颅脑损伤后血浆内皮素-1与经颅超声多谱勒的相关性研究

目的 探讨颅脑损伤后血浆内皮素－1（ET－1）水平的变化与经颅超声多谱勒（TCD）的关系。方法 动态测定33例成年颅脑损伤病人血浆ET－1水平的变化，同时地TCD检查以判定脑血管痉挛。结果 （１）伤后6-8d,13-15d血浆ET－1与血管痉挛呈明显正相关9r=0.533,P=0.002;r=0.423,P=0.02)，以伤后6－8d为著，ET－1水平高的时间与脑血管痉挛发生的时间一致。（2）伤后6－8d，发生血管痉挛者血浆ET－1水平明显高于无血管痉挛者（P＜0．05）。重度血管痉挛者血浆ET－1水平也高于轻度血管痉挛者，但未达到明显水平（＝0．134）。（3）伤后13－15d，血管痉挛者血浆ET－1水平较无血管痉挛者已无显著差异（P＝0．589），而重度血管痉挛者血浆ET－1水平明显高于无血管痉挛者（P＝0．0006＞结论 血浆ET－1水平和血管痉挛的发生和程度相关，其和TCD匀可以反映脑血管痉挛发生和严重程度；抗ET治疗，可以减轻或防止迟发性缺血性脑损害。     

颅内动脉瘤术后脑血管痉挛与血浆内皮素-1、一氧化氮含量的关系

目的　探讨内皮素 (ET) 1、一氧化氮 (NO)与颅内动脉瘤术后脑血管痉挛发生的关系。方法　颅内动脉瘤 3 0例 ,经颅多普勒 (TCD)检测脑血流速度 ,并抽取外周静脉血测定血浆ET 1和NO含量 ,进行手术前后对比研究。另选取 10例健康成人进行对比研究。结果　 (1)脑血管痉挛组术后 1～ 3d、5～ 7d血浆ET 1的平均含量明显高于同期未发脑血管痉挛组 (P <0 .0 1) ,与术前和正常组相比差异亦有显著性 (P <0 .0 1)。 (2 )脑血管痉挛组术后 1～ 3d血浆NO的平均含量明显低于术前 (P <0 .0 5 )和术后 5～ 7d(P <0 .0 1) ,术后 5～ 7d脑血管痉挛组的血浆NO平均含量明显高于未发生脑血管痉挛组和正常组 (P <0 .0 1)。结论　 (1)颅内动脉瘤术后脑血管痉挛的发生与血浆ET 1、NO平均含量呈明显相关性。 (2 )ET 1/NO在维持脑血管张力上起着重要作用 ,当两者动态平衡破坏时 ,可能导致脑血管痉挛发生。 (3 )对于术后血浆ET 1含量明显升高和 /或NO含量明显降低的患者应及时行经颅多普勒检查 ,有助于尽早发现脑血管痉挛 ,使脑缺血、脑梗死得到及时的预防和治疗     

纳络酮治疗急性重型颅脑损伤患者血浆内皮素含量变化及其临床意义

目的 探讨纳络酮治疗急性重型颅脑损伤患者血浆内皮素（ET）含量变化及其临床意义，评价纳络酮治疗急性重型颅脑损伤的意义。方法 观察了52例纳洛酮治疗急性重型颅脑损伤患者血浆ET含量在治疗前1d、治疗后3、8d及2周的变化，并且以46例颅脑损伤患者按常规治疗作对照组。结果 颅脑损伤24h内两组患者血浆内皮素较正常人均明显升高（P〈0．05），伤后第3天、第8天两治疗组血浆内皮素较治疗前均明显下降（P〈0．05），但纳络酮治疗组低于常规治疗组（P〈0．05），治疗2周后两组ET水平基本恢复到正常水平。结论 急性重型颅脑损伤患者血浆内皮素含量明显升高，与病情轻重相关，纳络酮治疗较常规治疗能更迅速地降低血浆ET水平。     

实验性脑血管痉挛兔基质金属蛋白酶-9的变化研究

目的观察实验性新西兰白兔蛛网膜下腔出血（SAH）后脑血管痉挛血清基质金属蛋白酶-9（MMP-9）及血浆血管内皮生长因子（VEGF）浓度的动态变化，探讨它们与脑血管痉挛的发生、发展及转归过程的关系，从而为临床诊断及治疗提供理论依据。方法新西兰白兔60只，随机分为假手术组（n=30）及模型组（n=30）。采用枕大池二次注血法进行蛛网膜下腔脑血管痉挛模型的制作。分别将两组实验动物于第1、3、5、7、9、14天采取兔空腹血，应用酶联免疫、双抗体夹心法化验血清中的MMP-9及血浆VEGF的浓度，同时进行经颅多普勒（TCD）检测基底动脉最大流速判定脑血管痉挛。结果假手术组血清MMP-9的浓度及血浆VEGF的浓度无明显变化，在模型组中血清MMP-9及血浆VEGF浓度于注血后24h开始升高，至5～7天达高峰，以后逐渐减退，14天时接近正常。结论血清MMP-9及VEGF的浓度变化可以预测蛛网膜下腔出血后脑血管痉挛的发作，判断其发展及预后，从而为临床治疗提供依据。     

实验性脊髓损伤后内皮素与前列环素含量的变化及意义

目的：探讨脊髓损伤后脊髓组织中内皮素（ＥＴ）与前列环素（ＰＧＩ２）变化的相互关系与意义。方法：３６只大鼠随机分为６组，Ａｌｅｎｓ法中度量（５０ｇ·ｃｍ）损伤脊髓。测定伤段脊髓中内皮素与６－酮－前列腺素Ｆ１α含量。结果：内皮素含量在伤后３０ｍｉｎ显著升高，２ｈ急剧升高达到高峰，以后逐渐下降；６－酮－前列腺素Ｆ１α含量在伤后３０ｍｉｎ即升高，２ｈ达到较高水平，其升高程度较内皮素小，以后缓慢上升。结论：脊髓损伤早期内皮素含量的急剧升高和前列环素的相对不足可能与脊髓损伤后早期缺血的产生有关，内皮素可能通过多种途经参与脊髓损伤后的继发损伤     

犬蛛网膜下腔出血腰大池引流内皮素、一氧化氮变化及其与经颅彩色多美勒超声相关性研究

目的 探讨犬蛛网膜下腔出血（SAH）后脑血管痉挛（CVS）与内皮素（ET）和一氧化氮（NO）的关系、腰大池持续引流后两者变化及与经颅彩色多普勒超声（TCCD）相关性。方法 采用犬SAH模型，测定SAH后腰大池持续引流前后不同时期，血浆和脑脊液中ET和NO含量。观察ET和NO动态变化，同时应用TCCD检查SAH模型不同时期脑动脉血流形态与流速。结果 SAH后引流组血浆和脑脊液中ET含量增加和NO含量下降不明显（P〉0．05），非引流组血浆和脑脊液中ET含量增加和NO含量下降明显（P〈0．01）。TCCD显示：血浆和脑脊液中ET含量变化与大脑中动脉平均流速呈正相关，NO含量变化与大脑中动脉平均流速呈负相关。结论 SAH后脑血管痉挛与ET含量增加和NO含量下降有关，腰大池持续引流有效清除引起脑血管痉挛因子ET，经颅彩色多普勒超声可以根据动脉血的流速和血流形态判断脑血管痉挛的程度及其预后。     

尼莫地平防治脑血管造影致血管痉挛的临床观察

目的观察尼莫地平防治脑血管造影所致脑血管痉挛的临床效果。方法将186例行脑血管造影的患者分为观察组（94例）和对照组（92例），对照组术前30min肌内注射苯巴比妥钠0．1，观察组在此基础上应用尼莫地平静脉泵入。持续至造影后4h。结果观察组无1例发生脑血管痉挛，对照组造影中出现脑血管痉挛2例，造影后5例，发生率7．6％，两组比较，差异有显著性意义（x^2=7．34，P〈0．01）。结论脑血管造影检查中微量静脉泵注尼莫地平可防治脑血管造影致脑血管痉挛，且安全可靠。     

组织细胞间粘附分子-1在阻塞性黄疸小肠粘膜损伤中的作用及丹参防治机制的研究

目的：研究组织细胞间粘附分子－1（ICAM－1）在阻塞性黄疸（阻黄）小肠粘膜损伤中的作用及丹参防治小肠粘膜损伤机制。方法：SD大鼠48只分为4组：假手术对照组（SO＋NS）、阻黄组（BDL＋NS）、治疗对照组（SO＋SM）及丹参治疗组（BDL＋SM），每组术后再随机分设7、14d两个时相点。在不同时相点检测小肠组织髓过氧化物酶活性（MPO）、ICAM－1、二胺氧化酶（DAO）、血浆内毒素水平变化，并与丹参治疗组进行比较。结果：BDL＋NS组7、14d时小肠DAO的活性降低，MPO活性增高P＜0．05），门表脉血浆内毒素增加，ICAM－1主要表达在小肠粘膜上皮组织，且表达逐渐增强（P＜0．05）；BDL＋SM组7、14d时小肠组织DAO活性显著升高，门静脉血浆内毒素降低，ICAM－1表达受到抑制（P＜0．05），MPO改变不明显。结论：阻黄引起小肠上皮细胞上的ICAM－1表达上调，参与了中性粒细胞（PMN）介导的小肠粘膜损伤；丹参是通过抑制ICAM－1的表达而减轻小肠粘膜的损伤。     

小鼠全层皮肤创伤愈合过程中基质细胞衍生因子-1及其受体CXCR4基因表达的研究

目的：研究小鼠全层皮肤创伤愈合过程中创面基质细胞衍生因子-1（stroma-cell derived factor-1,SDF-1）及其受体CXCR4的基因表达情况。方法：建立小鼠背部皮肤正中近颈侧1.5cm×1.5cm的正方形皮肤全层缺损模型,分别于伤后1、2、3、4、5、7、10和14d获取创缘组织,应用半定量逆转录-聚合酶链反应检测损伤后各时间点创面SDF-1及CXCR4的mRNA表达,并观察组织病理学变化。结果：伤后1～3d创面有大量炎症细胞浸润,4d时有肉芽组织形成,5d可见上皮细胞覆盖创面,7d时创面周围明显上皮化,14d创面基本完全愈合。SDF-1及CXCR4在创面愈合过程均呈双峰表达,SDF-1基因表达于伤后1d明显增高（P〈0.01）,随后下降,于伤后3d达最低,随后再次升高,于伤后5d达峰值（P〈0.01）,然后下降,14d时接近伤前值。CXCR4基因表达于伤后1d升高,然后继续升高,至伤后5d达峰值,随后下降,于伤后10d表达最少（P〈0.01）,伤后14d表达再次增加（P〈0.01）。结论：SDF-1/CXCR4轴参与了创伤愈合的炎症反应期和增殖期的愈合过程,在皮肤组织创伤愈合过程中起着重要作用。     

心肺复苏期血浆内皮素、心钠素、降钙素基因相关肽含量的变化

目的研究血浆内皮素(ET)、心钠素(ANP)、降钙素基因相关肽(CGRP)在心脏骤停缺血-再灌注损伤前后含量变化规律及意义。方法健康家兔40只,随机均分为A、B两组。制作家兔心脏骤停缺血-再灌注模型,观察心肺复苏期各时相血浆ET、ANP、CGRP、BP及ECG变化。结果动物在心脏骤停及复苏即刻血浆ET含量未见明显变化,心肺复苏后5min开始升高,而同期血浆ANP、CGRP水平降低(P<0.05),复苏后0.5h血浆ET明显升高(P<0.01),复苏后1、2h血浆ET、ANP、CGRP均较复苏前显著升高(P<0.05)。结论在心脏骤停缺血-再灌注损伤过程中ET、ANP、CGRP水平变化及相关关系可能是一种调节机制并在病理生理过程中起重要作用。     

星状神经节阻滞对颅内动脉瘤手术患者脑血管痉挛的影响

目的 评价星状神经节阻滞对颅内动脉瘤手术患者脑血管痉挛的影响.方法 择期行颅内动脉瘤夹闭术患者40例,ASA分级Ⅱ或Ⅲ级,采用随机数字表法,将其随机分为2组(n=20):对照组(C组)和星状神经节阻滞组(SGB组).两组均常规气管内插管,静吸复合维持麻醉.SGB组气管插管后立即以0.25%罗哌卡因10ml行左侧星状神经节阻滞.分别于切皮前、夹闭动脉瘤前、夹闭动脉瘤后30 min及术毕时采集静脉血样,测定血浆内皮素、降钙素基因相关肽及S100B蛋白水平;并于术后1、3 d时采用经颅多普勒技术监测双侧大脑中动脉和颈内动脉颅外段血流速率,记录脑血管痉挛的发生情况.术后1～7 d随访患者,记录脑缺血的发生情况.结果 与c组比较,SGB组血浆内皮素和S100B蛋白浓度降低,血浆降钙素基因相关肽浓度升高,术后脑血管痉挛及脑缺血的发生率降低(P＜0.05或0.01).结论 星状神经节阻滞可抑制颅内动脉瘤手术患者脑血管痉挛的发生,其机制与抑制血管内皮细胞释放内皮素,促进降钙素基因相关肽的释放有关.

Abstract：

Objective To evaluate the effect of stellate ganglion block (SGB) on cerebral vasospasm in patients undergoing intracranial aneurysm surgery. Methods Forty ASA Ⅱ or Ⅲ patients aged 14-64 yr weighing 40-81 kg undergoing intracranial aneurysm clipping were randomly divided into 2 groups ( n = 20 each): group control (group C) and group SGB. Left SGB was performed with 0.25% ropivacaine 10 ml immediately after intubation. Successful block was verified by development of Homer syndrome within 15 min after block. Anesthesia was induced with midazolam, propofol, fentanyl and vecuronium and maintained with isoflurane inhalation and intermittent iv boluses of fcntanyl and vecuronium. The patients were intubated and mechanically ventilated. PETCO2 was maintained at 30-35 mm Hg. BIS was maintained at 50-60. Right internal jugular vein was cannulated and the catheter was threaded cranially until resistance was met for blood sampling. Blood samples were collected before skin incision (T1), before clipping of aneurysm (T2), at 30 min after clipping (T3 ), and at the end of surgery (T4) for determination of plasma concentrations of endothelin (ET), calcium gene-related peptide (CGRP) and S100B protein. Transcranial Doppler was used to measure the flow rate of blood in bilateral middle cerebral artery and extracranial carotid artery at 1 and 3 days after surgery. All patients were observed for incidence of brain ischemia during 1-7 days after surgery. Results Plasma ET and S100B protein concentrations were significantly decreased, while plasma CGRP concentration was significantly increased after clipping of aneurysm at T3 and T4 in group SGB as compared with group C. The incidence of cerebral vasospasm and brain ischemia was significantly lower in group SGB than in group C. Conclusion SGB performed before operation can significantly reduce the incidence of cerebral vasospasm after clipping of intracranial aneurysm by inhibiting the release of ET and promoting the release of CGRP.     

胆管结石及急性重症胆管炎患者外周血中内皮素及降钙素基因相关肽变化的意义

目的　探讨胆管结石及急性重症胆管炎 (ACST)患者外周血中内皮素 (ET)及降钙素基因相关肽 (CGRP)浓度的变化及意义。方法　采用放射免疫分析法检测了 3 0例胆管结石及 5 5例 ACST患者术中、术后 7d、14 d外周血中 ET及CGRP的浓度。结果　胆管结石得从术中至术后 14 d外周血中 ET的浓度与对照组比较差异无显著性。ACST患者术中外周血的浓度显著高于对照组 (P<0 .0 5～ 0 .0 1) ,病情严重程度不同的两组病例术中外周血 ET的浓度差异也有显著性 (P<0 .0 5 ) ;术后外周血中 ET的浓度逐渐下降。胆管结石患者从术中至术后 14 d外周血中 CGRP的浓度与对照组比较差异无显著性。 ACST患者术中外周血中 CGRP的浓度显著高于对照组 (P<0 .0 1) ,术后外周血中 CGRP的浓度逐渐下降。结论　 ACST患者外周血中 ET的浓度可以反映出肝胆系统及全身的病理损害程度 ,外周血中 ET的浓度与 ACST病情严重程度呈正相关 ;外周血中 CGRP浓度增高 ,对拮抗 ET对组织细胞的损伤 ,促进组织器官功能恢复可能起重要的作用。     

Development of calcitonin gene-related peptide slow-release tablet implanted in CSF space for prevention of cerebral vasospasm after experimental subarachnoid haemorrhage

Summary The calcitonin gene-related peptide (CGRP), a known potent intrinsic cerebral vasodilator, is contained in the sensory nerves from trigeminal ganglia that inervate the cerebral arteries. We previously reported that human CGRP (hCGRP) dilates spastic cerebral arteries after experimental subarachnoid haemorrhage (SAH) in rabbits. In the present study, we investigated the prophylactic potential of a sustained higher cerebrospinal fluid level ofhCGRP against experimental cerebral vasospasm. AnhCGRP slow-release tablet (hCGRP s-r tablet) was developed for cisternal implantation. Experimental SAH was induced by percutaneous cisternal injection of autologous arterial blood. Angiography was initiated on day 1 (before SAH) and performed everyday. ThehCGRP s-r tablet was implanted into the cisterna magna on day 2 in the treated groups. The spastic response of the basilar artery was maximized on day 4 in the non-treated (80.7% of day 1) and the placebo-treated (79.3%) groups. In contrast, the arterial diameters on day 4 were 96.1% and 90.5% of day 1 in the groups implanted withhCGRP 24 g and 153 g s-r tablets, respectively. We also measured the concentration ofhCGRP in the cerebrospinal fluid (CSF) following implantation of thehCGRP 24 g s-r tablet in the cisterna magna. The hCGRP concentration before implantation was below the dectable level. Following implantation, thehCGRP level in the CSF was 23.12 nmol/L on the second day and remained at elevated levels until the fifth day. These experiments suggest that the intrathecal single implantation of thehCGRP s-r tablet could produce an elevated concentration ofhCGRP in the CSF over five days and have prevented the cerebral vasospasm after SAH in the rabbit. ThehCGRP s-r tablet may be clinically applicable in the treatment of patients with SAH against cerebral vasospasm.     

急性重症胆管炎患者胆汁中内皮素及降钙素基因相关肽的检测及意义

目的 探讨急性重症胆管炎（ACST）患者胆汁中内皮素（ET）及降钙素基因相关肽（CGRP）浓度的变化及意义。方法 采用放射性免疫分析法检测了55例ACST患者术中、术后7、14d胆汁中ET及ERCP的浓度。结果 ACST患者术中胆汁ET的浓度显著高于对照组（P＜0．01－0．001）,病情严重程度不同的两组病例术中胆汁ET的浓度差异也有显著性（P＜0．05）;术后胆汁中ET的浓度逐渐下降。术中胆汁CGRP的浓度显著低于对照组（P＜0．01）,术后胆汁中CGRP的浓度逐渐升高。结论 ET参与了ACST肝胆系统的病理损害过程,胆汁中ET的浓度与ACST病情严重程度呈正相关;胆汁中ET与CGRP二者间的平衡紊乱可能在ACST肝胆系统的病理损害过程中具有重要意义。     

髂股静脉血栓形成溶栓治疗过程中测定血浆降钙素基因相关肽的临床意义

目的　探讨急性髂股静脉血栓形成溶栓治疗过程中血浆降钙素基因相关肽 (CGRP)的水平及其临床意义。方法　选择 50例急性髂股静脉血栓形成及 3 0例本病后遗症接受尿激酶溶栓治疗的患者 ,利用放射免疫测定法动态观察其血浆CGRP水平。结果　急性组患者行尿激酶溶栓治疗后 6h、1d、3d、7d及 14d血浆CGRP水平明显升高 ,与治疗前比较差异有统计学意义 (P<0 .0 5,P<0 .0 1) ,而 3 0例后遗症患者及 12例第二次治疗者 ,血浆CGRP水平治疗前后无明显变化。结论　血浆CGRP水平可初步反映溶栓治疗效果 ,并可作为了解疾病转归的指标     

Regional CBF, intraventricular pressure, and cerebral metabolism in patients with ruptured intracranial aneurysms

Regional cerebral blood flow (rCBF), cerebral metabolic rate of oxygen (CMRO2), intraventricular pressure, and lactate/pH levels in the cerebrospinal fluid (CSF) were measured in 38 patients with ruptured intracranial aneurysms between the 3rd and 13th day after subarachnoid hemorrhage (SAH). Angiography was performed following the rCBF study and the degree of vasospasm was measured on the angiograms. The patients were graded clinically according to the system of Hunt and Hess. Cerebral vasospasm significantly influenced rCBF: global reductions and focal changes (ischemia, hyperemia, and tissue peaks) were commonly associated with vasospasm. Patients with severe diffuse spasm always had global ischemia (21 +/- 5 ml/100 gm/min), and cerebral infarctions were demonstrated subsequently, The CMRO2 was more reduced than rCBF, indicating an uncoupling between flow and metabolism. This relative luxury perfusion was associated with CSF lactic acidosis and intracranial hypertension. The arteriovenous difference of oxygen was equally reduced in all categories of patients, probably due to the primary insult of SAH. The CMRO2 decreased concomitantly with arterial caliber, indicating a secondary impairment of cerebral metabolism due to vasospasm.     

Posttreatment with adenovirus-mediated gene transfer of calcitonin gene-related peptide to reverse cerebral vasospasm in dogs

OBJECT: Gene transfer to cerebral vessels is a promising new therapeutic approach for cerebral vasospasm after subarachnoid hemorrhage (SAH). This study was undertaken to explore whether a delayed treatment with adenovirus encoding the prepro-calcitonin gene-related peptide (CGRP), 2 days after initial blood injection, reduces cerebral vasospasm in a double-hemorrhage model of severe vasospasm in dogs. METHODS: In 20 dogs, arterial blood was injected into the cisterna magna on Days 0 and 2. Thirty minutes after the second blood injection, the animals received either adenovirus encoding the prepro-CGRP gene (AdCMVCGRP-treated group, eight dogs) or adenovirus encoding the beta-galactosidase gene (AdCMVbeta gal-treated group, six dogs) under the cytomegalovirus (CMV) promoter. One group of dogs did not receive treatment and served as controls (control SAH group, six dogs). Angiography was performed on Days 0 and 7 to assess cerebral vasospasm. On Day 7 following angiography, the animals were killed and their brains were stained with X-gal to detect the distribution of gene expression. Cerebrospinal fluid (CSF) was also tested for CGRP immunoreactivity. Severe vasospasm was observed in control SAH dogs on Day 7, and the mean basilar artery (BA) diameter was 53.4 +/- 5.5% of the value measured on Day 0. Treatment with AdCMVbeta gal did not alter vasospasm (the BA diameter was 55 +/- 3.9% of that measured on Day 0). The leptomeninges and adventitia of the BAs of dogs treated using AdCMVbeta gal demonstrated positive staining with X-gal. High levels of CGRP were measured in CSF from dogs that received AdCMVCGRP. In the group treated with AdCMVCGRP, vasospasm was significantly reduced (the BA diameter was 78.2 +/- 5.3% of that measured on Day 0, p < 0.05 compared with the control SAH group and the AdCMVbeta gal group). CONCLUSIONS: In a model of severe vasospasm in dogs, gene transfer of CGRP after injection of blood attenuated cerebral vasospasm after SAH.     

Changes of endothelin and calcitonin gene-related peptide during desflurane anesthesia in patients undergoing intracranial aneurysm clipping

The purpose of this study was to explore whether the changes of plasma concentrations of endothelin (ET) and calcitonin gene-related peptide (CGRP) were possibly involved during desflurane anesthesia in patients undergoing intracranial aneurysm clipping. Forty-five consecutive patients scheduled for selective craniotomy and aneurysm clipping were anesthetized with desflurane in oxygen. Radial arterial catheter was inserted for blood sampling before anesthesia. Serial plasma concentrations of ET and CGRP were measured with radioimmunoassay prior to induction, after dura incision, after clipping of the aneurysm, and 30 minutes after clipping the aneurysm, respectively. Plasma concentrations of ET decreased significantly during the anesthesia and surgery compared with the baseline. An observed decrease in mean CGRP during anesthesia and surgery was not statistically significant. Considering the well-recognized vasoconstrictive effect of ET, it is possible that a decrease in its plasma concentration plays a role in the prevention of the acute cerebral vasospasm during desflurane anesthesia in patients undergoing intracranial aneurysm clipping.     

Cerebrovascular reactivity in patients with ruptured intracranial aneurysms

The cerebral vasomotor reactivity to arterial hypotension and hypocapnia was studied in 34 patients between the 3rd and 13th day after rupture of an intracranial saccular aneurysm. Using the intra-arterial xenon-133 injection method, regional cerebral blood flow (rCBF) and cerebral metabolic rate of oxygen (CMRO2) were measured. The intraventricular pressure and cerebrospinal fluid (CSF) lactate and pH levels were determined. The degree of vasospasm was measured on angiograms taken immediately following the rCBF study. The patients were graded clinically according to the system of Hunt and Hess. Cerebral autoregulation was intact in patients in good clinical condition, but was impaired in patients in poor clinical condition. There was a close correlation between the degree of vasospasm and the degree of autoregulatory impairment, which varied from focal disturbances to global impairment. Intracranial hypertension and CSF lactic acidosis were commonly found in association with vasoparalysis. Cerebrovascular response to hyperventilation was generally preserved, although often reduced. During hyperventilation, the cerebral perfusion pressure became elevated, and increases in CMRO2 were often found, even in patients with severe diffuse spasm and cerebral ischemia. The clinical significance of the results in relation to the treatment of delayed cerebral ischemia and to the use of intraoperative induced hypotension is discussed.