脑卒中急性期血脂代谢异常的临床分析

目的 观察脑梗死与脑出血患者急性期血脂与血清脂蛋白的差异.方法 回顾性分析94例脑出血与147例脑梗死患者急性期血清甘油三酯(TG)、总胆固醇(TC)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、载脂蛋白AⅠ(ApoAⅠ)、载脂蛋白B(ApoB)、脂蛋白a[Lp(a)]、ApoAⅠ/ ApoB之间的异同.结果 脑梗死组TG、TC、HDL-C、ApoAⅠ/ ApoB与脑出血组比较差异有统计学意义(P＜0.05).结论 脑出血与脑梗死血脂代谢异常有显著差异.     

分析血脂和血清脂蛋白谱检测对脑出血与脑梗死的诊断价值

目的分析脑梗死与脑出血患者血脂、血清脂蛋白谱的变化期差异。方法选取本院神经内科收治的60例脑梗死患者、60例脑出血患者及60例体检健康者(健康组)为观察对象,分别检测3组血脂、血清脂蛋白谱的变化及特点。结果脑梗死组、脑出血组TG、LDL-C、VLDL-C水平显著高于健康组(P0.05);脑梗死组、脑出血组HDL-C、ApoE水平显著低于健康组(P0.05);脑梗死组TG、TC、LDL-C水平显著高于脑出血组(P0.05)。3组血清脂蛋白谱指标PreβLP1、PreβLP2差异均无统计学意义(P0.05);脑梗死组、脑出血组血清脂蛋白谱指标AL、βLP显著高于健康组(P0.05),血清脂蛋白谱指标ɑLP显著低于健康组(P0.05)。结论脑梗死与脑出血患者的血脂、血清脂蛋白谱较健康人群改变显著,临床检测血脂、血清脂蛋白谱指标对临床诊断、治疗具有重要意义。     

急性脑梗死患者颈动脉粥样硬化斑块形成严重程度与血脂水平的关系

目的探讨急性脑梗死患者颈动脉粥样硬化斑块严重程度与血脂水平的关系。方法 253例急性脑梗死患者,根据颈动脉彩色多普勒超声检查结果分为无斑块组、内膜增厚组、轻度狭窄组、中度狭窄组及重度狭窄-闭塞组。检测患者血清总胆固醇(TC)、三酰甘油(TG)、高密度脂蛋白(HDL-C)、低密度脂蛋白(LDL-C)、脂蛋白(LP)(a)、载脂蛋白(Apo)A-Ⅰ及(Apo)B水平。比较各组患者脂蛋白、载脂蛋白及各血脂水平的差异,分析各组颈动脉粥样硬化斑块形成严重程度与脂蛋白、载脂蛋白及各血脂水平之间的相关性。结果组间比较各组患者血清TC、LDL-C、LP(a)、ApoB、ApoA-Ⅰ及ApoB/ApoA-Ⅰ水平比较,差异有统计学意义(P<0.05)。血清TC、LDL-C、LP(a)、ApoB、ApoB/ApoA-Ⅰ水平与颈动脉狭窄呈正相关。(r=0.15,P<0.05,r=0.24,r=0.29,r=0.37,r=0.50,P<0.01),血清ApoA-Ⅰ水平与颈动脉狭窄程度呈负相关(r=-0.21,P<0.01)。逐步回归分析显示,TC、ApoB/ApoA-Ⅰ水平与急性脑梗死患者颈动脉狭窄呈正相关(P<0.05)。结论急性脑梗死患者的颈动脉狭窄程度与血清TC、ApoB/ApoA-Ⅰ水平密切相关。ApoB/ApoA-Ⅰ水平是预测缺血性脑卒中的重要危险因素。     

急性脑梗死患者血清抵抗素水平及相关性研究

目的 探讨脑梗死患者血清抵抗素水平变化及其与糖代谢、脂质代谢、超敏C反应蛋白(hs-CRP)等的相关性.方法 采用酶联免疫吸附法测定82例脑梗死患者血清抵抗素水平,同时检测血清瘦素、胰岛素、空腹血糖(FBG)、三酰甘油(TG)、总胆固醇(TC)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)及hs-CRP水平,计算定量胰岛素敏感性检测指数(QUICKI).另收集健康体检者50名为对照组.对所有受试者进行身高、体质量、腰围、臀围、收缩压(SBP)、舒张压(DBP)测量,并计算体质量指数(BMI)及腰臀比(WHR).结果(1)两组间性别比、年龄和BMI差异无统计学意义(P＞0.05),脑梗死组WHR、SBP和DBP均明显高于对照组(P＜0.01).(2)脑梗死组血清抵抗素、瘦素、胰岛素、FBG、LDL-C及hs-CRP均明显高于对照组(P＜0.05),而血清HDL-C和QUICKI均低于对照组(P＜0.05),两组间TC和TG比较差异无统计学意义(P＞0.05).(3)单因素直线相关分析结果显示,抵抗素与BMI、SBP、DBP、胰岛素、FBG、LDL-C和hs-CRP呈正相关(P＜0.05),与QUICKI和HDL-C呈负相关(P＜0.05),与WHR、瘦素、TC和TG无相关性(P＞0.05).(4)多元逐步回归分析结果显示,抵抗素与BMI、SBP、LDL-C和hs-CRP呈正相关(P＜0.05),而与HDL-C和QUICKI呈负相关(P＜0.05).结论 急性脑梗死患者血浆抵抗素水平明显升高,提示抵抗素在动脉粥样硬化性脑梗死的发生过程中具重要调控作用.抵抗素不但参与糖代谢紊乱和脂质代谢紊乱的发生,而且与高血压、肥胖以及动脉粥样硬化炎性反应等有关.     

LDL-C/HDL-C比值与急性脑梗死危险因素的关系及在疗效评估中的价值

目的探讨低密度脂蛋白(LDL-C)与高密度脂蛋白(HDL-C)比值与急性脑梗死危险因素的关系及其对急性脑梗死疗效的评估价值。方法选取我院2012-06—2014-06神经内科收治的68例急性脑梗死患者为研究对象,另选取60例正常体检者为对照组,测定2组收缩压(SBP)、舒张压(DBP)、空腹血糖(FBG)、糖化血红蛋白(HbA1c)、甘油三脂(TG)、总胆固醇(TC)、低密度脂蛋白(LCL-C)、高密度脂蛋白(HCL-C)、载脂蛋白B(APOB)、颈动脉内-中膜厚度(IMT),并计算LDL-C/HDL-C比值。急性脑梗死患者入院后给予阿托伐他汀钙片治疗,分析治疗效果及LDL-C/HDL-C对疗效的评估价值。结果急性脑梗死组患者SBP、DBP、FBG、HbA1c、TG、TC、LCL-C、APOB、APOA1、IMT及LDL-C/HDL-C水平均高于对照组(P0.05),而HDL-C水平低于对照组(P0.05)。经Person相关因素分析,LDL-C/HDL-C与SBP、LCL-C、HDL-C、IMT水平呈正相关(P0.05)。经Logistic多因素分析,LDL-C/HDL-C、IMT、SBP为急性脑梗死的独立危险因素。与治疗前相比,急性脑梗死患者美国国立卫生院神经功能缺损评分(NIHSS)显著下降,且与LDL-C/HDL-C、IMT呈正相关(P0.05)。结论LDL-C/HDL-C比值是急性脑梗死独立危险因素,且与患者NIHSS具有密切的关系,可与IMT作为患者预后的评价指标。     

多发性脑梗死性痴呆及脑梗死患者血清载脂蛋白E测定及意义

目的检测多发性脑梗死性痴呆(MID)及脑梗死(CI)患者血清载脂蛋白E(ApoE)含量，探讨ApoE测定的临床意义。方法选取20例MID患者、24例CI患者及24例正常对照者，分别运用单克隆抗体ELISA法测定血清ApoE含量，同时测定血清TC、TG、HDL-C、LDL-C、ApoA和ApoB含量，并进行相关分析。结果与对照组比较，MID和CI患者血清ApoE、ApoB及LDL-C含量显著升高(P＜0.05)，HDL-C和ApoA含量显著降低(P＜0.01)，TC及TG含量升高，但无统计学意义(P＞0.05)。结论MID和CI患者均有脂代谢异常，血清ApoE可作为检测其脂代谢异常的重要指标。     

β-受体阻滞剂对高血压病人血脂水平影响的研究

目的探讨β受体阻滞剂对高血压病人血脂水平的影响。方法60例高血压病人随机分成四组,分别服用普萘洛尔、阿替洛尔、美托洛尔、比索洛尔。用药前后分别测定血清甘油三酯(TG)、总胆固醇(CH)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、载脂蛋白AI(APO AI)、载脂蛋白B(APOB),将用药前后血脂数据进行统计学处理。结果 普萘洛尔组治疗后TG明显升高,HDL-C明显下降,差异显著。阿替洛尔和美托洛尔组治疗后TC、LDL-C明显升高,HDL-C明显下降,差异显著。比索洛尔组治疗后TG明显升高,HDI-C明显下降,差异显著。结论研究结果提醒医生在选择治疗方案时要考虑到β受体阻滞剂对血脂水平的影响,应定期复查血脂,长期治疗可使冠心病恶化,若高血压病伴严重高血脂症慎用,从而提高医疗质量。     

血脂、血尿酸及凝血功能与急性脑梗死 和脑出血的相关性

目的 探讨血脂、血尿酸（UA）及凝血功能与急性脑梗死（ACI）和脑出血（ICH）的相关性。 方法 测定同期住院的62例ACI和50例ICH患者的血脂、UA及凝血功能等指标，并以同期住院的50例非 脑血管病患者为对照进行相关分析。 结果 ACI组总胆固醇（TC）、甘油三酯（TG）水平显著高于对照组（P＜0.01），载脂蛋白A1（ApoA1）水平 显著低于对照组（P＜0.01）；高密度脂蛋白胆固醇（HDL-C）、低密度脂蛋白胆固醇（LDL-C）、载脂蛋 白B（ApoB）水平与对照组比较差异无统计学意义（P＞0.05）。ACI组血UA、纤维蛋白原（Fib）显著高于对 照组和ICH组（P＜0.01）；ICH组血脂指标、血UA、Fib与对照组比较差异无统计学意义（P＞0.05）。 结论 血脂代谢紊乱、高尿酸血症、高纤维蛋白原血症与脑梗死明显相关，是脑梗死的危险因素，与 ICH则无明显相关性。     

载脂蛋白E及血脂水平联合检测对早期脑梗死的诊断价值

目的探讨载脂蛋白E及血脂水平联合检测对早期脑梗死的诊断价值。方法以我院2013-02—2015-02就诊的50例脑梗死患者为研究组,选择同期50例健康体检者为对照组,均通过免疫比浊法、酶法测定2组受试者血清载脂蛋白E及血脂指标。结果2组载脂蛋白E[(114.1±20.8)vs(509.5±82.6)]mg/L、TC[(7.13±0.85)vs(4.20±0.53)]mmol/L、TG[(2.01±0.38)vs(1.32±0.30)]mmol/L、HDL-C[(0.70±0.22)vs(1.25±0.04)]mmol/L、LDL-C[(7.81±1.12)vs(2.27±0.28)]mmol/L水平比较差异有统计学意义(P0.001)。载脂蛋白E+TC+LDL-C诊断脑梗死敏感度、特异度、诊断效率分别为32.0%、100.0%、58.0%。结论载脂蛋白E联合血脂水平检测在早期脑梗死诊断中有一定的应用价值。     

脑梗死与血脂、血糖的关系分析

目的探讨中老年人脑梗死的发病与血压、血脂、血糖的关系。方法240例患者根据脑CT或MRI检查结果分为脑梗死组120例和非梗死组(对照组)120例。对2组患者的血压、血脂、血糖等指标用t检验分析。结果脑梗死组合并高血压的(?-)生率明显高于对照组(P<0.05);2组甘油三酯(TG)、高密度脂蛋白-胆固醇(HDL-C)、载脂蛋白-A(APOA)等生化指标差异无显著性(P>0.05);但胆固醇(CHO)、低密度脂蛋白-胆固醇(LDH-C)、血糖(GLU)、载脂蛋白-B(APOB)方面差异有显著性(P<0.05)。结论高血压作为老年人脑梗死的独立危险因素,是老年人防治脑梗死的重点内容,而控制血脂、血糖水平在一个正常的范围对防治脑梗死亦有积极意义。     

Quantitative measurement of cerebral blood flow and cerebral blood volume after cerebral ischaemia

CBF obtained by the hydrogen clearance technique and cerebral blood volume (CBV) calculated from the [14C]dextran space were measured in three groups of rats subjected to temporary four-vessel occlusion to produce 15 min of ischaemia, followed by 60 min of reperfusion. In the control animals, mean CBF was 93 +/- 6 ml 100 g-1 min-1, which fell to 5.5 +/- 0.5 ml 100 g-1 min-1 during ischaemia. There was a marked early postischaemic hyperaemia (262 +/- 18 ml 100 g-1 min-1), but 1 h after the onset of ischaemia, there was a significant hypoperfusion (51 +/- 3 ml 100 g-1 min-1). Mean cortical dextran space was 1.58 +/- 0.09 ml 100 g-1 prior to ischaemia. Early in reperfusion there was a significant increase in CBV (1.85 +/- 0.24 ml 100 g-1) with a decrease during the period of hypoperfusion (1.33 +/- 0.03 ml 100 g-1). Therefore, following a period of temporary ischaemia, there are commensurate changes in CBF and CBV, and alterations in the permeability-surface area product at this time may be due to variations in surface area and not necessarily permeability.     

Effects of ATP on cerebral circulation--morphological observation of cerebral circulation and cerebral vasculature]

Review was made on the effect of adenosine triphosphate, 1.0-3.0 mg/kg intravenously, on the cerebral circulation and the presence of the dilating action on the cerebral blood-vessels in cats. 1. The group of the normal intra-cranial pressure showed, as reported previously, the transient hypotension and its complicated decrease of cerebral blood-circulation at the initial period for 30-100 check, then demonstrating the increase of cerebral blood-flow for 200-1000 check. Its increased volume and duration were dose-dependent. 2. The group of the loaded intracranial pressure of 20-30 mmHg (slightly elevated group) showed the increase of cerebral blood-flow, like the group of the normal intracranial pressure. However, the effect of ATP showed the decrease or disappearance in accordance with the elevation of the loaded pressure. 3. Cerebral vasodilating effect of ATP was promptly observed after the administration, and its degree was 30-50% in photographical observation. 4. Increasing effect on cerebral blood-flow and cerebral vasodilating action of ATP were similar in the pattern to that of vasodilators such as papaverine hydrochloride.     

Regional cerebral blood flow correlates of aphasia outcome in cerebral hemorrhage and cerebral infarction

The relationship between recovery from aphasia and regional cerebral blood flow (CBF) was compared in 87 patients, 44 with cerebral hemorrhage and 43 with non-embolic cerebral infarction. CBF values correlated poorly with aphasia outcome in patients with cerebral hemorrhage whereas a tight correlation was demonstrated in patients with non-embolic cerebral infarction. A marked variability of CBF values in the acute and subacute stage might account for the poor correlation between CBF and aphasia outcome in patients with cerebral hemorrhage. On the other hand, a sharp discrimination was achieved between those with a good recovery from aphasia and those with a poor recovery by the dimensions of the hematoma on CT. In non-embolic cerebral infarction, a relative frontal ischemia was associated with motor aphasia while a relative temporal ischemia was associated with sensory aphasia. This dichotomy was not demonstrated in the regional CBF values in patients with cerebral hemorrhage.     

脑动脉瘤显微手术治疗及脑血管痉挛的综合防治

目的探讨脑动脉瘤破裂出血后的最佳手术时机和方法,分析影响脑动脉瘤患者预后的因素,探讨防治脑血管痉挛的最佳措施.方法回顾性分析412例脑动脉瘤患者的临床资料,着重探讨不同时期开颅手术的效果和急性期锁孔手术的相对适应证,分析影响颅内动脉瘤患者预后的因素,比较各种防治脑血管痉挛措施的效果.结果使用常规开颅显微手术治疗361例,其中急性期手术222例,92%动脉瘤夹闭成功;发病后4～14d手术63例;延期手术76例.非急性期手术患者在等待手术期间发生动脉瘤再破裂出血27例(27/139).经眉眶上锁孔入路动脉瘤夹闭31例.未行手术治疗20例.术后脑血管痉挛的总发生率为45.5%,其中静脉联合使用尼莫同加硫酸镁组为32.7%;尼莫同加环孢菌素-A组为33.3%.术后3个月时预后良好333例,中残29例,重残及植物人15例,死亡23例,自动出院12例.病程中有意识障碍、癫痫发作、动脉瘤多次破裂的预后较差.结论脑动脉瘤一旦发现应积极争取早期手术治疗,锁孔手术同样适合急性期手术.病程中有意识障碍、癫痫发作、病情危重及动脉瘤多次破裂是影响患者预后的重要因素.静脉联合使用尼莫同加硫酸镁或尼莫同加环孢菌素-A是防治脑血管痉挛的较好方法.     

The effects of naloxone on cerebral blood flow and cerebral function during relative cerebral ischemia

CBF and somatosensory evoked potentials (SEPs) were measured in a model of moderate cerebral ischemia in anesthetized spontaneously hypertensive rats. The rats were bled to reduce SEP amplitudes to about 50% of prebleeding control. The consequent blood pressure fall reduced CBF to 77% of control as measured by the laser-Doppler technique. Naloxone (5 mg kg-1 i.v. plus 25 mg kg-1 h-1 i.v. for 30 min) caused a significant increase in SEP amplitudes, while CBF did not change significantly. In addition, the latency of the first SEP component decreased toward prebleeding values. Heart rate (HR) decreased, but MABP was held constant by a pressure-regulating reservoir. In unbled rats, naloxone (5 mg kg-1 i.v.) caused a transient small increase in MABP and SEP amplitudes and decrease in HR. These results indicate that sensory input is regulated by opioid systems. Increased opioid activity may inhibit ascending sensory pathways during relative cerebral ischemia and thereby depress SEP responses. Thus, naloxone can release this inhibition and enhances SEP independently of CBF during relative cerebral ischemia. Similar mechanisms might explain the apparently beneficial effects of naloxone in some stroke models.     

颅脑损伤后炎症反应与脑水肿

创伤性脑水肿是创伤性脑损伤（traumatic brain iniury，TBI）后的主要继发性病理生理过程之一，也是导致颅内压增高的主要原因。目前国内外多数学者主张将脑水肿分为血管源性、细胞毒性、渗透压性和脑积水性（间质性）四类。过去几十年，根据冷冻性脑损伤模型的研究结果，普遍认为创伤性脑水肿以血脑屏障（BBB）破坏后的血管源性脑水肿为主。但新近研究发现，创伤性脑水肿是血管源性和细胞毒性的混合性水肿，并且以细胞毒性脑水肿为主。[第一段]