CT灌注成像评价血肿穿刺置管引流术对血肿周围脑组织血流动力学的影响

目的探讨血肿穿刺置管引流术(简称引流术)对自发性幕上出血患者血肿周围组织血流动力学的影响。方法 30例自发性幕上出血患者于引流术后行CT灌注成像,以血肿侧和对侧镜像区血肿中央区、血肿周围水肿区、血肿周围水肿区外侧(距离水肿边缘1 cm)和远隔皮质区作为兴趣区,测量各区域脑血流量(CBF)、脑血容量(CBV)、平均通过时间(MTT)和达峰时间(TTP)。结果 (1)脑出血后血肿周围组织存在不同程度低灌注。与对侧镜像区相比较,血肿侧血肿中央区CBF值(P=0.000)和CBV值(P=0.000)降低、MTT值延长(P=0.000),但未见峰值;血肿周围水肿区CBF值(P=0.000)和CBV值(P=0.000)降低、MTT值延长(P=0.000);血肿周围水肿区外侧CBF值(P=0.000)和CBV值(P=0.000)降低;而血肿侧与对侧镜像区远隔皮质区CBF、CBV、MTT和TTP值差异均无统计学意义(P0.05)。(2)脑出血后自血肿中央区至远隔皮质区灌注参数呈阶梯样改变。血肿侧自血肿中央区至远隔皮质区CBF值和CBV值逐渐增大(均P 0.05)、MTT值逐渐减少(均P 0.05),而TTP值差异无统计学意义(P 0.05);对侧镜像区血肿中央区、血肿周围水肿区、血肿周围水肿区外侧与远隔皮质区CBF、CBV、MTT和TTP值差异均无统计学意义(P 0.05)。(3)引流术后血肿周围水肿区CBF值(P=0.000)和CBV值(P=0.000)高于术前。结论血肿穿刺置管引流术可以明显提高血肿周围组织血流灌注。     

SHR大鼠脑出血急性期氨氯地平血压干预和血肿周围水肿的相关性研究

目的采用自发性高血压大鼠(SHR)脑出血模型,研究脑出血后急性期血压和血肿周围水肿的相关性。方法胶原酶法制备SHR大鼠脑出血模型,出血部位为右侧基底节区。动物随机分为脑出血组、脑出血常规剂量氨氯地平降压组、脑出血强化剂量氨氯地平降压组。MRI检查并计算血肿周围水肿大小;免疫组化及荧光定量PCR法检测血肿周围水肿的AQP4表达。结果 (1)氨氯地平治疗组MRI检测值显示,脑血肿周围水肿减轻,降压组均优于未干预组,强化降压组优于常规降压组,差异有统计学意义,第3、5、7天的F值分别为16.987、35.448、37.174(P<0.05);收缩压降低幅度和血肿周围水肿体积之间有相关性,在第3、5、7天的相关系数r分别为0.83、0.89、0.83,P=0.000;舒张压降低幅度和血肿周围水肿体积之间有相关性,在第3、5、7天的相关系数r分别为0.82、0.89、0.84,P=0.000)。(2)降压组血肿周围水肿的AQP4表达下调均优于未干预组,强化降压组优于常规降压组,差异有统计学意义,第3、5、7天的F值分别为217.058、21、51.706(P<0.05)。结论 (1)氨氯地平有效降压能使脑出血血肿周围水肿缩小;(2)氨氯地平可能通过抑制AQP4表达促使血肿周围脑水肿减轻;(3)收缩压、舒张压的升高均可促使血肿周围脑水肿扩大。     

脑出血急性期合并高血压患者血压与血肿、水肿的相关性研究

目的研究脑出血急性期合并高血压患者血压与血肿、水肿的相关性。方法选取我院接诊的30例脑出血急性期合并高血压患者为研究对象。调查分析30例患者脑出血后1d、3d、5d、7d血压、血肿体积以及血肿周围水肿体积,进而计算出1~3d、3~5d及5~7d的血压变化率、血肿变化率以及血肿周围水肿变化率。结果患者脑出血后,随着出血时间的增加,收缩压、舒张压以及平均血压均持续升高,但血肿体积及血肿周围水肿体积并未随着脑出血时间的增加而持续增加。患者收缩压变化率与血肿变化率呈正相关(r=0.764 1,P=0.0000),收缩压变化率与血肿周围水肿变化率呈正相关(r=0.518 2,P=0.025 3),平均血压变化率与血肿变化率以及血肿周围水肿变化率无相关性,舒张压变化率与血肿变化率以及血肿周围水肿变化率无相关性。结论脑出血急性期合并高血压患者脑出血后血压显著升高,收缩压波动可能促使血肿以及血肿周围水肿扩大。     

脑出血患者血肿周围水肿形成机制:脑内细胞因子的作用

目的 :探讨脑出血患者脑内炎性细胞因子与血肿周围水肿的形成是否相关。方法 :32例脑出血患者行血肿清除术后 ,留取脑血肿液 ,放免法测定其中肿瘤坏死因子α(TNFα)和白细胞介素 - 6 (IL - 6 )的含量 ,测量术前检查的头 CT上的血肿周围水肿带大小 ,用 SPSS10 0对两者进行相关分析。结果 :脑出血患者脑血肿液中 IL - 6和 TNFα的含量明显高于正常人溶血血清中的含量 (P<0 .0 1) ;脑血肿液中 TNFα和 IL - 6含量与血肿周围水肿带大小呈正相关 (r TNF=0 .5 39,P<0 .0 1;r IL- 6 =0 .5 6 9,P<0 .0 1)。结论 :脑出血患者急性期脑血肿液中 IL - 6和 TNFα含量升高 ;脑内炎性细胞因子可能参与血肿周围水肿的形成     

早期强化降压治疗与高血压脑出血血肿、血肿周围水肿的关系

目的探讨早期强化降压治疗与高血压脑出血(HICH)血肿、血肿周围水肿的关系。方法将50例HICH患者随机分为强化降压组(23例)及对照组(27例)。所有患者采用常规治疗,强化降压组患者加用氨氯地平10 mg/d。入院时及入院24 h后各进行一次头颅CT检查,比较两组的血肿及血肿周围水肿体积。结果入院时强化降压组及对照组SBP、血肿体积及周围水肿体积差异均无统计学意义(均P0.05)。与对照组比较,强化降压组24 h SBP、血肿及血肿周围水肿体积显著缩小(均P0.05)。Pearson相关分析显示,SBP与血肿、血肿周围水肿体积呈正相关(r=0.291,P=0.040;r=0.312,P=0.027)。结论早期强化降压治疗可减少血肿、血肿周围水肿体积。     

阻塞性睡眠呼吸暂停低通气综合征与高血压性脑出血血肿周围水肿的相关性

目的 分析阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep apnea-hypopnea syndrome,OSAHS)与高血压性脑出血血肿周围水肿的相关性.方法 收集高血压性脑出血患者144例,其中合并OSAHS患者78例.不合并OSAHS的高血压性脑出血患者66例,作为空白对照组,两组患者均接受常规脱水降颅压、降压、保护脑细胞治疗.在入院时行头CT检查并于24h内行夜间多导睡眠图(polymonography,PSG)监测.入院后24 h及第4天均复查CT,测量脑血肿体积和血肿周围水肿体积,动态观察脑血肿及血肿周围水肿变化.结果 伴或不伴OSAHS两组在年龄、性别组成、体重指数、血糖、血脂等方面差异均无统计学意义.两组患者的相对水肿体积指数(relative edema index,REI)在入院时和24 h后差异均无统计学意义；入院第4天,OSAHS组水肿体积变化指数为0.96±1.35,明显高于对照组(0.40±0.45,t=4.149,P=0.000).不同程度OSAHS患者的水肿体积及水肿变化的分析结果表明,入院时不同程度OSAHS的脑出血患者的脑水肿程度差异无统计学意义(无OSAHS组和轻、中、重组分别为1.05士0.65、0.84±0.48、1.20±0.54、1.10±0.40,F=1.061,P=0.374)；入院24h和第4天时,随着OSAHS严重程度的增加,脑出血患者的脑水肿程度增加.水肿体积变化差异性分析显示,重度OSAHS合并症的患者,水肿体积增加更明显.水肿变化指数与OSAHS程度指标呼吸暂停低通气指数呈明显正相关,Pearson相关系数为0.652(P =0.000).结论 OSAHS可加重高血压性脑出血患者的水肿恶化程度,且恶化程度与OSAHS严重程度呈正相关.     

铁蛋白在高血压脑出血后血肿周围脑水肿中的作用及机制研究

目的探讨血清铁蛋白与高血压脑出血后血肿周围脑水肿的关系,并分析其在血肿周围脑水肿发生中的作用。方法采集2012-05—2013-11于我院住院治疗的38例高血压脑出血患者的临床资料和实验室数据,所有患者均在入院时及入院3~4d后行血清铁蛋白及头颅CT检查,计算入院时及入院3~4d后血肿体积、脑水肿总体积及经校正后的相对水肿体积,采用Spearman相关分析相对血肿周围脑水肿体积与血清铁蛋白的关系。结果与入院当天比较,入院第3~4天后血肿体积增加19%,但差异无统计学意义(P0.05);脑水肿体积增大71%,差异有统计学意义(P0.05)。血肿周围脑水肿体积与血肿体积的比值即相对水肿体积增加1.13倍。入院当天,患者血清铁蛋白水平和相对水肿大小间无明显相关性(P0.05);入院后第3~4天时相对水肿体积与血清铁蛋白呈正相关(r=0.67,P=0.006)。结论血清铁蛋白是反映高血压脑出血后血肿周围脑水肿程度的一个重要指标,其在血肿周围继发性脑水肿的发生中起重要作用。     

脑出血后水肿体积相关危险因素分析

目的探讨脑出血后周围脑水肿严重程度与相关危险因素的关系。方法前瞻性分析河南科技大学附属黄河三门峡医院2013-01—2015-12住院诊断为自发性脑出血患者共168例。收集上述病人的基本资料,包括姓名、性别、年龄、体重指数、吸烟史、出血部位、高血压史、糖尿病史、有无合并腔隙性梗死、有无合并脑白质疏松及严重程度,实验室指标包括血脂、CRP、胱抑素C。脑出血住院患者于发病当天、发病后24h、72h、7d和14d进行头部CT扫描,计算脑出血血肿体积及周围水肿体积,分析脑出血周围水肿体积的严重程度与相关危险因素的关系。结果 (1)168例入选的脑出血患者,发病当天脑出血平均体积(16.22±5.13)mL,随着发病时间延长,脑血肿体积逐渐缩小,水肿指数随时间延长逐渐增加,7d时达最高峰,14d下降明显。(2)对发病1周时水肿指数相关因素进行单因素分析结果显示:体重指数(P=0.004)、高血压史及其程度(P=0.021)、糖尿病史(P=0.039)、CRP(P=0.018)、脑白质病变(P=0.008)对脑出血1周时幕上脑出血后周围水肿指数影响差异具有统计学意义(P0.05)。结论 (1)脑出血后血肿周周围水肿严重程度随时间进展逐渐增加,7d时达最高峰,之后逐渐下降。(2)脑出血1周时周围水肿严重程度与体质量指数、高血压病史、糖尿病病史、脑白质疏松严重程度、CRP相关。     

无创性脑电阻抗测定在脑出血患者脑水肿监测中的应用

目的 应用无创性脑电阻抗测定探讨急性脑出血患者脑水肿的变化规律及意义.方法 分别检测200名健康志愿者和78例脑出血患者的脑电阻抗扰动系数及其动态变化,通过多媒体图像分析系统计算头颅CT上血肿和血肿周围水肿的体积,并进行相关分析.结果 ①健康志愿者左、右大脑半球扰动系数分别为(7.98±0.95)和(8.02±0.71),基本对称(P＞0.05).性别、年龄及3～6 h连续检测前后对其无明显影响(P＞0.05).②脑出血患者的总体检测阳性率为73.1%.血肿位于基底节区时阳性率最高(83.3%),病灶体积大于20 ml者阳性率(80.0%～88.9%)明显高于体积小于20 ml者(48.1%).③脑出血患者血肿侧扰动系数由低于血肿对侧至逐渐升高并超过血肿对侧,这个"交叉"时间平均为起病后(19.67±11.52)h,在该时间点后血肿周围水肿体积较前明显增大(P＜0.05),同时扰动系数亦明显升高(P＜0.01).④起病24h内的血肿侧扰动系数变化与血肿体积及血肿周围组织水肿体积无相关关系(P＞0.05);而病后3 d的血肿侧扰动系数变化与血肿周围组织水肿体积具有显著正相关关系(r=0.5977,P＜0.01).结论 脑电阻抗测定可较敏感地反映脑出血患者脑水肿的变化,扰动系数越高,则提示脑水肿越重.病灶位于基底节区时检测阳性率最高.该方法为临床上进行动态、床旁连续无创性脑水肿监测提供了新的有意义的手段.     

老年自发性脑出血患者血肿变化与阻塞性睡眠呼吸暂停低通气综合征的相关性

目的分析老年自发性脑出血血肿变化与阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep apnea hypopnea syndrome,OSAHS)的相关性。方法收集自发性脑出血患者156例,其中有OSAHS的自发性脑出血患者88例为试验组,无OSAHS的自发性脑出血患者68例为空白对照组。在患者入院第24h及第4天采用CT或MRI测量脑血肿体积,检测患者脑血肿的变化。结果入院第4天相对血肿体积指数(RHI),试验组为2.18±0.81,明显高于对照组的1.72±0.51(P=0.02)。另外,不同程度OSAHS患者的脑血肿体积及血肿变化的结果表明,入院第24h和第4天时,随着OSAHS严重程度的增加,脑出血患者的脑血肿程度增加(P0.05)。且重度OSAHS并发症患者的脑血肿体积增加更显著(P=0.002)。血肿变化指数与OSAHS程度呈明显正相关(r=0.687,P=0.000)。结论伴OSAHS的老年自发性脑出血患者血肿的体积变化程度高于无OSAHS者,且OSAHS严重程度与脑血肿的变化程度呈正相关。     

Perihematoma cerebral blood flow is unaffected by statin use in acute intracerebral hemorrhage patients

Statin therapy has been associated with improved cerebral blood flow (CBF) and decreased perihematoma edema in animal models of intracerebral hemorrhage (ICH). We aimed to assess the relationship between statin use and cerebral hemodynamics in ICH patients. A post hoc analysis of 73 ICH patients enrolled in the Intracerebral Hemorrhage Acutely Decreasing Arterial Pressure Trial (ICH ADAPT). Patients presenting <24 hours from ICH onset were randomized to a systolic blood pressure target <150 or <180 mm Hg with computed tomography perfusion imaging 2 hours after randomization. Cerebral blood flow maps were calculated. Hematoma and edema volumes were measured planimetrically. Regression models were used to assess the relationship between statin use, perihematoma edema and cerebral hemodynamics. Fourteen patients (19%) were taking statins at the time of ICH. Statin-treated patients had similar median (IQR Q25 to 75) hematoma volumes (21.1 (9.5 to 38.3) mL versus 14.5 (5.6 to 27.7) mL, P=0.25), but larger median (IQR Q25 to 75) perihematoma edema volumes (2.9 (1.7 to 9.0) mL versus 2.2 (0.8 to 3.5) mL, P=0.02) compared with nontreated patients. Perihematoma and ipsilateral hemispheric CBF were similar in both groups. A multivariate linear regression model revealed that statin use and hematoma volumes were independent predictors of acute edema volumes. Statin use does not affect CBF in ICH patients. Statin use, along with hematoma volume, are independently associated with increased perihematoma edema volume.     

Quantitative evaluation for secondary injury to perihematoma of hypertensive cerebral hemorrhage by functional MR and correlation analysis with ischemic factors

OBJECTIVES: To analyse quantitatively for the secondary injury to the perihematoma region of intracerebral hemorrhage (ICH) patients by functional MR imaging technique. METHODS: 35 ICH patients were recruited and performed T1, T2, perfusion weight imaging (PWI), diffusion weight imaging (DWI) and FLAIR sequence scanning. Hematoma volume and edema volume of perihematomal area as well as parameters of blood volume [regional cerebral blood volume (rCBV), mean transit time (MTT)] alteration were calculated. RESULTS: Varied blood flow decline was detected in the patients on the perihematoma sides, compared with the corresponding area of the opposite sides. There was significant difference of rCBV and MTT (p=0.00) and mild negative correlation between rCBV and hematoma volume (p=0.00) among groups; edema volume of perihematoma region and hematoma volume showed a linear correlation (p=0.00). Moreover, positive correlation between edema intensity and rCBV was detected, (p=0.00); the most significant perihematoma edema was in the group of day 10 to day 14; the lowest rCBV occurred in the early stage. (days 2-5 from symptom onset). CONCLUSION: We have concluded that rCBV and MTT of perihematoma region decreased remarkably compared with the contralateral side, and the decline would last over 3 weeks. Quantitative research suggested edema intensity is closely related with rCBV. We believe that the reduced regional blood flow of perihematoma contributes to the secondary ischemic injury of perihematoma tissue. However, the peak of edema would appear later than the onset of the peak of ischemia, it suggests that edema surrounding the hematoma is not only the result from the single ischemic factor, but also results from multiple disadvantage mechanisms.     

Nimodipine treatment to assess a modified mouse model of intracerebral hemorrhage

One of the main limitations of intracerebral hemorrhage (ICH) research is lack of reproducible animal models. ICH appears to be associated with a volume of edema and ischemic injury surrounding the hematoma that may be reduced by nimodipine due to its vasodilating and cytoprotective effects. The present study was designed to produce a modified ICH model in mice based on the double-injection method initially developed by Dr. Belayev and accordingly performed in 3 groups: to evaluate this model itself and to assess the pharmacological effects of nimodipine in this model, respectively. In 80 ICR mice (32 +/- 3 g), ICH was induced by 30 microL whole blood injection into the caudate nucleus. ICH animals were then randomly received either nimodipine (5 mg/kg) or vehicle intraperitoneal injection just before and every 24 h after ICH (total of four times). The changes for cortical blood flow (CBF) were studied by the technique of Laser Doppler Perfusion Measure (LDPM). Animals were rated on a behavioral test and sacrificed at 72 h after ICH. The brains were removed, and hematoma volume and brain edema were subsequently determined. Due to the vasodilating effect of nimodipine, ICH animals treated with nimodipine had marked improved CBF accompanied by the improvement of forelimb placing performance compared with vehicle-treated ICH animals, though there was no marked difference in the hematoma volume and brain water content. In conclusion, the 30 microL whole blood injection closely mimicked natural ischemic events that occurred in human massive ICH and confirmed the anti-ischemia effect of nimodipine. This study suggested that nimodipine could be markedly effective to reduce edema and hematoma volume when administered in combination with other neuroprotective agents because ICH can induce brain injury by multiple mechanisms.     

Dynamic single-section CT demonstrates reduced cerebral blood flow in acute intracerebral hemorrhage

Optimum blood pressure (BP) management in acute intracerebral hemorrhage (ICH) remains controversial. BP reduction may limit hematoma expansion, but may also exacerbate ischemia. Reduced regional cerebral blood flow (rCBF) has been reported in ICH. Its extent and precise pattern, however, remain uncertain. Dynamic single-section CT perfusion (CTP) is rapid, easily performed and offers superior spatial resolution to PET, SPECT and MRI. It may be the most applicable method for assessing the effects of BP management on rCBF in ICH. We sought to assess whether CTP can identify rCBF abnormalities in acute ICH in 5 patients with ICH who underwent CTP within 24 h of symptom onset. rCBF was measured in serially expanded 2-mm rings around the hematoma and compared with rCBF in the uninvolved hemisphere. Mean time to CTP was 9 h (range 3-23). Mean ICH volume was 25 ml (range 9-64). Perihematoma perfusion was reduced in all patients compared with contralateral hemisphere rCBF. rCBF reduction was most pronounced immediately adjacent to the hematoma (p < 0.05 at 2 mm, p = 0.084 at 4 mm, p > 0.2 at 6 and 8 mm). Perihematoma rCBF increased as a function of the distance from hematoma perimeter. Rate of rCBF increase over distance correlated with time from onset (p = 0.006). We conclude that CTP identifies a rim of reduced rCBF in ICH. A gradient of hypoperfusion appears to extend at least 4 mm beyond the hematoma edge and may be time dependent. Whether reduced CBF is associated with perihematoma ischemia requires additional study.     

脑出血后继发性脑水肿的形成、发展及影响因素研究

【摘要】 目的 研究急性脑出血（intracerebral hemorrhage,ICH）患者继发性脑水肿的相关因素及对ICH患者预后的影响。 方法 本研究为前瞻性研究,连续收集发病24 h内的ICH住院患者51例。患者到院时收集临床基线信息、完成实验室检查和常规头颅平扫计算机断层扫描（computed tomography,CT）以评价基线脑水肿情况。发病（12±2）d行常规头颅平扫CT及CT血管成像一站式检查,以完成高峰期水肿情况及脑血管系统评价。分别在就诊、出院和发病后90 d进行神经功能评价。 结果 在51例入组患者中,基底节区出血36例,丘脑出血7例,脑叶出血8例。本研究发现初始水肿体积（V初始水肿）与初始血肿体积（V初始血肿）正相关（r=0.799,P＜0.001）;初始水肿指数（EI初始）与服用抗血小板药物负相关（r=－2.456,P=0.014）。高峰期水肿体积（V高峰水肿）与V初始水肿（r=0.720,P＜0.001）、V初始血肿（r=0.779,P＜0.001）和高峰期血肿体积（V高峰血肿）（r=0.788,P＜0.001）呈正相关;高峰期水肿指数（EI高峰）与EI初始正相关（r=0.357,P=0.010）。本组患者中V初始水肿与就诊ICH功能预后量表（Functional Outcome after ICH,FUNC）评分（r=-0.355,P=0.011）、格拉斯哥昏迷量表（Glasgow Coma Scale,GCS）评分（r=－0.419,P=0.002）、原始脑出血量表（the Original ICH Scale,oICH）评分（r=0.364,P=0.009）、出院（r=0.520,P＜0.001）及发病后90 d（r=0.481,P＜0.001）改良Rankin量表（modified Rankin Scale,mRS）评分以及出院时美国国立卫生研究院卒中量表（National Institutes of Health Stroke Scale,NIHSS）评分（r=0.526,P＜0.001）相关;V高峰水肿与就诊时NIHSS评分（r=0.455,P=0.001）、FUNC评分（r=－0.327,P=0.019）、GCS评分（r=－0.436,P=0.001）、出院（r=0.564,P＜0.001）及发病后90 d（r=0.590,P＜0.001）mRS评分以及出院时NIHSS评分（r=0.541,P＜0.001）相关。 结论 ICH患者存在继发性脑水肿,初始水肿严重程度与初始血肿体积、既往应用抗血小板药物等因素相关,高峰期水肿严重程度与初始水肿、血肿体积,高峰血肿体积以及初始水肿指数等因素相关。ICH患者急性期疾病严重程度和90 d预后与初始和高峰期脑水肿体积相关。     

Hypoperfusion without ischemia surrounding acute intracerebral hemorrhage.

A zone of hypoperfusion surrounding acute intracerebral hemorrhage (ICH) has been interpreted as regional ischemia. To determine if ischemia is present in the periclot area, the authors measured cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2), and oxygen extraction fraction (OEF) with positron emission tomography (PET) in 19 patients 5 to 22 hours after hemorrhage onset. Periclot CBF, CMRO2, and OEF were determined in a 1-cm-wide area around the clot. In the 16 patients without midline shift, periclot data were compared with mirror contralateral regions. All PET images were masked to exclude noncerebral structures, and all PET measurements were corrected for partial volume effect due to clot and ventricles. Both periclot CBF and CMRO2 were significantly reduced compared with contralateral values (CBF: 20.9 +/- 7.6 vs. 37.0 +/- 13.9 mL 100 g(-1) min(-1), P = 0.0004; CMRO2: 1.4 +/- 0.5 vs. 2.9 +/- 0.9 mL 100 g(-1) min(-1), P = 0.00001). Periclot OEF was less than both hemispheric OEF (0.42 +/- 0.15 vs. 0.47 +/- 0.13, P = 0.05; n = 19) and contralateral regional OEF (0.44 +/- 0.16 vs. 0.51 +/- 0.13, P = 0.05; n = 16). In conclusion, CMRO2 was reduced to a greater degree than CBF in the periclot region in acute ICH, resulting in reduced OEF rather than the increased OEF that occurs in ischemia. Thus, the authors found no evidence for ischemia in the periclot zone of hypoperfusion in acute ICH patients studied 5 to 22 hours after hemorrhage onset.     

脑出血患者血清基质金属蛋白酶水平与脑水肿和神经损害的关系

目的探讨脑出血患者血清基质金属蛋白酶(MMPs)水平与脑水肿和神经功能损害的关系。方法应用酶联免疫吸附法测定31例脑出血患者发病后1d、3d、7d和14d时血清MMP-9和MMP-2水平;发病当日及14d时头颅CT测定血肿及其周围脑水肿体积,同时进行卒中评分量表(NIHSS)评分。结果血清MMP-9、MMP-2水平发病后各时间点明显高于正常对照组(均P<0.05);发病7d及14d时MMP-9水平与血肿周围水肿体积呈正相关(r=0.748,P<0.001;r=0.436,P<0.05),与血肿体积及NIHSS评分无相关;各时间点MMP-2水平与血肿体积、血肿周围水肿体积及NIHSS评分无相关。结论脑出血后MMP-9过表达参与血肿周围水肿的形成。     

脑出血患者血肿周围脑组织中P75NTR、TrkA的表达及其与细胞凋亡的关系

目的 通过对人脑出血后血肿周围不同区域组织中的P75NTR、TrkA表达的检测,探讨其在脑出血后血肿周围组织细胞凋亡中的作用. 方法采集脑出血血肿清除术患者的脑组织标本,分别运用DNA断裂原位末端标记(TUNEL)法及免疫组化技术检测血肿周围及远隔部位组织中细胞凋亡率与P75NTR、TrkA的表达. 结果相对于远隔部位组织,脑出血后血肿周围组织中的细胞凋亡率与P75NTR的表达水平明显增加(P<0.05),而TrkA的表达水平并没有明显变化(P>0.05).P75NTR的阳性细胞率与TUNEL阳性细胞率呈正相关(r=0.628,p=0.000). 结论脑出血后血肿周围组织中凋亡细胞明显增多,P75NTR介导的细胞凋亡通路可能发挥了重要的作用;TrkA在脑出血发生后并没有增量表达以增加细胞存活,未起到拮抗P75NTR介导的细胞凋亡作用.     

Comparison of cerebral blood flow and injury following intracerebral and subdural hematoma in the rat

Subdural hematomas (SDH) can induce ischemia and neuronal damage in the underlying cortex. However, the extent to which intracerebral hematomas (ICH) produce reductions in cerebral blood flow (CBF) sufficient to cause ischemic damage is uncertain. Intracranial hemorrhage was induced by the injection of 100 or 200 microl of blood into the subdural space (SDH) or into the caudate nucleus (ICH) of the rat. CBF was measured using [14C]-iodoantipyrine autoradiography at 4 h. Brain damage was measured using 2,3, 5-triphenyl tetrazolium chloride (TTC) staining at 24 h and brain edema was measured using the wet/dry weight method. Brain ion contents were measured at 24 h using a flame photometer and chloridometer. In the CBF studies, the volume of tissue perfused below the ischemic threshold (<20 ml/100 g/min) for SDH was 122+/-35 mm3 (sham: 3.3+/-1.7 mm3). Following ICH, there was a small volume of tissue perfused below the ischemic threshold 50+/-11 mm3 (sham: 3. 3+/-2.5 mm3) but this volume corresponded closely to the volume of clot (71+/-5 mm3). The extent of brain damage, measured by TTC staining, in the cerebral cortex correlated with the increasing volume of the subdural blood clot (sham: 9+/-3 mm3; 200 microl: 81+/-19 mm3; P<0.01). Conversely, minimal brain damage was detected following ICH. The injection of blood into the subdural space or into the brain parenchyma induced blood volume-dependent increases in brain water content at 24 h. Increases in brain water content after SDH, were confined to the cerebral cortex (sham: 0.1+/-0.1 g/g dry weight; 200 microl: 0.8+/-0.3 g/g dry weight; P<0.001). In contrast, increases in brain water content after ICH were predominantly in the subcortical region (sham: 0.1+/-0.1 g/g dry weight; 200 microl: 0.4+/-0.2 g/g dry weight; P<0.01). The present investigations demonstrate differences in CBF, brain injury and edema formation following SDH and ICH indicating that these conditions may require different therapeutic interventions.