The ferric iron chelator 2,2′-dipyridyl attenuates basilar artery vasospasm and improves neurological function after subarachnoid hemorrhage in rabbits

We investigated the efficacy of the ferrous iron (Fe²⁺) chelator 2,2′-dipyridyl (DP) to attenuate cerebral vasospasm after subarachnoid hemorrhage (SAH). Thirty-six New Zealand white rabbits were randomly assigned to four groups: untreated control, SAH, SAH + dimethyl sulfoxide (DMSO) vehicle, and SAH + DP. SAH was induced by injection of autologous blood into the cisterna magna and then DP or vehicle was infused into the cistern magna for 5 days (20 mg/kg/day or an equal volume of DMSO). Neurological deficit score (NDS) was used to assess neurological function and cerebral angiography to measure basilar artery (BA) diameter following SAH. TUNEL staining was used to detect BA endothelial cell apoptosis, and immunohistochemistry and Western blotting to assess changes in caspase-3 protein levels 5 days post-SAH. The SAH + DP group had a significantly larger mean BA diameter and lower mean NDS post-SAH compared to the SAH + DMSO and SAH groups (p < 0.05). TUNEL-positive cell numbers and caspase-3 levels were significantly reduced in BA endothelial cells of the SAH + DP group as compared to the SAH and SAH + DMSO groups (p < 0.05). The iron chelator DP reduced vasospasm and neurological sequelae in rabbits, likely by chelating the Fe²⁺ in oxyhemoglobin and reducing oxidative stress-induced endothelial cell apoptosis.     

Rosiglitazone Attenuates Cerebral Vasospasm and Provides Neuroprotection in an Experimental Rat Model of Subarachnoid Hemorrhage

Background

Glutamate and oxidative stress play important roles after subarachnoid hemorrhage (SAH). The ability to modulate glutamate transporter 1 (GLT-1) and the antioxidative effect of rosiglitazone have been demonstrated. We investigated the neuroprotective effect of rosiglitazone after SAH.

Methods

SAH was induced by double blood injection. The rats were randomly divided into sham, SAH + vehicle, and SAH + rosiglitazone groups and treated with dimethyl sulfoxide, dimethyl sulfoxide, and 6 mg/kg of rosiglitazone, respectively, at 2 and 12 h after SAH induction and then daily for 6 days. Cerebrospinal fluid dialysates were collected 30 min before SAH induction and then daily for 7 days for glutamate measurement. Mortality, body weight, and neurological scores were also measured daily. On day 7 after SAH, the wall thickness and the perimeter of the basilar artery (BA), neuron variability, GLT-1 levels, glial fibrillary acidic protein (GFAP) expression and activity, and malondialdehyde, superoxide dismutase, and catalase activities were also evaluated.

Results

Rosiglitazone improved survival (relative risk = 0.325) and neurological functions and reduced neuronal degeneration (5.7 ± 0.8 vs. 10.0 ± 0.9; P < 0.001) compared with the SAH + vehicle group. Rosiglitazone also lowered glutamate levels by 43.5-fold and upregulated GLT-1 expression by 1.5-fold and astrocyte activity by 1.8-fold compared with the SAH + vehicle group. The increase in BA wall thickness was significantly attenuated by rosiglitazone, whereas the perimeter of the BA was increased. In addition, rosiglitazone abated the 1.9-fold increase in malondialdehyde levels and the 1.6-fold increase in catalase activity after SAH.

Conclusion

Rosiglitazone reduced SAH mortality, neurological deficits, body weight loss, GFAP loss, and cerebral vasospasm by preventing the neurotoxicity induced by glutamate and oxidative stress.     

动物蛛网膜下腔出血后脑血管痉挛与内皮素、一氧化氮的关系

目的:研究兔症状性蛛网膜下腔出血(ＳＡＨ)后脑血管痉挛(ＣＶＳ)与内皮素(ＥＴ)和一氧化氮(ＮＯ)的关系。方法:采用兔ＳＡＨ模型,观察ＳＡＨ前后动物进食量、神经功能和局部脑血流量(ｒＣＢＦ)改变,测定血液和脑脊液中ＥＴ和ＮＯｘ－含量。结果:ＳＡＨ后动物进食量和ｒＣＢＦ下降、神经功能障碍,血液和脑脊液中ＥＴ含量增加,ＮＯｘ－含量下降(Ｐ＜０．０１)。结论:兔双侧颈动脉结扎后枕大池二次注血可制成可靠的症状性ＳＡＨ后ＣＶＳ模型。ＳＡＨ后ＥＴ和ＮＯ含量的改变与ＣＶＳ的发生密切相关,并进而导致临床症状的恶化。     

The rise of soluble platelet-derived growth factor receptor β in CSF early after subarachnoid hemorrhage correlates with cerebral vasospasm

Platelet-derived growth factor β (PDGFβ) has been proposed to contribute to the development of cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH), and soluble PDGFRβ (sPDGFRβ) is considered to be an inhibitor of PDGF signaling. We aimed at determining the sPDGFRβ concentrations in the cerebrospinal fluid (CSF) of patients with aneurysmal SAH (aSAH) and analyzing the relationship between sPDGFRβ level and CVS. CSF was sampled from 32 patients who suffered aSAH and five normal controls. Enzyme-linked immunosorbent assay was performed to determine the sPDGFRβ concentrations in the CSF. Functional outcome was assessed using modified Rankin scale (mRS) at 6 months after aSAH. CVS was identified using transcranial Doppler or angio-CT or DSA. The cutoff of sPDGFRβ for CVS was defined on the ROC curve. The concentrations of sPDGFRβ following aSAH were both higher than those of normal controls on days 1–3 and 4–6, and peaked on days 7–9 post-SAH. The cutoff value of sPDGFRβ level on days 1–3 for CVS was defined as 975.38 pg/ml according to the ROC curve (AUC?=?0.680, p?=?0.082). In addition, CSF sPDGFRβ concentrations correlated with CVS (r?=?0.416, p?=?0.018), and multivariate analysis indicated that sPDGFRβ level higher than 975.38 pg/ml on days 1–3 was an independent predictor of CVS (p?=?0.001, OR?=?19.22, 95% CI: 3.27–113.03), but not for unfavorable outcome after aSAH in the current study. CSF sPDGFRβ level increases after aSAH and is higher in patients who developed CVS, and sPDGFRβ level higher than 975.38 pg/ml on days 1–3 is a potential predictor for CVS after SAH.     

Inhibitory effect of deuterium oxide on cerebral vasospasm after experimental subarachnoid hemorrhage in a rabbit model

Abstract

Object: We wished to determine the inhibitory effect of deuterium oxide (D₂O) on cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH).

Methods and results: An established rabbit single-hemorrhage was used. Thirty-five rabbits were randomly divided into four groups: non-treatment, sham control, lower-D₂O, and higher-D₂O treatment groups. Angiography was performed before (day 0) and after (day 2) SAH and the CVS ratio was calculated by comparing the diameter of the basilar artery (BA) on day 2 with that on day 0. After death, blood clot volume was assessed and the BA was dissected from the brain for histological examination. The CVS ratio in D₂O-treatment groups was significantly higher in comparison with that in non-treatment and sham control groups (p < 0.0001). Furthermore, the volume of blood clot around the BA was reduced significantly in D₂O-treatment groups, compared with those in both the non-treatment and the sham control groups (p < 0.05). Histological examination showed that the BA represented less folding of the internal elastic lumina in D₂O-treatment groups, while a corrugation of the intima with the thickened vessel wall was seen in both the non-treatment and sham control groups.

Conclusion: Therapeutic administration of D₂O into the cisterna magna exhibited an inhibitory effect on CVS after SAH in rabbits.     

Inhibitory effect of deuterium oxide on cerebral vasospasm after experimental subarachnoid hemorrhage in a rabbit model

OBJECT: We wished to determine the inhibitory effect of deuterium oxide (D(2)O) on cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH). METHODS AND RESULTS: An established rabbit single-hemorrhage was used. Thirty-five rabbits were randomly divided into four groups: non-treatment, sham control, lower-D(2)O, and higher-D(2)O treatment groups. Angiography was performed before (day 0) and after (day 2) SAH and the CVS ratio was calculated by comparing the diameter of the basilar artery (BA) on day 2 with that on day 0. After death, blood clot volume was assessed and the BA was dissected from the brain for histological examination. The CVS ratio in D(2)O-treatment groups was significantly higher in comparison with that in non-treatment and sham control groups (p < 0.0001). Furthermore, the volume of blood clot around the BA was reduced significantly in D(2)O-treatment groups, compared with those in both the non-treatment and the sham control groups (p < 0.05). Histological examination showed that the BA represented less folding of the internal elastic lumina in D(2)O-treatment groups, while a corrugation of the intima with the thickened vessel wall was seen in both the non-treatment and sham control groups. CONCLUSION: Therapeutic administration of D(2)O into the cisterna magna exhibited an inhibitory effect on CVS after SAH in rabbits.     

川芎嗪对实验性SAH后CVS防治作用的研究

目的研究兔症状性蛛网膜下腔出血(SAH)后脑血管痉挛(CVS)与内皮素(ET)和一氧化氮(NO)的关系及川芎嗪的保护作用.方法采用双侧颈动脉结扎和枕大池二次注血制成兔SAH模型,观察SAH前后动物进食量和神经功能改变,用放射免疫方法和硝酸还原酶法分别测定血液和脑脊液中ET和NOx-含量,以氢清除法测定局部脑血流量(rCBF).结果SAH后大部分动物进食量有不同程度的下降,所有动物均有不同程度的神经功能障碍和rCBF下降.SAH后血液和脑脊液中ET含量增加,NOx-含量下降(P＜0.01).上述变化随出血时间延长和出血量的增大而增加.川芎嗪治疗组上述变化均有不同程度的改善.结论双侧颈动脉结扎后枕大池二次注血可制成可靠的兔症状性SAH后CVS的动物模型.兔SAH后ET和NO含量的改变与CVS的发生密切相关,并进而导致临床症状的恶化.川芎嗪可通过抑制SAH后ET和NO的变化而对CVS的发生和发展起到防治作用.     

Glycyrrhizic acid exerts anti-inflammatory effect to improve cerebral vasospasm secondary to subarachnoid hemorrhage in a rat model

This study aimed to investigate the therapeutic effect of glycyrrhizic acid (GA) on the cerebral vasospasm (CVS) in a rat subarachnoid hemorrhage (SAH) model and to explore the potential mechanism. A total of 44 healthy male rats were randomly assigned into 3 groups: control group (n = 12), SAH group (n = 16) and GA group (n = 16). No treatment was conducted in control group; in SAH group and GA group, experimental CVS was induced using a double-hemorrhage model and then rats were intraperitoneally injected with normal saline and GA at 10 mg/kg, respectively, once daily. Three days later, neurological function was evaluated. Then, animals were sacrificed, and the basilar artery was collected. The inner diameter and vascular wall thickness were determined. Western blotting was employed to detect high mobility group protein B1 (HMGB1) protein expression and RT-PCR to detect the mRNA expression of IL-1β, IL-6, TNF-α, and IL-10 in the basilar artery. GA treatment significantly improved the neurological function following SAH. In GA group, the basilar artery diameter increased markedly and vascular wall thickness reduced significantly when compared with SAH group (p < 0.05). HMGB1 protein expression and mRNA expression of IL-1β, IL-6, TNF-α, and IL-10 in SAH group were significantly higher than in control group (p < 0.05). However, GA dramatically reduced IL-1β, IL-6, and TNF-α, and further elevated IL-10 expression as compared to SAH group (p < 0.05). GA may inhibit HMGB1 expression and subsequent production of inflammatory cytokines to prevent CVS following SAH.     

Endothelin and aneurysmal subarachnoid haemorrhage: a study of subarachnoid cisternal cerebrospinal fluid.

Endothelin (ET) is considered one of the most potent vasoconstrictor polypeptides; several experimental studies have suggested its possible role in the pathogenesis of arterial vasospasm after subarachnoid haemorrhage (SAH). Previously reported data on plasma and CSF levels of endothelin in patients with a diagnosis of SAH have been controversial. Cisternal endothelin CSF levels and the possibility that they could be related to vasospasm and other clinical patterns of SAH were investigated. CSF samples were obtained from 55 patients admitted after angiographic diagnosis of intracranial aneurysm. Levels of ET-1 and ET-3 were measured through radio-immunoassay technique. Twelve patients who had operations for unruptured aneurysms were considered control cases; 43 patients with SAH were classified according to: Hunt and Hess grading at admission, vasospasm grading, CT classification and timing of surgery. In all 55 patients ET-1 was measured, while positive levels of ET-3 were found only in 17 cases of 48. No linear correlation was found between cisternal CSF ET-1 levels when considering time of surgery, CT classification, Hunt and Hess grading at admission, and vasospasm grading. The results of ET-3 assay should be considered with great caution because of the low percentage of positive cases. Cisternal CSF levels of ET-1 and ET-3 are not directly related to the occurrence of arterial vasospasm after the aneurysm rupture, or to other major clinical patterns of SAH; however, ET-1 expression occurs either in paraphysiological (unruptured aneurysm) or in pathological conditions (SAH). It is suggested that ET may potentiate, or may be potentiated by, other factors playing a consistent pathophysiological role in the development of vasospasm.     

大鼠蛛网膜下腔出血后MMP-9在基底动脉壁中的表达变化

目的探讨大鼠蛛网膜下腔出血（subarachnoid hemorrhage,SAH）后基质金属蛋白酶-9（MMP-9）在基底动脉壁中的表达变化及其与脑血管痉挛（Cerebral Vasospasm,CVS）的关系。方法健康成年雄性SD大鼠51只,并随机分为正常组、对照组和SAH组,应用枕大池一次注血法制成SAH动物模型,对照组和SAH组大鼠在SAH后1 d,3 d,5 d,7 d,14 d时间点通过HE染色光镜下观察基底动脉的病理学变化,测定血管壁厚度及血管腔内径,以此评价脑血管痉挛;应用免疫组化法评估大鼠基底动脉管壁中MMP-9在不同时间点的表达水平。结果 HE染色显示SAH组基底动脉管腔狭窄,管壁增厚,3 d时最明显,之后狭窄程度渐减轻,14 d时基本正常;SAH后基底动脉壁MMP-9表达增加,表达高峰为注血后3～5 d,随后开始下降,14 d恢复正常。结论大鼠SAH存在明确的CVS,SAH后MMP-9在基底动脉壁中的表达上调,并与CVS的时相一致,提示MMP-9可能参与了CVS的病理过程。     

Effect of 18β-glycyrrhetinic acid on cerebral vasospasm caused by asymmetric dimethylarginine after experimental subarachnoid hemorrhage in rats

Abstract

Objectives:

Cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH) is characterized by the severe constriction of an artery, which often leads to unfavorable outcomes. CVS after SAH is closely associated with asymmetric dimethylarginine (ADMA) and connexin. The effect of 18β-glycyrrhetinic acid (18β-GA), an inhibitor of gap junction, on ADMA, connexin, and CVS after SAH were investigated.

Methods:

Sprague–Dawley rats (n = 120), weighing 300–350 g, were divided into the control group, sham, SAH, and SAH + 18β-GA groups. In the SAH group, blood was injected into the prechiasmatic cistern of the rats, and 18β-GA (10 mg/kg) was intraperitoneally injected. The neurological score, basilar artery diameter, ADMA, and connexin protein contents (Cx40, Cx43, and Cx45) were measured using Kaoutzanis scoring system, pressure myograph, enzyme linked immunosorbent assay kit, and Western blot, respectively, 1, 3, 5, 7, and 14 days after SAH.

Results:

The neurological score significantly decreased 3, 5, 7, and 14 days after SAH. The basilar artery diameter significantly decreased, and the ADMA level in the cerebrospinal fluid (CSF) significantly increased at all time points. The level of Cx40 significantly decreased on days 3, 5, 7, and 14, and the level of Cx43 and Cx45 significantly increased at all time points. ADMA and Cx43 are positively correlated. However, the upregulated level of ADMA, Cx43, and Cx45 were attenuated. The neurology result significantly improved in the SAH + 18β-GA group.

Conclusions:

Treatment with 18β-GA in SAH rats decreases Cx43 and Cx45 in basilar artery and ADMA in CSF. ADMA is probably involved in the pathophysiological events of CVS after SAH by altering connexin proteins. The mechanism of connexin protein changes caused by ADMA needs to be further studied.     

颅底肿瘤术后脑脊液中ET-1的动态变化与脑血管痉挛的相关性研究

目的探讨颅底肿瘤术后脑脊液中内皮素-1（ET-1）的动态变化规律及其与脑血管痉挛（CVS）的相关性。方法颅底肿瘤病人33例，在术后第3、5、7、10和14天用放免法测定脑脊液中ET-1的含量；手术前1天和术后第1、3、5、7、10和14天用经颅多普勒超声动态监测双侧颈内动脉、双侧大脑前动脉和中动脉的血流速度。结果术后发生CVS的患者第3天脑脊液中ET-1水平即升高，第7天达到高峰，而后逐渐下降；术后第5、7和10天，中、重度CVS组ET-1水平明显高于对照组（P〈0.05），术后第7和10天，重度CVS组ET-1水平高于轻、中度CVS组和无CVS组（P〈0.05）；术后脑脊液中ET-1的水平与大脑中动脉平均血流速度呈正相关（r=0.635，P〈0.01）。结论颅底肿瘤术后患者脑脊液中ET-1水平的升高参与了术后CVS的发生，且其变化与术后CVS呈正相关，提示其含量可预测颅底肿瘤病人术后CVS的严重程度和预后。     

丹参对实验性蛛网膜下腔出血后脑血管痉挛的影响

目的 探讨中药丹参防治蛛网膜下腔出血(SAH)后脑血管痉挛(CVS)的作用机制。方法 采用兔枕大池2次注血法制作实验性兔SAH模型,放免法测定SAH后2d、4d、7d时的血及脑脊液中的内皮素(ET)和降钙素基因相关肽(CCRP)的含量,并于第2次注血后30min从耳缘静滴复方丹参注射液,以后1次/d(2ml/kg),至第7d,测定时间点同上。结果 丹参组在第2次注血后血浆及脑脊液中ET含量较对照组高,较单纯注血组低,而CGRP较对照组低,较单纯注血组高。结论 丹参可以通过抑制ET升高和CCRP降低达到防止SAH后CVS的目的。     

实验性SAH后CVS与ET、NO的关系

目的　研究兔症状性蛛网膜下腔出血（SAH）后脑血管痉挛（CVS）与内皮素（ET）和一氧化氮（NO）的关系。方法　采用双侧颈动脉结扎和枕大池二次注血法制成兔SAH模型，观察SAH前后动物进食量和神经功能改变，用放射免疫方法和硝酸还原酶法分别测定血液和脑脊液中ET和NOx     

血浆脑利钠肽与蛛网膜下腔出血后脑血管痉挛及低钠血症的关系

目的　探讨血浆脑利钠肽(BNP)与蛛网膜下腔出血(SAH)后脑血管痉挛(CVS)及低钠血症的关系。方法　动态测定30例SAH患者发病后1~3d、4~6d、7~9d及10~12d4个时段的血浆BNP和血钠水平,对血浆BNP和血钠水平进行相关性分析;比较有无CVS及有症状与无症状CVS患者的血浆BNP水平。同时检测18名健康人的血浆BNP水平作为对照。结果　SAH患者血浆BNP水平明显高于对照组(P<0. 01),虽然无CVS及无症状CVS患者血浆BNP水平在SAH后4个时段中逐渐下降,但有症状CVS患者第3时段血浆BNP水平明显高于第1时段(P<0. 01 );第2 ~4时段血钠与血BNP水平呈显著负相关(r2 =-0 .763,r3 =-0 .681,r4 =-0 .764,均P<0 .01)。结论　BNP可能导致和参与了SAH后CVS及低钠血症的发生,并在SAH后CVS的发病机制中起重要的作用。     

糖尿病大鼠蛛网膜下腔出血后海马组织中caspase-3、Bax和Bcl-2的表达及醒脑静干预的研究

目的探讨醒脑静对糖尿病大鼠蛛网膜下腔出血（sAH）后海马组织凋亡相关因子天冬氨酸特异性半胱氨酸蛋白酶（casDase-3）、Bax和Bcl-2表达的影响。方法成年雄性Wistar大鼠28只,按随机数字表法随机分为空白对照组（n=7）、糖尿病对照组（n=7）、糖尿病SAH组（n=7）和醒脑静治疗组（n=7）;采用链脲佐菌素（STZ）腹腔注射方法建立糖尿病大鼠模型,然后采用枕大池两次注血法建立糖尿病大鼠SAH模型。SAH后48h取海马组织,用实时聚合酶链式反应检测caspase-3、Bax及Bcl-2的mRNA的表达,并用免疫印迹法测定它们蛋白表达,进行验证。结果空白对照组和糖尿病对照组大鼠海马组织中的caspase-3、Bax和Bcl-2的mRNA表达量均无显著差异（P〉0．05）;与空白对照组和糖尿病对照组相比,糖尿病SAH组和醒脑静治疗组其mRNA表达量均显著升高（P〈0．05）;醒脑静治疗组caspase-3和BaxmRNA表达水平均显著低于糖尿病SAH组大鼠（P〈0．05）,而Bcl-2mRNA表达水平却明显高于糖尿病SAH组（P〈0．05）。它们蛋白表达变化与mRNA表达基本相符。结论醒脑静抑制糖尿病SAH大鼠海马组织促凋亡相关因子表达,而促进抗凋亡相关因子表达,从而发挥保护作用。     

Brain natriuretic peptide and cerebral vasospasm in subarachnoid hemorrhage. Clinical and TCD correlations

BACKGROUND AND PURPOSE: Hyponatremia has been shown in association with cerebral vasospasm (CVS) following aneurysmal subarachnoid hemorrhage (SAH). In the past few years there has been increasing evidence that brain natriuretic peptide (BNP) is responsible for natriuresis after SAH. The purpose of the present study was to investigate the relationship between BNP plasma concentrations and CVS after aneurysmal SAH. METHODS: BNP plasma concentrations were assessed at 4 different time periods (1 to 3 days, 4 to 6 days, 7 to 9 days, and 10 to 12 days) in 19 patients with spontaneous SAH. BNP plasma levels were investigated with respect to neurological condition, SAH severity on CT, and flow velocities measured by means of transcranial Doppler. RESULTS: Thirteen patients had Doppler evidence of CVS; 7 of these had nonsymptomatic CVS. In 6 patients, CVS was severe and symptomatic, with delayed ischemic lesion on CT in 5 of these. CVS was severe and symptomatic in 6 patients, and delayed ischemic lesions were revealed on CT in 5 of these. BNP levels were found to be significantly elevated in SAH patients compared with control subjects (P=0.024). However, in patients without CVS or with nonsymptomatic CVS, BNP concentrations decreased throughout the 4 time periods, whereas a 6-fold increase was observed in patients with severe symptomatic CVS between the first and the third periods (P=0.0096). A similar trend in BNP plasma levels was found in patients with severe SAH compared with those with nonvisible or moderate SAH (P=0.015). CONCLUSIONS: In conclusion, our results show that BNP plasma levels are elevated shortly after SAH, although they increase markedly during the first week in patients with symptomatic CVS. The present findings suggest that secretion of BNP secretion after spontaneous SAH may exacerbate blood flow reduction due to arterial vasospasm.     

细胞间粘附分子-1在蛛网膜下腔出血后痉挛血管内的表达

目的：研究细胞间粘附分子－1（ICAM－1）在蛛网膜下腔出血（SAH）后脑血管壁内的表达变化规律及其与脑血管痉挛（CVS）的关系。方法：应用免疫组织化学及逆转录－聚合酶链式反应（RT－PCR）等方法，检测大鼠2次注血SAH模型基底动脉壁内ICAM－1在蛋白质和mRNA水平上的表达。结果：在大鼠脑池内注血后第3d，基底动脉血管腔狭窄已非常明显，第5d达到高峰。注血后第1d,ICAM-1表达开始上调，主要在内膜及内膜下，第3dg表达明显增强并持续到第5d。ICAM－1在蛋白和mRNA水平上表达基本一致，且在时程上的变化与CVS的程度密切相关。结论：由ICAM－1介导的血管壁炎症反应可能在CVS发生和发展过程中起重要作用。     

The Value of CT Angiography and Transcranial Doppler Sonography in Triaging Suspected Cerebral Vasospasm in SAH Prior to Endovascular Therapy

Background  Transcranial Doppler sonography (TCD) is a noninvasive method for detecting arterial cerebral vasospasm (CVS) in aneurysmal subarachnoid hemorrhage (SAH). Computed tomographic angiography (CTA) has been increasingly used for CVS diagnosis. The purpose of this study was to evaluate the degree of agreement between TCD and CTA in diagnosing clinical CVS following SAH, and to define the role of CTA in triaging patients prior to digital subtraction angiography (DSA) and endovascular intervention. Methods  Fifty-five consecutive patients with aneurysmal SAH who underwent sequential TCD and CTA were analyzed. TCD CVS was defined as anterior circulation peak mean velocity (PMV) >160 cm/s, basilar artery (BA) PMV >90 cm/s, and Lindegaard ratio (LR) >6. CTA CVS was defined as >50% luminal narrowing in the affected vessel. Clinical CVS was defined as the onset of new focal neurological deficit attributed to delayed ischemic injury. Results  Thirteen patients (24%) had clinical CVS and 42 patients (76%) were asymptomatic. All patients with clinical CVS had also radiological evidence of CVS (agreement 100%). In 35 patients without clinical CVS, both tests agreed for absence of CVS in 28 cases (agreement 83%). The remaining 7 asymptomatic patients had radiological CVS only, in disagreement with clinical absence of CVS (17%). Conclusions  Clinical evaluation and TCD can reliably diagnose CVS in symptomatic patients and PMV >180 cm/s, or can rule out CVS in asymptomatic patients with PMV <140 cm/s. In this category of patients, adding a CTA to clinical evaluation and TCD may not be warranted.     

蛛网膜下腔出血大鼠基底动脉血小板源性生长因子的表达变化

目的探讨血小板源性生长因子(PDGF)在大鼠蛛网膜下腔出血(SAH)后脑血管痉挛(CVS)血管壁的表达及关系。方法将30只大鼠按照枕大池二次注血的方法建立模型,然后分别于建立模型后的1 d、3 d、5 d、7 d、14 d将大鼠处死,取出基底动脉制作石蜡切片在光镜下观察。采用免疫组化法检测大鼠基底动脉血管壁PDGF的表达水平。结果模型组中PDGF在基底动脉血管壁上的表达,3 d和5 d组最明显,与脑血管痉挛程度的变化是一致的。结论通过枕大池二次注血能够成功的模拟SAH后CVS的发生。PDGF参与了SAH后CVS的过程,并可能起了重要的作用。