蛛网膜下腔出血后鼠脑底动脉内皮素-1能神经纤维的表达变化

本文旨在探讨大鼠蛛网下腔出血(SAH)诱发脑血管痉挛时脑底动脉内皮素-1(endothelin-1,ET-1)能神经纤维的表达变化及其诱发脑血管痉挛的作用。大鼠随机分为正常组、SAH组(3d、14d)。SAH组大鼠取股动脉自体血注入蛛网膜下腔,应用免疫组织化学ABC法,观察正常组、SAH组大鼠脑底动脉ET-1能神经纤维的表达。结果显示正常组大鼠脑底动脉可见棕褐色,细线状ET-1能免疫反应阳性纤维。SAH后3d组大鼠脑底动脉与正常组大鼠脑底动脉比较ET-1能神经纤维密度明显增多,统计学检验(P<0.05);而SAH14d组大鼠脑底动脉ET-1能阳性神经纤维密度与正常组比较无明显变化。以上结果提示脑底动脉ET-1能神经纤维在蛛网膜下腔出血诱发脑血管痉挛的病理生理过程中可能发挥重要的作用。     

In vitro evidence of the role of hemoglobin during vasospasm on the modifications of the expression of PKCalpha and zeta

The cellular events leading to cerebral vasospasm after subarachnoid hemorrhage (SAH) are poorly understood, although the family of protein kinase C (PKC) is already known to play crucial roles in this pathology. Hemoglobin (Hb) is one of the major causes of the cerebral vasospasm that follows SAH. In the present study we investigated whether Hb can in vitro regulate PKC expression in endothelial as opposed to smooth-muscle cells. The levels of expression of PKCalpha and PKCzeta were quantitatively determined by means of computer-assisted fluorescence microscopy in the A7r5 smooth-muscle rat cells and human umbilical endothelial cells (HUVECs). Hb significantly modified both calcium-dependent PKCalpha and calcium-independent PKCzeta expression in HUVECs and A7r5 smooth-muscle rat cells. Our data showed that, in vitro, Hb promptly and markedly modified the levels of expression of both calcium-dependent PKCalpha and calcium-independent PKCzeta. We are currently investigating the effects of specific PKC antagonists associated or not with calcium channel blockers on the expression of PKC and the in vivo severity of SAH-induced vasospasm. Our results encourage the prophylactic use of specific PKC isoform antagonists associated with calcium channel blockers early after SAH to prevent cerebral vasospasm.     

Patient-specific flow analysis of brain aneurysms at a single location: comparison of hemodynamic characteristics in small aneurysms

The purpose of this study is to examine and compare the hemodynamic characteristics of small aneurysms at the same anatomical location. Six internal carotid artery-ophthalmic artery aneurysms smaller than 10 mm were selected. Image-based computational fluid dynamics (CFD) techniques were used to simulate aneurysm hemodynamics. Flow velocity and wall shear stress (WSS) were also quantitatively compared, both in absolute value and relative value using the parent artery as a baseline. We found that flow properties were similar in ruptured and unruptured small aneurysms. However, the WSS was lower at the aneurysm site in unruptured aneurysms and higher in ruptured aneurysms (P < 0.05). Hemodynamic analyses at a single location with similar size enabled us to directly compare the hemodynamics and clinical presentation of brain aneurysms. The results suggest that the WSS in an aneurysm sac can be an important hemodynamic parameter related to the mechanism of brain aneurysm growth and rupture.     

A clinical analysis of twelve cases of ruptured cerebral de novo aneurysms

Formation of cerebral de novo aneurysms (CDNA) is rare, and the pathogenesis remains obscure. In this study, we investigated the factors that contribute to the formation of CDNA and suggest guidelines for following patients treated for cerebral aneurysms. We retrospectively reviewed 2,887 patients treated for intracranial aneurysm at our institute from January of 1976 to December of 2005. Of those patients, 12 were readmitted due to recurrent rupture of CDNA, which was demonstrated by cerebral angiography. We assessed clinical characteristics, such as gender, size and site of rupture, past history, and the time to CDNA rupture. Of the 12 patients, 11 were female and 1 was male, with a mean age at rupture of the first aneurysm of 44.7 years (range: 30-69 years). The mean time between the first episode of subarachnoid hemorrhage (SAH) and the second was 8.9 years (range: 1.0-16.7 years). The most common site of ruptured CDNA was the internal carotid artery (5 patients, 41.7%), followed by basilar artery bifurcation (3 patients, 25.0%). In the remaining 4 patients, rupture occurred in the anterior communicating, middle cerebral, anterior cerebral (A1), or posterior cerebral (P1) arteries. In 5 cases (41.7%), the CDNA occurred contralateral to the initial aneurysm. Eleven patients (91.7%) had a past history of arterial hypertension. There was no history of habitual smoking or alcohol abuse in any of the patients. Eight patients underwent clipping for CDNA and three patients were treated with coiling. One patient who had multiple aneurysms was treated with clipping following intra-aneurysmal coiling. Assessment according to the Glasgow Outcome Scale (GOS) of the patients after the treatment was good in 10 cases (83.3%) and fair in 2 cases (16.7%). Although formation of CDNA after successful treatment of initial aneurysm is rare, several factors may contribute to recurrence. In our study, female patients with a history of arterial hypertension were at higher risk for ruptured CDNA. We recommend follow-up imaging studies every five years after treatment of the initial aneurysm, especially in women and those with a history of arterial hypertension.     

Endothelial nitric oxide gene T-786C polymorphism and subarachnoid hemorrhage in Korean population

We aimed to elucidate whether the eNOS T-786C mutant allele is implicated in subarachnoid hemorrhage (SAH) susceptibility or vasospasm after SAH, and whether the mutant allele is differentially expressed in those with small and large ruptured aneurysms in Korean population. 136 consecutive patients diagnosed with aneurismal SAH and 113 controls were recruited. Polymerase chain reaction and direct sequencing of both strands were performed to determine genotypes with respect to the eNOS T-786C mutation. No significant difference was found between cases and controls with respect to the distributions of the two eNOS T-786C single nucleotide polymorphism (SNP) genotypes. No significant differences in the distributions of the eNOS T-786C SNP genotypes were found with regard to the sizes of ruptured aneurysms or the occurrence of vasospasm after SAH. Multiple logistic regression analysis after controlling for age and sex showed the eNOS T-786C SNP T/C geno-type was independently associated with an unfavorable outcome (GOS grade 3-5) of SAH (Exp (beta)=4.27, 95% CI 1.131-16.108, p=0.032). In conclusion, the eNOS T-786C mutation was not found to be associated with either a susceptibility to SAH or vasospasm after SAH, or with aneurysm size in Korean population. The eNOS T-786C SNP T/C genotype could be used as a prognostic marker in individuals with SAH.     

Potentials of magnesium treatment in subarachnoid haemorrhage.

Subarachnoid hemorrhage from a ruptured aneurysm is a subset of stroke. The young age (median 55 years) and poor outcome (50% of patients die; 30% of survivors remain dependent) explain why in the population the loss of productive life years from aneurysmal subarachnoid hemorrhage (SAH) is as large as that from brain infarcts, the most common type of stroke. Ischemia plays an important role in the pathophysiological process after SAH. A period of global cerebral ischemia firstly occurs in the acute phase, immediately after rupture of the aneurysm, due to acute vasoconstriction and elevated intracranial pressure, which leads to a drop in perfusion pressure. This is quite distinct from the secondly, delayed cerebral ischemia (DCI), which is focal or multi-focal. DCI usually occurs between 4 and 10 days after the initial bleeding, has a gradual onset and is multi-focal, and is an important cause of death and dependency after SAH. The interval between the bleeding and the onset of ischemia provides an opportunity for preventive treatment. Magnesium is readily available, inexpensive and has a well-established clinical profile in obstetrical and cardiovascular practice. It is beneficial in the treatment of eclampsia, a disease with a pathophysiology comparable to DCI after subarachnoid hemorrhage. Neuroprotective mechanisms of magnesium include inhibition of the release of excitatory amino-acids and blockade of the NMDA-glutamate receptor. Magnesium is also a non-competitive antagonist of voltage dependent calcium channels, has cerebrovascular dilatory activity and is an important co-factor of cellular ATPases, including the Na/K-ATPase. Magnesium can reverse delayed cerebral vasospasm and reduces the extent of acute ischemic cerebral lesions after experimental subarachnoid hemorrhage in rats. In this article we discuss the neuroprotective potency of magnesium in SAH by describing the pathophysiology of ischaemia after SAH and the many ways magnesium may interfere with this.     

Recurrent cerebral aneurysm formation and rupture within a short period due to invasive aspergillosis of the nasal sinus; pathological analysis of the catastrophic clinical course

Destructive infiltration of invasive fungal sinusitis can easily occur into the central nervous system (CNS). Cerebral aneurysms associated with fungal infection are highly vulnerable to rupture, and can frequently and rapidly take a serious clinical course. We experienced a patient who twice developed cerebral aneurysm followed by rupture due to invasive fugal sinusitis. This 77-year-old man was admitted for progressive bilateral visual disturbance, which was initially treated as idiopathic hypertrophic pachymeningitis. The patient subsequently suffered subarachnoid hemorrhage (SAH) twice in only 12 days. Both SAH originated from different newly formed cerebral aneurysms. Trapping was performed for both ruptured aneurysms. Pathological examination of the resected aneurysms indicated the presence of fungi determined to be Aspergillus. This Aspergillus infection was also discovered inside the frontal sinus by endoscopic biopsy, so a regimen of antifungal agents was instituted. Prolonged antifungal therapy caused renal impairment, which ultimately led to the patient’s death. Autopsy detected no mycotic infiltration of the major cerebral arteries, except for the 2 ruptured cerebral aneurysms. However, prolonged mycosis of the CNS, such as in the deep part in the falx cerebri and in the small veins proximal to the tentorium cerebelli, was observed, indicating that mycosis invading the cranium is refractory even to long-term administration of antifungal agents. The present case strongly suggests that urgent and proactive definitive diagnosis is essential to successfully treat invasive paranasal sinus aspergillosis. If infiltration of the CNS is suspected, early surgical resection and antifungal therapy must be initiated immediately.     

蛛网膜下腔出血后鼠脑底动脉降钙素基因相关肽能神经纤维的变化

本文旨在探讨大鼠蛛网膜下腔出血(SAH)诱发脑血管痉挛时脑底动脉降钙素基因相关肽(CGRP)能神经纤维的变化。大鼠随机分为正常组、蛛网膜下腔出血组。SAH组大鼠取股动脉自体血注入蛛网膜下腔,正常组动物不做任何处理。3d后灌注固定后,应用免疫组织化学ABC法,对两组大鼠脑底动脉CGRP能神经纤维变化进行观察。结果显示:正常组大鼠脑底动脉可见棕褐色,细线状CGRP能免疫反应阳性纤维;而SAH后3d组大鼠脑底动脉与正常组大鼠脑底动脉相比CGRP能神经纤维密度明显减少,具有统计学意义。以上结果提示脑底动脉CGRP能神经纤维在蛛网膜下腔出血诱发脑血管痉挛的病理生理过程中可能发挥重要的作用。     

Risk Factors for Intraprocedural Rerupture during Embolization of Ruptured Intracranial Aneurysms

BackgroundIntraprocedural rupture (IPR) is a devastating complication in endovascular treatment of ruptured intracranial aneurysms, but its risk factors have not been fully assessed. This study was performed to explore the risk factors for IPR during embolization of ruptured cerebral aneurysms.MethodsA total of 1,494 patients with ruptured intracranial aneurysms who underwent endovascular interventional embolization were enrolled. Clinical characteristics were collected for each patient. Univariate and multivariate logistic regression analysis was employed to identify the factors independently associated with IPR. A receiver operating characteristic (ROC) curve analysis was performed to determine the cutoff values of continuous variables predicting IPR.ResultsForty-one patients suffered from IPR (2.7%). Multivariate logistic regression analysis indicated that aneurysm size (odds ratio [OR], 0.819; 95% confidence interval [CI], 0.732–0.916), aneurysms with irregular morphology (OR, 2.162; 95% CI, 1.143–4.091), time from symptom onset to intervention (OR, 1.615; 95% CI, 1.207–2.161), and vasospasm during embolization (OR, 2.021; 95% CI, 1.038–3.934) were the independent risk factors of IPR. ROC curve analysis showed that the area under the curve for aneurysm size and time from onset to intervention were 0.697 (cutoff value, 3.4 mm; sensitivity, 78.8%; and specificity, 53.7%) and 0.659 (cutoff value, 2 days; sensitivity, 78.0%; and specificity, 45.2%), respectively.ConclusionAneurysms with irregular morphology, aneurysms ≤ 3.4 mm in diameter, time from onset to intervention > 2 days and cerebral vasospasm during embolization are independent risk factors for IPR during coil embolization of ruptured aneurysms. More attention should be paid to the factors increasing the risk of IPR in patients with ruptured aneurysms so as to minimize this complication.     

Mouse Models of Intracranial Aneurysm

Subarachnoid hemorrhage secondary to rupture of an intracranial aneurysm is a highly lethal medical condition. Current management strategies for unruptured intracranial aneurysms involve radiological surveillance and neurosurgical or endovascular interventions. There is no pharmacological treatment available to decrease the risk of aneurysm rupture and subsequent subarachnoid hemorrhage. There is growing interest in the pathogenesis of intracranial aneurysm focused on the development of drug therapies to decrease the incidence of aneurysm rupture. The study of rodent models of intracranial aneurysms has the potential to improve our understanding of intracranial aneurysm development and progression. This review summarizes current mouse models of intact and ruptured intracranial aneurysms and discusses the relevance of these models to human intracranial aneurysms. The article also reviews the importance of these models in investigating the molecular mechanisms involved in the disease. Finally, potential pharmaceutical targets for intracranial aneurysm suggested by previous studies are discussed. Examples of potential drug targets include matrix metalloproteinases, stromal cell‐derived factor‐1, tumor necrosis factor‐α, the renin‐angiotensin system and the β‐estrogen receptor. An agreed clear, precise and reproducible definition of what constitutes an aneurysm in the models would assist in their use to better understand the pathology of intracranial aneurysm and applying findings to patients.     

影响颅内小型动脉瘤破裂的影像解剖特征分析

目的 探讨颅内小型动脉瘤的破裂与其影像解剖特征的关系,建立动脉瘤破裂风险评分的预测模型,为颅内小型动脉瘤破裂高危患者的早期识别干预提供参考。方法 回顾性分析2015年1月—2020年5月郑州大学附属郑州中心医院经头颈CT血管造影或全脑血管造影证实的182例颅内小型动脉瘤(最大径＜5 mm)患者的临床资料,其中男62例、女120例,年龄31~83(56.85±11.51)岁,动脉瘤破裂组95例、未破裂组87例。两组患者动脉瘤的部位、形状、有无子囊、生长方向及相关解剖学参数等临床特征和影像解剖特征的比较采用单因素分析方法;动脉瘤破裂的独立危险因素分析采用多因素logistic分析方法,建立动脉瘤破裂的影像解剖特征的预测模型。结果 两组患者基线资料比较差异均无统计学意义(P值均＞0.05)。单因素分析显示,两组间动脉瘤部位、瘤壁形状、子囊、入射夹角、瘤高与瘤颈的比值(AR)差异均有统计学意义(P值均＜0.05)。多因素logistic回归分析显示,有子囊、入射夹角＞117.75°、AR值＞1.65是动脉瘤破裂的独立危险因素(P值均＜0.01)。根据logistic预测模型,其动脉瘤破裂风险评分(R),受试者操作特征曲线下面积为0.812(95%可信区间0.750~0.874,P＜0.01),R=2为最佳截断值,灵敏度72.6%,特异度78.2%。结论 颅内小型未破裂动脉瘤患者符合以下两种及两种以上影像解剖特征者,即动脉瘤位于颈内动脉后交通段或前交通动脉、瘤壁不规则、有子囊、入射夹角＞117.75°、AR值＞1.65等,为动脉瘤破裂的高危人群。     

3D Shape Analysis of Intracranial Aneurysms Using the Writhe Number as a Discriminant for Rupture

Intracranial aneurysms are polymorphic focal arterial dilations, which harbor a variable risk of rupture leading to high morbidity and mortality. Increased detection of incidental aneurysms by non-invasive imaging has created a need for rupture risk stratification tools, in addition to simple aneurysm size, to guide optimal treatment strategy. To this end, shape analysis has emerged as a possible differentiator of rupture likelihood. A novel set of morphological parameters based on the writhe number are introduced here to describe aneurysms and discriminate rupture status. Classification in 117 saccular aneurysms (52 ruptured and 65 unruptured) is based on statistical analysis of writhe number distribution on the aneurysm surface. Aneurysms are analyzed both in isolation and including a portion of their parent vessel. Sidewall and bifurcation aneurysm subtypes were found to be best described by disjoint sets of shape parameters, yielding a morphological dichotomy between the two aneurysm classes. Writhe number analysis results in 86.7% accuracy on sidewall (SW) aneurysms and 71.2% accuracy on bifurcation (BF) aneurysms. This represents a 12% accuracy increase for both subtypes compared to the performance of seven established 2D and 3D indexes. The results support the utility of writhe number aneurysm shape analysis, with potential clinical value in rupture risk stratification.     

Long-lasting narrowing of the parent artery after bilateral clipping of mirror-image aneurysms of distal anterior cerebral arteries: a case report

Because multiple intracranial aneurysms are not rare, accurate preoperative detection of asymptomatic aneurysms is important. In this paper, we report a ruptured distal anterior cerebral artery (DACA) aneurysm associated with an unruptured mirror-image aneurysm in a 62-year-old man presenting with headache. Although delayed vasospasm after subarachnoid hemorrhage has been reported to persist for 2 to 3 weeks, angiographic parent artery narrowing was far more prolonged in our case. Computed tomography revealed a subarachnoid hemorrhage in the interhemispheric and right sylvian fissures and a right frontal lobe hematoma. Digital subtraction angiography demonstrated bilateral symmetric saccular aneurysms of DACAs. On the day of admission, both aneurysms were clipped using an interhemispheric approach in a one-stage procedure, and the hematoma was aspirated. Angiography performed 8 days after the surgery demonstrated a residual aneurysm neck on the left side. Follow-up digital subtraction angiography performed on day 42 from onset showed resolution of the residual aneurysm neck along with narrowing of the left A2. However, at 7 months, the A2 narrowing had lessened. The location of the bilateral aneurysms near the midline facilitated a single approach but necessitated the application of juxtaposed clips. Regarding the pathogenesis of the bilateral aneurysms, previous reports have suggested symmetry of congenital anatomic defects and hemodynamic stress as potential causes. The persistent narrowing that was observed could have resulted from proliferative vasculopathy or from fibrosis possibly induced by the clips.     

Three-Dimensional Geometrical Characterization of Cerebral Aneurysms

The risk of rupture of cerebral aneurysms has been correlated with the size of the aneurysm sac. It is conceivable that geometrical shape, not just size may also be related to aneurysm rupture potential. Further, aneurysm shape may also be a factor in deciding on treatment modalities, i.e., to clip or coil. However, our ability to make use of available information on aneurysm shape remains poor. In this study, methods were developed to quantify the seemingly arbitrary three-dimensional geometry of the aneurysm sac, using differential and computational geometry techniques. From computed tomography angiography (CTA) data, the three-dimensional geometry of five unruptured human cerebral aneurysms was reconstructed. Various indices (maximum diameter, neck diameter, height, aspect ratio, bottleneck factor, bulge location, volume, surface area, Gaussian and mean curvatures, isoperimetric ratio, and convexity ratio) were utilized to characterize the geometry of these aneurysm surfaces and four size-matched hypothetical control aneurysms. The physical meanings of various indices and their possible role as prognosticators for rupture risk and presurgical planning were discussed.     

The CSF concentration of ADMA,but not of ET-1, is correlated with the occurrence and severity of cerebral vasospasm after subarachnoid hemorrhage

Under physiological conditions, vasoconstrictors and vasodilators are counterbalanced. After aneurysmal subarachnoid hemorrhage (SAH) disturbance of this equilibrium may evoke delayed cerebral vasospasm (CVS) leading to delayed cerebral ischemia (DCI). Most studies examined either the vasoconstrictor endothelin-1 (ET-1) or the vasodilative pathway of nitric oxide (NO) and did not include investigations regarding the relationship between vasospasm and ischemia. Asymmetric dimethyl-l-arginine (ADMA), an endogenous inhibitor of nitric oxide synthase (NOS), decreases the concentration of NO. Studies have correlated increasing concentrations of ADMA with the course and degree of CVS after SAH. We sought to determine, if ADMA and endothelin-1 (ET-1) are associated with CVS and/or DCI after SAH. CSF concentrations of ADMA and ET-1 were retrospectively determined in 30 patients after SAH and in controls. CVS was detected clinically and by arteriogaphy. DCI was monitored by follow-up CT scans. 17 patients developed arteriographic CVS and 4 patients developed DCI. ADMA but not ET-1 concentrations were correlated with occurrence and degree of CVS. However, ET-1 concentrations were correlated with WFNS grade on admission. Neither ADMA nor ET-1 correlated with DCI in this cohort. ET-1 concentrations seem to be associated with the impact of the SAH bleed. ADMA may be directly involved in the development and resolution of CVS after SAH via inhibition of NOS disturbing the balance of vasodilative and -constrictive components.     

The efficacy of apolipoprotein E deficiency in cerebral aneurysm formation

Subarachnoid hemorrhage due to the rupture of a cerebral aneurysm is a life-threatening disease. Despite this, the detailed mechanisms underlying the initiation and progression of cerebral aneurysm are unclear. The relation of hypercholesterolemia and apolipoprotein E (ApoE) to cerebral aneurysm formation, has been unclear until now. We used, in the present study, a previously established cerebral aneurysm model of rats and mice whose histological features were closely similar to human cerebral aneurysms. ApoE protein was expressed mainly in the endothelial cells of arterial walls both in control arteries and cerebral aneurysms. The expression of ApoE was reduced during aneurysm formation in the immunohistochemistry. The mRNA expression of ApoE in arterial walls was not different between the controls and cerebral aneurysms. Owing to the deficiency of ApoE, mice presented marked hypercholesterolemia, but there was no difference in cerebral aneurysm formation. In the present study, we clarified that ApoE was not responsible for cerebral aneurysm formation.     

The Familial Intracranial Aneurysm (FIA) study protocol

Background  

Subarachnoid hemorrhage (SAH) due to ruptured intracranial aneurysms (IAs) occurs in about 20,000 people per year in the U.S. annually and nearly half of the affected persons are dead within the first 30 days. Survivors of ruptured IAs are often left with substantial disability. Thus, primary prevention of aneurysm formation and rupture is of paramount importance. Prior studies indicate that genetic factors are important in the formation and rupture of IAs. The long-term goal of the Familial Intracranial Aneurysm (FIA) Study is to identify genes that underlie the development and rupture of intracranial aneurysms (IA).     

银杏叶制剂对蛛网膜下腔出血大鼠血浆及脑组织内皮素-1含量的影响

目的探讨蛛网膜下腔出血（ＳＡＨ）后内皮素－１（ＥＴ－１）变化和银杏叶制剂（ＧＢＥ）对其影响。方法对单纯ＳＡＨ组和ＧＢＥ处理组大鼠检测ＳＡＨ后２４ｈ内颅内血浆及脑组织ＥＴ－１含量的动态改变。结果 ＳＡＨ组血浆及脑组织 ＥＴ－１含量分别于 ＳＡＨ后即刻和 １ｈ明显增加,并维持 ２４ｈ（Ｐ＜０．０５,０．０１）。ＧＢＥ组ＳＡＨ后ＥＴ－１增加的程度显著小于ＳＡＨ组（Ｐ＜０．０５,０．０１）。结论血浆及脑组织ＥＴ－１增多可能是造成脑部大血管和微血管痉挛及其缺血性脑损伤的原因之一,ＧＢＥ则可逆转ＥＴ－１的上述病理性改变。     

Adiponectin activates endothelial nitric oxide synthase through AMPK signaling after subarachnoid hemorrhage

Adiponectin is produced from fatty tissue and has been reported to be involved with metabolic syndrome. Recently, adiponectin has been demonstrated to play a neuroprotective role against cerebral ischemia. In this study, we explored the time-course serial expression changes of adiponectin in cerebrospinal fluid (CSF) after subarachnoid hemorrhage (SAH) and the effects of adiponectin on cerebral arteries. The concentrations of adiponectin were measured serially until day 14 in CSF of 8 patients with SAH. The CSF samples obtained from 6 patients suffering from an unruptured aneurysm were used as controls. Serum samples were collected from 6 healthy adult volunteers. Rat cerebral arteries were incubated with adiponectin (2μg/ml). Western blot analysis using AMP-activated protein kinase α (AMPKα), phosphorylated (p)-AMPKα at Thr(172), endothelial nitric oxide synthase (eNOS), p-eNOS at Ser(1177) and actin antibodies was then performed. The adiponectin concentrations in serum and control CSF were 17,670±3748ng/ml and 9.2±3.0ng/ml, respectively. After SAH, the concentration of adiponectin in the CSF significantly increased on the first post-SAH day and gradually decreased thereafter. Adiponectin significantly phosphorylated both the AMPKα and eNOS of the cerebral arteries. Our findings suggest that adiponectin is significantly increased in the CSF after SAH, resulting in the activation of AMPKα and eNOS. Adiponectin plays an important role against cerebral vasospasm via the AMPK/eNOS signaling pathway.