诱导升压对动脉瘤性蛛网膜下腔出血患者脑血流量的影响

目的本文旨在探讨对于动脉瘤性蛛网膜下腔出血患者,诱导升压对其脑血流量的影响。方法选取2015年1月至2018年12月在我院就诊的诊断为动脉瘤性蛛网膜下腔出血的患者,随机分为诱导组和对照组。分别对两组患者实行诱导升压以及无诱导操作,在24～36小时后,评估两组患者的脑血流量(CBF),同时评估两组患者的动脉血压。结果共有24名患者被纳入到本研究中,对照组和诱导组的临床资料无统计学的差异。在本研究中,在CTP1和CTP2两个时间点之间,诱导组患者的平均动脉血压为12 mmHg(95%置信区间,8.7～14.8 mm Hg),高于对照组。诱导组的所有患者在CTP2时间点时,仍然能够耐受诱导血压的升高。诱导组患者的总CBF变化为0.1(-31～43) ml/100g/min,而对照组为-8.3(-41～30) ml/100g/min,差异没有显著的统计学意义(P=0.24)。结论诱导升压对于动脉瘤性蛛网膜下腔出血患者的脑血流量无显著的统计学影响。     

复合手术治疗颅内动脉瘤破裂致蛛网膜下腔出血疗效观察

目的 对比研究复合手术与栓塞手术治疗颅内动脉瘤破裂致蛛网膜下腔出血疗效。方法 回顾性描述性研究2016年1月至2018年12月开封市中医院和河南大学第一附属医院治疗颅内动脉瘤破裂致蛛网膜下腔出血的13例复合手术与16例栓塞手术病例。结果 术后栓塞组术后发生2例脑积水、1例脑梗死、1例脑血管痉挛,复合组未发生;两组各有1例发生术后肺部感染;复合组2例发生术后颅内感染,栓塞组未发生;两组各有1例发生术后下肢深静脉血栓形成。两组均无围手术期死亡病例。两组并发症发生有统计学差异（P<0.05）。出院时复合组有4例功能障碍,栓塞组有8例功能障碍;两组出院及随访GOS分级有统计学差异（P<0.05）。栓塞组1例1年内动脉瘤再破裂出血,复合组未发生,两组有统计学差异（P<0.05）。结论 复合手术在颅内动脉瘤致蛛网膜下腔出血治疗上有一定优势。     

头颅移动CT灌注扫描对重型颅脑损伤患者的临床价值

目的 探讨移动CT灌注扫描（CTP）在重型颅脑损伤（TBI）患者中的临床应用价值。方法 2015年4~9月我院神经外科重症监护室收住重型TBI患者26例,受伤24 h之内同时进行头颅CT平扫（CT1）和移动CTP,并在5 d后复查头颅CT平扫（CT5）。CTP提供脑血流量（CBF）影像、脑血容量（CBV）影像及平均转运时间（MTT）影像;将CTP影像、CT1及CT5进行比较。结果 CTP平均在伤后（15.6±4）h进行。16例（61.5%）患者CTP影像显示灌注改变区域大于CT1显示的病灶区域,其中7例（27%）患者低灌注程度达到缺血水平。3例（11.5%）患者通过CTP扫描发现严重的脑灌注不足,尽管在CT5上并没有明显的缺血梗死表现,根据CTP结果,改变此3例患者的治疗方案,最终只有1例发生严重脑梗死,另外2例恢复良好。与CT1相比,CTP与CT5结果具有更好的一致性。结论 头颅移动CTP可以在创伤后早期对重型TBI患者的脑血流灌注情况作出较为准确的评估,为临床干预提供有力依据。     

动脉瘤性蛛网膜下腔出血后低血钾对短期预后的影响分析

目的 研究患者入院时血钾水平与动脉瘤性蛛网膜下腔出血短期预后的关系。方法 回顾性收集张家界市人民医院神经外科于2014年1月-2018年6月诊治的动脉瘤性蛛网膜下腔出血患者的临床资料,对符合纳入标准患者入院时的血钾水平、一般情况、Hunt-hess分级、白细胞计数、PCO₂、住院时间等进行有序线性回归分析,探讨血钾水平对患者短期预后的影响并阐述其可能的机制。结果 有序多因素分析结果显示：低血钾（0~3.5mmol/L）与短期预后不良有关（P<0.05）,其中0~2.9mmol/L、2.9~3.1mmol/L、3.5~5.5mmol/L（P均<0.001）,趋势P值<0.05;其他危险因素包括Hunt-hess分级为Ⅰ级、Ⅱ级、Ⅲ级,动脉瘤位于前交通动脉与后交通动脉,白细胞计数正常（P<0.05）;箱线图显示：随mRS14评分增高,血钾水平呈下降趋势,低血钾组mRS14评分的分布区间偏高。结论 血钾水平越低,短期预后不良可能性越大,导致住院时间延长。其他可能影响因素有Hunt-hess分级、动脉瘤部位、白细胞计数。     

虾青素对小鼠蛛网膜下腔出血早期脑损伤的保护机制的研究

目的 研究虾青素对小鼠蛛网膜下腔出血（SAH）早期脑损伤的保护机制。方法 ICR雄性小鼠采用随机数字法随机分为四组：蛛网膜下腔出血组、假手术组、蛛网膜下腔出血+溶剂组（DMSO）、蛛网膜下腔出血+虾青素组。通过建立小鼠视交叉注血方法建立蛛网膜下腔出血模型，于手术后24 h记录神经功能评分，并应用末端脱氧核苷酸转移酶介导的生物素脱氧尿嘧啶核苷酸缺口末端标记法（TUNEL）、western blot法检测脑组织中的NOX2蛋白含量、ELISA法检测TNF-a/IL-1β水平，干湿法检测脑组织中含水量。结果 与对照组相比，SAH后小鼠神经功能损伤评分加重，脑水肿加重，脑组织中的NOX2蛋白及脑组织中凋亡阳性细胞数也显著增多，TNF-a/IL-1β值明显升高；应用虾青素干预以后，小鼠神经功能改善，脑组织凋亡阳性细胞明显减少。同时，虾青素能够降低SAH后小鼠脑组织中NOX2蛋白，TNF-a/IL-1β水平值也明显降低。结论 虾青素对sAH后早期脑损伤（EBI）具有保护作用，其作用机制可能与其抗氧化性有关。     

多巴胺升压疗法对脑血管痉挛的评价

脑动脉瘤破裂出血患者由于血凝块及溶血物质的刺激,常可继发脑血管痉挛.尽管早期作动脉瘤根治手术,清除血肿,以及脑室清洗和引流,但发生脑血管痉挛仍难予避免,所以时常引起脑血流量(CBF)减少而发生脑缺血.又由于蛛网膜下腔出血后CBF之生理调节功能障碍,以及这些患者的脑血     

CT血管成像和CT灌注点征的联合应用在选择中等量脑出血超早期手术方式中的价值

目的 探讨联合应用CT血管成像（CTA）、CT灌注（CTP）点征在基底节中等量脑出血超早期抽吸术或开颅手术的手术方式选择中的应用价值。方法 选择中等量基底节脑出血（出血量30~60ml）且家属同意超早期手术治疗221例，根据入院后患者是否同意行颅脑CTA及CTP检查，分为研究组（同意检查者）105例，对照组（不同意检查者）116例，研究组CTA或CTP点征阳性者，入开颅手术亚组32例，CTA和CTP点征阴性者入抽吸亚组73例。对照组根据患者家属知情同意后选择的手术方式，分为开颅亚组39例，抽吸亚组77例。对比研究组与对照组患者治疗效果的差异，评估联合应用CTA、CTP点征在基底节中等量脑出血超早期手术方式选择中的应用价值。结果 研究组有效率、术后血肿增大率、病死率、颅内感染率分别为77.1%、3.8%、3.8%、2.9%，对照组分别为52.6%、18.1%、15.6%、12.1%，2组比较差异有统计学意义。（P<0.05）。结论 联合应用CTA、CTP点征选择基底节中等量脑出血手术方式，可明显改善患者预后。     

利多卡因对颅内动脉瘤夹闭术后患者呛咳、血压和心率的影响

目的 观察静脉注射利多卡因对颅内动脉瘤夹闭术患者麻醉恢复期的呛咳、躁动、血压和心率的影响。方法 前瞻性选择我院2013年8月至2014年5月开颅夹闭术治疗的颅内动脉瘤患者60例,随机分为对照组和试验组,每组30例。两组患者均给予相同药物进行麻醉诱导和麻醉维持。术毕对照组静脉注射生理盐水（0.15 ml/kg）,试验组静脉注射1%利多卡因（0.15 ml/kg）。结果 术后气管导管留置期间和拔管期间,试验组患者咳嗽评分明显低于对照组（P<0.05）,试验组拔管时间、丙泊酚和佩尔地平用量均明显少于对照组（>P<0.05）。气管导管拔管后5 min内,两组收缩压、舒张压和心率均随时间变化显著下降（P<0.05）,但均高于手术结束时（>P<0.05）,且对照组明显高于试验组（>P<0.05）。>结论 静脉注射利多卡因可降低颅内动脉瘤夹闭术患者麻醉恢复期的呛咳和躁动,减少拔管期间的血压和心率波动。     

蛛网膜下腔出血并迟发性脑血管痉挛大鼠脑能量代谢与脑血流量变化的实验研究

目的探讨实验性蛛网膜下腔出血导致的迟发性脑血管痉挛时脑能量代谢的变化规律，及其与皮质脑血流量（CBF）变化的相关性。方法50只雄性SD大鼠随机分为对照组和蛛网膜下腔出血第1、3、5、7天组．应用非抗凝自体动脉血枕大池两次注血法制备蛛网膜下腔出血大鼠模型；另5只大鼠用于颅内血液大体分布的观察。应用微透析仪监测各组大鼠脑组织间液中葡萄糖（Glu）、乳酸（Lac）及丙酮酸（Pyr）含量，并计算乳酸／丙酮酸比值；激光多普勒血流仪监测各组大鼠皮质脑血流量；于光学显微镜及透射电子显微镜下观察基底动脉血管壁的病理学改变。结果（1）5只用于观察颅内血液大体分布的大鼠中4只蛛网膜下腔出血模型鼠血液主要分布于基底池、脚间池及额叶底面，亚甲蓝与血液混合物主要沉积于颅底．同时在脑室及纵裂池亦可见血液分布；余1只注入人工脑脊液后未发生颅内出血及血液沉积。表明蛛网膜下腔出血动物模型制备成功。（2）与对照组相比，蛛网膜下腔出血组大鼠葡萄糖及丙酮酸含量明显降低（P〈0．01）；乳酸／丙酮酸比值明显升高（P〈0．01），以第5、7天组升高最为明显（P〈0．01）；第5天组乳酸含量亦明显升高（P〈0．01）。（3）激光多普勒监测显示，蛛网膜下腔出血组大鼠脑血流量减少率高于对照组（P〈0．05），其中第5天组减少最为显著。与其他各亚组比较差异有统计学意义（尸〈0．05）；脑血流量变化与乳酸／丙酮酸比值、乳酸水平的改变呈正相关（r=0．721，0．477；均P〈0．01），与葡萄糖、丙酮酸水平的改变呈负相关（r=-0．447，-0．579；均P〈0．01）。结论微透析指标与脑血流量变化具有一致性，可作为蛛网膜下腔出血脑组织间液生化指标的动态监测，用于预测迟发性脑血管痉挛的发生。     

血管紧张素转换酶基因多态性与自发性蛛网膜下腔出血后脑血管痉挛的相关性研究

目的 探讨血管紧张素转换酶（ACE）基因插入/缺失（I/D）位点多态性与自发性蛛网膜下腔出血（SAH）后脑血管痉挛（CVS）的关系。方法 166例自发性SAH患者按照是否合并CVS分为CVS组72例和对照组94例,采用ELISA法检测患者血清ACE水平,采用聚合酶链反应﹣限制性片段长度多态性法检测ACE基因I/D位点多态性。结果 SAH后13 d内血清ACE水平无显著变化（均P>0.05）。CVS组患者入院时血清ACE基线水平高于对照组（t=2.136,P=0.048）。ACE组和对照组比较,两组ACE基因I/D位点基因型和等位基因分布频率差异均具有统计学意义（χ²=7.086,P=0.029;χ²=6.080,P=0.014）。多因素logistic回归法分析结果显示对于自发性SAH患者,携带ACE基因I/D位点D等位基因是发生CVS的危险因素（OR=1.473,95%CI：1.068～2.610,P=0.021）。结论 对于自发性SAH患者,ACE基因I/D位点多态性可能与CVS发生相关。     

Changes of the plasma ketone body level and arterial ketone body ratio at the onset of mild aneurysmal subarachnoid hemorrhage

Abstract

Objective: The purpose of this study was to investigate the physiologic changes of ketone bodies in patients with aneurysmal subarachnoid hemorrhage. We tested the hypothesis that the plasma ketone bodies are associated with the vasoconstrictor and lipolysis effect of circulating catecholamine.

Methods: Twenty-four patients with mild aneurysmal subarachnoid hemorrhage and 18 healthy volunteers were enrolled in this study. We collected arterial blood samples immediately after admission and 30 days later to measure the levels of 3-hydroxybutyrate, acetoacetate, epinephrine and norepinephrine.

Result: At the onset of aneurysmal subarachnoid hemorrhage, the plasma ketone body (3-hydroxybutyrate + acetoacetate) level and the epinephrine and norepinephrine concentrations were significantly elevated, but the arterial ketone body ratio (acetoacetate/3-hydroxybutyrate) was significantly decreased compared with that of the control group. There was a negative correlation between the plasma ketone body level and the arterial ketone body ratio. There was a positive correlation between the plasma ketone body level and epinephrine level. Thirty days after admission, the ketone body, epinephrine and norepinephrine levels, as well as the arterial ketone body ratio, showed no significant differences between the patients and controls.

Conclusion: At the onset of mild aneurysmal subarachnoid hemorrhage, the plasma ketone body level was significantly increased, while the arterial ketone body ratio was significantly decreased.     

Relationship of hypotension and cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage

OBJECTIVES: Changes in systemic arterial blood pressure and the degree of cerebral vasospasm were investigated in 125 patients with aneurysmal subarachnoid hemorrhage.METHODS: Systemic arterial blood pressure was measured every 2 hours in each patient for a period of more than 2 weeks, and a fall in systemic blood pressure (FBP) was defined as a decrease of >40 mmHg of systolic blood pressure between two consecutive measurements.RESULTS: A total of 91 FBPs occurred in 52 (41.6%) of 125 patients despite specific post-operative management to prevent hypovolemia. Five (5.5%) of the 91 FBPs occurred just before the onset of symptomatic vasospasm. Symptomatic vasospasm was observed in 36 (69.2%) of 52 patients with FBP and in 32 (43.8%) of 73 patients without FBP (p<0.01, chi-squared test). A hypodense area on computed tomographic scans in association with cerebral vasospasm was observed in 25 (48.1%) of 52 patients with FBP and in 21 (28.8%) of 73 patients without FBP (p<0.05).DISCUSSION: We conclude that FBP might result from delayed cerebral vasospasm and/or brain dysfunction owing to subarachnoid hemorrhage itself.     

The effect of low dose dopamine on CBF in patients with subarachnoid hemorrhage

Cerebral blood flow was measured in 10 patients with subarachnoid hemorrhage using the 133Xe inhalation methods. Regional cerebral blood flow (r-CBF) values were calculated with initial slope index, their values were compared with the blood flow response to the administration of low dose dopamine (DA). CBF values of just after and continuous administration of DA were compared with control values. The measurement of r-CBF was performed immediately after the infusion of 5 micrograms/kg/min DA for 30 min. The focal ischemic lesions decreased, bi-hemispheric mean CBF value (7 cases without A-Com patients) increased by 10.3% significantly (paired T test), affected hemispheric mean CBF value increased by 8.7% significantly and non-affected hemispheric mean CBF value increased by 16.6% significantly. The PaCO2 value didn't change but the mean systemic blood pressure increased by 5.1% significantly. The CBF values of continuous administration of DA for 10 days to 2 weeks were measured. The CBF values increased during the administration of DA. The mean CBF values increased without the steal phenomenon and the mean arterial blood pressure increased slightly after the administration of DA. These phenomena were observed more significantly in non affected side than affected side. We suggest that the administration of DA increase the CBF values in patients with subarachnoid hemorrhage due to the stimulation of DA receptor.     

Autoregulation of cerebral blood flow surrounding acute (6 to 22 hours) intracerebral hemorrhage.

BACKGROUND: Arterial hypertension is common in the first 24 hours after acute intracerebral hemorrhage (ICH). Although increased blood pressure usually declines to baseline values within several days, the appropriate treatment during the acute period has remained controversial. Arguments against treatment of hypertension in patients with acute ICH are based primarily on the concern that reducing arterial blood pressure will reduce cerebral blood flow (CBF). The authors undertook this study to provide further information on the changes in whole-brain and periclot regional CBF that occur with pharmacologic reductions in mean arterial pressure (MAP) in patients with acute ICH. METHODS: Fourteen patients with acute supratentorial ICH 1 to 45 mL in size were studied 6 to 22 hours after onset. CBF was measured with PET and (15)O-water. After completion of the first CBF measurement, patients were randomized to receive either nicardipine or labetalol to reduce MAP by 15%, and the CBF study was repeated. RESULTS: MAP was lowered by -16.7 +/- 5.4% from 143 +/- 10 to 119 +/- 11 mm Hg. There was no significant change in either global CBF or periclot CBF. Calculation of the 95% CI demonstrated that there is less than a 5% chance that global or periclot CBF fell by more than -2.7 mL x 100 g(-1) x min(-1). CONCLUSION: In patients with small- to medium-sized acute ICH, autoregulation of CBF was preserved with arterial blood pressure reductions in the range studied.     

Subarachnoid blood infusion versus raised intracranial pressure: effects on the amino acid pattern in the extracellular fluid of the rabbit hippocampus.

In order to evaluate the role of a hemorrhage versus that of a transient increase in intracranial pressure in subarachnoid hemorrhage, the two components were induced separately in rabbits. Extracellular glutamate, sampled from the hippocampus with microdialysis, was used to evaluate the degree of CNS tissue damage. In four rabbits, autologous arterial blood was infused in the cisterna magna in a volume that would not affect the intracranial pressure. The other group of animals was infused with saline to elevate the intracranial pressure from 10 to > 100 mmHg. The increase of intracranial pressure per se did not induce significant changes in extracellular glutamate. However, 20-60 min after infusion of blood, a significant glutamate increase was recorded. Furthermore, aspartate, alanine, glycine and serine were also raised. The results indicate that blood in the subarachnoid space damages the brain primarily by inducing ischemia. Furthermore, the parameters employed gave no indication that an increase in intracranial pressure had a deleterious effect on CNS tissue.     

Critical care of intracerebral and subarachnoid hemorrhage

The acute management of primary intracerebral or aneurysmal subarachnoid hemorrhage requires a comprehensive approach involving stabilization of the patient, surgical intervention, and continued intensive care treatment of medical and neurologic complications. The are several causes of intracerebral hemorrhage (ICH), including hypertension, cerebral amyloid angiopathy, sympathomimetic drugs, and coagulopathies. More recently, use of thrombolytic agents in the treatment of acute ischemic stroke has increased the risk of ICH. Treatment of intracerebral hemorrhage is based on blood pressure control, and, in selected cases, surgical evacuation of clot. Patients with aneurysmal subarachnoid hemorrhage may experience rebleeding, symptomatic vasospasm, or hydrocephalus. Medical management in the intensive care unit with careful attention to fluid and electrolyte balance, nutrition, cardiopulmonary monitoring, and close observation for changes in the neurologic exam is vital. This review examines the diagnosis and intensive care management of patients with intracerebral or subarachnoid hemorrhage, and reviews some of the newer therapies for treatment of these disorders.     

Subarachnoid blood infusion versus raised intracranial pressure: Effects on the amino acid pattern in the extracellular fluid of the rabbit hippocampus

Abstract

In order to evaluate the role of a hemorrhage versus that of a transient increase in intracranial pressure in subarachnoid hemorrhage, the two components were induced separately in rabbits. Extracellular glutamate, sampled from the hippocampus with microdialysis, was used to evaluate the degree of CNS tissue damage. In four rabbits, autologous arterial blood was infused in the cisterna magna in a volume that would not affect the intracranial pressure. The other group of animals was infused with saline to elevate the intracranial pressure from 10 to > 100 mmHg. The increase of intracranial pressure per se did not induce significant changes in extracellular glutamate. However, 20-60 min after infusion of blood, a significant glutamate increase was recorded. Furthermore, aspartate, alanine, glycine and serine were also raised. The results indicate that blood in the subarachnoid space damages the brain primarily by inducing ischemia. Furthermore, the parameters employed gave no indication that an increase in intracranial pressure had a deleterious effect on CNS tissue. [Neurol Res 1999; 21: 404-408]     

动脉瘤性蛛网膜下腔出血并发脑血管痉挛患者血清血管内皮生长因子表达的变化

目的:探讨动脉瘤性蛛网膜下腔出血(SAH)并发脑血管痉挛(CVS)与血清血管内皮生长因子(VEGF)表达的关系.方法:27例动脉瘤性SAH患者为试验组(SAH组),再依据是否并发不同程度CVS分为:无CVS亚组(11例),轻度CVS亚组(9例)、中度CVS亚组(4例)和重度CVS亚组(3例);另设10名健康体检者为对照组.采用ELISA法检测血清VEGF水平.结果:SAH各时间点各组血清VEGF水平为①SAH组发病第1天起即明显高于对照组;②无CVS组不增高.SAH后第1、3、5、7天时血清VEGF水平为①轻度CVS组与中度CVS组相同时间点比较,差异无统计学意义;②重度CVS组明显高于轻度和中度CVS组.SAH后出现脑梗死患者血清VEGF水平明显高于未出现脑梗死患者.结论:SAH后出现CVS患者和出现脑梗死的患者血清VEGF水平明显增高,血清VEGF水平能反映脑血管痉挛的程度.