,2 4h可见到少量的 MMP- 2表达 ( P>0 .0 5 ) ,5～ 7d时逐渐达高峰 ( P<0 .0 1) ,主要在巨噬细胞上表达 ,2周时仍保持较高水平 ( P<0 .0 1)。结论　脑出血后出血侧血肿边缘有 MMP- 9、MMP- 2表达 ,推测 MMP- 9在急性期参与了脑水肿的形成 ,而 MMP- 2在脑出血后期可能参与了脑组织的修复.     

AQP4、MMP-2及MMP-9 mRNA在高血压脑出血中的早期表达

目的探讨水通道蛋白4(AQP4)及基质金属蛋白酶2,基质金属蛋白酶9(MMP-2, MMP-9)在高血压性脑出血后的早期表达,为临床上防止脑组织进一步损伤提供实验依据。方法应用半定量RT-PCR方法检测高血压性脑出血患者出血后24 h内血肿周围脑组织中AQP4及MMP-2、 MMP-9的表达。结果 AOP4、MMP-2及MMP-9在高血压脑出血血肿周围组织中其相对表达量明显升高,相对表达量分别为0．517±0．028、0．502±0．054和1．003±0．013,与正常对照组0．021±0．004、 0．271±0．103和0．239±0．021相比差异均具有显著性(P<0．001)。结论 AQP4、MMP-2及MMP-9的早期上调表达在高血压性脑出血后早期脑水肿的发生、发展过程中具有重要的作用。     

自发性蛛网膜下腔出血后血液及脑脊液纤溶活性的研究

目的探讨自发性蛛网膜下腔出血(SAH)后血及脑脊液(CSF)中纤溶活性的变化规律及正常CSF中的纤溶状态。方法组织型纤溶酶原激活物的活性(tPA:A)及纤溶酶原抑制物的活性 (PAI:A)测定采用发色底物法,纤溶酶原抑制物-1(PAI-1)及D-二聚体(D-D)定量测定采用酶联免疫吸附试验(ELISA)双抗体夹心法,血及CSF标本在SAH后0-3 d(急性期),4-9 d(再出血高峰期),及 14-21 d(吸收期)留取三次;正常对照组留取一次。结果 SAH患者血液中,急性期tPA:A显著低于对照组,并随病程延长显著升高,至14-21 d达正常水平,与对照组差异无显著意义;急性期PAI:A 及D-D水平显著高于对照组,并随病程延长而显著降低,至14-21 d降至正常水平,与对照组差异无显著意义;各期PAI-1含量与对照组差异无显著意义。对照绀CSF中,测不到tPA:A及PAI:A及 PAI-1,D-D测得值很小,为(0．28±0．36)mg/L。 SAH患者CSF中,各期测不到tPA:A及PAI:A,但 PAI-1含量急性期显著升高并随病程延长而显著降低,D-D急性期显著升高并随病程延长而显著降低,至14-21 d 与对照组无显著性差异。结论 SAH后血中不存在纤深活性亢进。对照组CSF中不含有纤溶酶系。SAH患者CSF中纤溶活性急性期升高而后降低,于14-21 d恢复到正常水平。再出血高峰期血及CSF中反映纤溶活性的指标变化均显著低于急性期,提示再出血与血及CSF中纤溶活性无关。故SAH后不宜长期大剂量应用抗纤溶药物来预防再出血。     

Gender disparities in serum electrolytes levels after subarachnoid hemorrhage.

We retrospectively studied 133 patients with subarachnoid hemorrhage (SAH) to assess whether there was any gender disparity in serum electrolytes levels throughout the clinical course. Serum concentrations of sodium and potassium were measured in all patients, while catecholamines or antidiuretic hormone were assessed in a number of cases. Female SAH-patients had lower potassium level (3.29 +/- 0.47 mEq/L) than did male patients (3.68 +/-0.38) on the first day of SAH. This gender disparity continued to the beginning of the chronic phase and disappeared several months later. Mean serum sodium level was lower in the male group than in the female group throughout the clinical course. Mean serum levels of adrenaline and antidiuretic hormone were characterized by their prominent high value on the first day. Serum potassium levels were inversely related to serum levels of catecholamines, especially adrenaline, during the acute and subacute phases, particularly on the first day.     

MMP-9对大鼠脑出血后DCX表达的影响

目的 探讨脑出血后MMP-9对大鼠神经修复的影响.方法 采用立体定向技术制作 大鼠脑出血模型,用免疫组化方法测定脑出血后血肿周围及SVZ区DCX及MMP-9表达.结果 与对照组(MMP-9:116.865±5.126;DCX:121.34±2.76)相比,在第14天时脑出血组MMP9、DCX表达最强,灰度值最小(MMP-9:102.801±2.422,P＜0.05;DCX:110.58±2.29,P＜0.05),干预组较脑出血组表达弱,灰度值增大(MMP-9:109.31±2.13,P＜0.05;DCX:115.50±3.12,P＜0.05).结论 脑出血恢复期MMP-9可能是促进神经再生因子,多西环素能通过调节MMP-9的表达与活性影响神经再生.     

大鼠脑出血后MMP-9对血管生成影响

目的 探讨脑出血后MMP-9对血管生成的影响.方法 采用立体定向技术作大鼠脑出血模型,用免疫组化方法测定脑出血后CD34阳性新生微血管及MMP-9表达.结果 MMP-9阳性区平均灰度值高CD34阳性新生血管较多.结论 脑出血后MMP-9可能是促血管生成因子,强力霉素能通过调节MMP-9的表达与活性影响血管生成.     

Acute decrease in cerebral nitric oxide levels after subarachnoid hemorrhage.

Disturbances in the nitric oxide (NO) vasodilatory pathway have been implicated in acute vasoconstriction and ischemia after subarachnoid hemorrhage (SAH). The authors hypothesize that blood released during SAH leads to vasoconstriction by scavenging NO and limiting its availability. This was tested by measuring the major NO metabolites nitrite and nitrate in five different brain regions before and after experimental SAH. The basal NO metabolites levels were as follows (mean +/- SD, micromol/mg wet weight): brain stem, 0.14 +/- 0.07; cerebellum, 0.12 +/- 0.08; ventral convexity cortex, 0.22 +/- 0.15; dorsal convexity cortex, 0.16 +/- 0.11; and hippocampus, 0.26 +/- 0.17. In sham-operated animals, no effect of the nitric oxide synthase (NOS) inhibitor L(G)-nitro-L-arginine-methyl-ester (30 mg/kg) was found on NO metabolites 40 minutes after administration, but a significant decrease was seen after 120 minutes. The NO metabolites decreased significantly 10 minutes after SAH in all brain regions except for hippocampus, and recovered to control levels in cerebellum at 60 minutes and in brain stem and dorsal cerebral cortex 180 minutes after SAH, while remaining low in ventral convexity cortex. Nitrite recovered completely in all brain regions at 180 minutes after SAH, whereas nitrate remained decreased in brain stem and ventral convexity cortex. Our results indicate that SAH causes acute decreases in cerebral NO levels by a mechanism other than NOS inhibition and provide further support for the hypothesis that alterations in the NO vasodilatory pathway contribute directly to the ischemic insult after SAH.     

蛛网膜下腔出血继发癫痫发作

目的　探讨蛛网膜下腔出血继发癫痫的临床特点。方法　回顾性分析近 2 0年来经腰穿及CT证实的 2 84例蛛网膜下腔出血患者中 3 6例继发性癫痫的临床资料。结果　蛛网膜下腔出血继发癫痫的发病率为 12 68% (3 6/2 84) ,其中全身性强直 -阵挛发作占 61 11% (2 2 /3 6) ,简单部分性运动发作占 19 44(7/3 6) ,复杂部分性运动发作占 19 44% (7/3 6) ;2周内癫痫发作 3 3例 ,其中以癫痫为首发症状 16例 ,18例临时用过抗癫痫药 ;2周后癫痫发作的 3例 ,需长期服抗癫痫药。结论　蛛网膜下腔出血较易继发癫痫 ,且与出血量及出血部位密切相关 ;早期发作较易控制 ,晚期发作较难控制 ,需长期服用抗癫痫药。     

CXCR2 antagonism attenuates neuroinflammation after subarachnoid hemorrhage

ObjectivesOveractivation of neuroinflammation can worsen the prognosis of subarachnoid hemorrhage (SAH) patients. CXCR2 is a widely expressed G protein-coupled receptor that participates in the regulation of inflammation, indicating a potential role of CXCR2 in SAH.Materials and methodsHerein, we examined the expression pattern of CXCR2 in the ipsilateral brain tissue of SAH mice. Then, we evaluated the effects of CXCR2 antagonist on neuroinflammation and neurological function after SAH.ResultsWestern blotting and immunohistochemistry revealed that CXCR2 expression was upregulated following SAH. Our results demonstrated that treatment with SB225002 inhibited inflammatory cytokine (IL-1β, IL-6, TNF-α, MCP-1) production in the brain and cerebrospinal fluid (CSF) following SAH. Our further findings confirmed that treatment with SB225002 ameliorated astrocytosis and microgliosis after SAH. Interestingly, SB225002 significantly improved neurological impairment after SAH.ConclusionsAltogether, these results suggest that pharmacologically targeting CXCR2 may be an effective disease-modifying treatment for SAH.     

A survey of blood pressure parameters after aneurysmal subarachnoid hemorrhage

Purpose/aim: Blood pressure (BP) regulation is recommended following aneurysmal subarachnoid hemorrhage (aSAH) to prevent re-bleeding and to treat delayed cerebral ischemia. However, optimal BP thresholds are not well established. There is also variation with regard to the BP component (e.g. systolic vs. mean) that is targeted or manipulated. Materials and methods: An 18-question survey was distributed to physicians and advanced practitioner members of the Neurocritical Care Society. Respondents were asked which BP parameter they manipulated and what their thresholds were in different clinical scenarios. They were also asked whether they were influenced by the presence of incidental aneurysms. Answers were analyzed for differences in training background and treatment setting. Results: There were 128 responses. The majority were neurointensivists (47 neurology and 37 non-neurology) and treated patients in dedicated neurointensive care units (n = 98). Systolic BP (SBP) was preferred over mean arterial pressure (MAP). Prior to aneurysm treatment, SBP limits ranged from 140 to 180 mm Hg. After aneurysm treatment, SBP limits ranged from 160 to 240 mm Hg. The maximum and minimum MAPs varied by as much as 50%. Nearly two-thirds of the respondents were influenced by the presence of incidental aneurysms. Training background influenced tolerance to BP limits with neurology-trained neurointensivists accepting higher BP limits when treating delayed ischemia (?p = .018). They were also more likely to follow SBP (?p = .018) and have a limit of 140 mm Hg prior to aneurysm treatment (?p = .001). Conclusions: There is large practice variability in BP management following aSAH. There is also uncertainty over the importance of incidental aneurysms. Further research could evaluate whether this variability has clinical significance.     

Trends in blood pressure, osmolality and electrolytes after subarachnoid hemorrhage from aneurysms

Daily trends in blood pressure, osmolality and electrolytes were analyzed in a series of 173 operated aneurysm cases who had subarachnoid hemorrhage (SAH) and were admitted within 4 days of the ictus. High blood pressure was associated with a greater risk of mortality and the development of clinically significant vasospasm (VSP). High osmolality shortly after admission was related to mortality but not VSP. Changes in sodium and potassium had no obvious relationship to mortality or VSP.     

Epileptic seizures after subarachnoid hemorrhage

We srudied predictive factors for the occurrence of epilepsy in 381 consecutive patients admitted within 72 hours after they had a subarachnoid hemorrhage from a reprued itracranial aneursym. Fits occurring in the presence of byponattremia or within 12 hours after the initial bleed, rebleeding, or aneurysm surgery were classifed as associated with these acute events and we did not regard these fits subsequent epileptic seizures. Thirty-five patients (9%) had one or more epileptic seizures, 12 hours to 1,761 days after the initial bleed (median value, 18 days). The following variables were included in the analysis: sex age, history of hypertension, historyof cardiovascular disease, loss of consciousness at ictus, sum score on the Glasgow Coma Scale on admission, sum score for the amount of cisternal blood and and presence of intraventricular blood based on the initial computed tomography(CT) scan, occurrence of ictal seizures (seizures occurring within 12 hours after the onset), acute hydrocephalus, rebleeding, delayed cerebral ischemia, fluid intake, treatment with tranexamic acid, ventricular drainage, and aneurysm surgery. After multivariate analysis by means of Cox proportional hazards model with stepwise forward selection of the variables, a high cisternal blood score and rebleeding proved to be significantly related to epilepsy (hazard ratio = 2.06, p = 0.040; and hazard ration = 3.02 p = 0016), even after the exclusion of 28 patients who receive perioperative prophylactic anticonvulsant therapy (hazard ratio = 2.31, P = 0.022; and hazard ratio =3.65, p = 0.006, respectively). We conclude that the frequency of epilepsy after the occurrence of subarachnoid hemorrhage is substantial and that except for rebleeding and a high cisternal blood score on the intitial CT scan, none of the investigated variables, including the occurrence of epieptic seizures within the first 12 hours following the intial bleed, are related to epilepsy.     

凝血酶对大鼠脑内MMP-9、MMP-2表达的影响

目的探讨凝血酶对大鼠脑内MMP-9、MMP-2表达的影响。方法Wistar大鼠随机分为假手术组及实验组。实验组脑内注入凝血酶,在不同时间点采用干湿重法测脑水含量,免疫组化方法检测脑内MMP-9、MMP-2的表达。假手术组注入等量生理盐水。结果脑组织水含量在凝血酶注入后6h开始增加,3d达高峰。MMP-9阳性细胞在注射凝血酶后6h即开始表达增加,与对照组相比差异显著(P<0.01),3d达高峰,随后持续下降。阳性微血管数也有相似的变化趋势。MMP-2阳性细胞在注射凝血酶后1d才开始有少量表达,后持续增多,5d达高峰,随后有所下降,但14d仍有明显表达,与对照组相比差异显著(P<0.01)。阳性微血管数也有相似的变化趋势。结论凝血酶在脑出血后脑水肿及脑组织损伤中起了关键的作用,MMP-9、MMP-2参与了急性期脑水肿、炎症反应等过程,MMP-2在损伤修复中可能有重要作用。