迷走神经刺激预处理对急性心肌缺血大鼠心肌P物质和降钙素基因相关肽的影响

目的观察迷走神经刺激预处理对急性心肌缺血大鼠心肌组织缺血区和非缺血区P物质(SP)和降钙素基因相关肽(CGRP)表达的影响。方法健康成年雄性SD大鼠24只,体质量270~300g,随机分为3组,每组8只,假手术组(S组)、单纯冠状动脉结扎组(I组)和迷走神经刺激预处理冠状动脉结扎组(VS组)。S组大鼠开胸后在冠状动脉左前降支下穿线不结扎;Ⅰ组大鼠开胸后结扎冠状动脉左前降支;VS组大鼠实施迷走神经刺激30min后结扎冠状动脉左前降支。各组在手术后计时3h。采用免疫组织化学、酶免疫法和反转录-聚合酶链反应法从蛋白和基因水平观察各组大鼠缺血区和非缺血区心肌SP和CGRP的表达。结果Ⅰ组大鼠缺血区心肌SP/SP mRNA和CGRP/β-CGRP mRNA的水平较S组升高(P<0.05),VS组低于Ⅰ组(P<0.05),但仍高于S组(P<0.05)。非缺血区各组的变化趋势类同缺血区,但各扎闭冠状动脉组SP/SP mRNA和CGRP/β-CGRP mRNA的水平均低于相应组缺血区的水平(P<0.05)。结论迷走神经刺激预处理可降低急性心肌缺血大鼠心肌组织SP和CGRP的表达,提示迷走神经刺激预处理可能参与缺血心肌的保护。     

葛根素干预对糖尿病肾病大鼠降钙素基因相关肽的影响研究

目的研究葛根素对糖尿病肾病（DN）大鼠降钙素基因相关肽（CGRP）的影响。方法链脉佐菌素（STZ）诱导糖尿病大鼠模型,随机分为糖尿病组（D组）、葛根素治疗组（S组）,同时另设正常对照组（CN组）,给药干预14周后,测定空腹血糖（FBG）、尿微量白蛋白（U—mAIb）、血浆内皮素（ET）和CGRP含量。结果糖尿病大鼠UAER增加,ET升高,CGRP下降,给予葛根素治疗14周后,S组DN大鼠U—mAIb较D组显著降低,ET显著下降,CGRP明显升高。结论葛根素对糖尿病大鼠肾脏病变有一定的保护作用,其部分机制可能是通过上调CGRP含量而实现的。     

Calcitonin gene-related peptide (CGRP) causes redistribution of blood flow in humans

Summary In normal human subjects (n=6), blood flow in the common carotid artery, assessed with an ultrasonic duplex-scanning unit, was increased up to 152% of basal levels by 60-min infusions of human calcintonin gene-related peptide I (CGRP) 80 pmol·kg^–1·h^–1, but it was not affected by 20 pmol·kg^–1·h^–1 CGRP or 88 pmol·kg¹·h^–1 human calcitonin.In the superior mesenteric artery, on the other hand, blood flow was reduced by 80 pmol·kg^–1·h^–1 CGRP to 58% of the basal level, but not by 20 pmol·kg^–1·h^–1 CGRP or with 88 pmol·kg^–1·h^–1 calcitonin.Blood flow in the abdominal aorta remained largely unchanged under the same conditions.Skin blood flow, assessed by a laser Doppler unit, was increased up to 682% of the basal level by 80 pmol·kg^–1·h^–1 CGRP, but not by 20 pmol·kg^–1·h^–1 CGRP or calcitonin.Thus CGRP increased regional blood flow to the brain and the skin at the expense of the gastrointestinal tract.     

创伤性脑损伤大鼠P物质和降钙素基因相关肽变化及其意义

目的建立液压创伤性脑损伤(TBI)模型,探讨创伤性脑损伤大鼠P物质(SP)和降钙素基因相关肽(CGRP)变化及其意义。方法健康雄性Wistar大鼠168只,体质量250～300 g,随机分为损伤组(126只)及对照组(42只)。损伤组随机分为:轻度、中度、重度3组,每组42只大鼠。3种损伤组及对照组,分别再随机分为0.5、2、6、12、24、48、72 h各7个亚组,每亚组6只。采用液压颅脑损伤仪,对轻度、中度、重度组分别给予0.5～1.0atm、1.5～2.0 atm、2.5～3.0 atm液压冲击力,制成轻、中、重3型液压颅脑损伤模型。分别于致伤后相应观察时间点对损伤组及对照组行心脏采血。采用酶联免疫吸附测定(ELISA)法测定血浆SP、CGRP的含量。结果创伤性脑损伤(TBI)中SP与CGRP血浆含量变化呈正相关(r=0.879,P<0.01)。变化规律基本都是损伤后立即升高,随之迅速下降,12 h或24 h之后缓慢回升。不同程度TBI组及对照组之间SP、CGRP血浆总含量不同,差异有统计学意义(P<0.01)。TBI中相同程度不同时间点之间SP、CGRP血浆含量不同,差异有统计学意义(P<0.01)。TBI中损伤程度和时间对于SP、CGRP血浆含量有交互效应。SP血浆含量中度组0.5 h时最高,重度组24 h时最低。CGRP血浆含量中度组2 h时最高,重度组24 h时最低。结论TBI中SP与CGRP在血浆含量变化呈正相关,且与损伤程度有关,通过测定SP及CGRP血浆含量可以间接推测TBI病变及损伤程度。     

降钙素基因相关肽对人皮肤成纤维细胞增殖的影响

目的探讨降钙素基因相关肽(CGRP)在不同浓度下对人皮肤成纤维细胞(Fb)增殖的影响。方法以含不同浓度的降钙素基因相关肽(CGRP)培养基培养成纤维细胞,在不同时间用细胞计数板进行细胞计数,四甲基偶氮唑盐比色法(MTT)法检测细胞的活性,选择最适浓度生长因子干预的细胞,用流式细胞仪检测细胞的DNA倍体情况及细胞周期,对所得数据进行统计学处理。结果降钙素基因相关肽(CGRP)促皮肤成纤维细胞(Fb)增殖作用的强度与CGRP的浓度和作用时间有关,在一定范围内随降钙素基因相关肽浓度递增作用增强,时间是在48 h促增殖作用最强。结论降钙素基因相关肽能够促进人皮肤成纤维细胞的增殖。     

针药结合对急性脑梗死患者血浆降钙素基因相关肽水平的影响

目的 观察针药结合对急性脑梗死患者血浆降钙素基因相关肽(CGRP)水平的影响.方法 90例急性脑梗死患者随机分为针药组(45例)和药物组(45例).两组患者治疗前、治疗后1个月检测血浆CGRP水平及观察临床疗效.结果 针药组总有效率91.1%(41/45)明显高于药物组总有效率77.8%(36/45),差异有统计学意义(P<0.05).治疗后两组血浆CGRP水平较治疗前明显升高(P<0.05),且针药组明显高于药物组(P<0.05).结论 针药结合具有降低急性脑梗死患者的神经细胞损伤作用,且可能与其调节患者CGRP水平有关.     

高压氧对颅脑损伤鼠内皮素及降钙素基因相关肽的影响

目的观察高压氧(HBO)治疗急性颅脑损伤大鼠血浆和损伤皮层内皮素(ET)和降钙素基因相关肽(CGRP)含量的变化。方法32只SD大鼠,随机为分正常组,急性颅脑损伤组(分颅脑损伤后6、24、48h组),高压氧治疗组(分颅脑损伤后6、24、48h组),常氧高氮处理组(分颅脑损伤后6、24、48h组)。每组各8只大鼠。各组动物出舱后按时间要求尽量在安静状态下快速断头取血及损伤皮层,采用放免法测定血浆及损伤皮层ET及CGRP含量。结果SD大鼠急性颅脑损伤后,其血浆和损伤皮层组织ET含量有不同程度的升高,而CGRP含量有不同程度的降低;高压氧治疗后,各组血浆及损伤皮层组织ET含量均有不同程度地降低,而血浆及损伤皮层CGRP含量亦有不同程度升高。结论急性颅脑损伤的发生发展与血浆和损伤皮层组织ET含量升高和CGRP含量降低有关;高压氧治疗可能通过降低ET含量和升高CGRP含量,从而起到治疗急性颅脑损伤的作用     

肝硬化患者血浆降钙素基因相关肽和内皮素-1含量分析

目的　观察肝硬化患者血浆降钙素基因相关肽 (CGRP)和内皮素 (ET 1)含量变化。方法　选择肝硬化患者 6 0例 (其中腹水患者 4 3例 )、正常对照 30例 ,用放射免疫法检测其血浆CGRP和ET 1含量。结果　肝硬化组血浆CGRP和ET 1明显高于对照组 (P <0 0 1) ;肝硬化腹水患者高于无腹水患者 (P <0 0 1) ;肝功能Child Pugh分级中C级高于B级、B级高于A级。结论　肝硬化患者血浆CGRP和ET 1水平增高 ,CGRP及ET 1在肝功能损伤及肝硬化高动力循环状态的发生中具有重要作用     

Release of calcitonin gene-related peptide in cardiac anaphylaxis

We have investigated the antigen-stimulated release of calcitonin gene-related peptide (CGRP) from ovalbumin-sensitized guinea-pig isolated hearts and the interaction with other mediators of anaphylaxis released concomitantly. It was found that antigen challenge caused a significant increase of CGRP release (from basal 31.2 ± 2.9 to 51.6 ± 4.9 fmol/5 min). Anaphylactic CGRP release was significantly attenuated in the presence of the cyclooxygenase inhibitor indomethacin while the 5-lipoxygenase inhibitor Bay-X1005 ((R)-2-[4-quinolin-2-yl-methoxy)phenyl]-2-cyclopentyl acetic acid) had no significant effect. Combined treatment with the histamine receptor (H₁,H₂) antagonists mepyramine and cimetidine also significantly attenuated anaphylactic release of CGRP. Under control conditions antigen injection increased release of cysteinyl-leukotrienes (LT), thromboxane (TXB₂) and 6-keto-prostaglandin (PG)F_1α from basal values of 0.96 ± 0.09, 2.7 ± 0.7 and 3.4 ± 0.28 ng/5 min respectively, to 5.9 ± 0.9, 48.4 ± 3.4 and 6.9 ± 1.4 ng/5 min. Indomethacin abolished the release of cyclooxygenase products of arachidonate metabolism and simultaneously increased cysteinyl-LT release significantly (8.8 ± 1.4 ng/5 min). Conversely Bay-X1005 completely abolished cysteinyl-LT release and had no significant effect on anaphylactic release of TXB₂ and 6-keto-PGF_1α. Simultaneous blockade of H₁ and H₂ receptors abolished release of 6-keto-PGF_1α, while release of TXB₂ and cysteinyl-LT was not significantly affected. The results indicate that CGRP is not a primary mediator of the immediate hypersensitivity reaction of the heart, but is in turn released by arachidonic acid metabolites of the cyclooxygenase pathway and histamine. In contrast, LT obviously do not contribute to anaphylactic CGRP release. CGRP is a potent coronary vasodilator and could act as endogenous functional antagonist of vasoconstrictor mediators also released during cardiac anaphylaxis such as cysteinyl-LT, platelet activating factor and TXA₂. Received: 8 May 1996 / Accepted: 11 October 1996     

不同程度创伤性脑损伤大鼠降钙素基因相关肽表达变化及其意义

目的建立液压创伤性脑损伤(TBI)模型,探讨创伤性脑损伤大鼠降钙素基因相关肽(CGRP)表达变化及其意义。方法健康雄性Wistar大鼠168只,体质量250～300g,随机分为损伤轻度、中度、重度及对照组各42只。各组分别再随机分为0.5、2、6、12、24、48、72h各7个亚组每组6只。采用液压颅脑损伤仪,对轻度、中度、重度组分别给予0.5～1.0atm(1atm=101.3kPa)、1.5～2.0atm、2.5～3.0atm液压冲击力,制成轻、中、重3型液压颅脑损伤模型。分别于致伤后相应时间点对各组大鼠断头取脑。采用苏木素-伊红(HE)染色观察TBI中组织病理改变,免疫组织化学检测创伤区大脑皮层CGRP表达。结果①光镜观察显示:创伤后12～48h时脑组织损伤最严重。②不同程度TBI中创伤区大脑皮层CGRP神经元表达的阳性单位呈现规律性变化,损伤程度越重,CGRP表达的阳性单位变化幅度越大。不同程度TBI组及对照组之间创伤区大脑皮层中CGRP神经元表达的阳性单位不同,差异有统计学意义;重度组明显低于轻度、中度及对照组,差异有统计学意义;轻度、中度及对照组之间,差异无统计学意义。TBI中损伤程度和时间对于创伤区大脑皮层中CGRP神经元表达的阳性单位有交互效应,中度2h时最高,重度24h时最低。结论不同程度TBI中创伤区大脑皮层CGRP神经元表达的阳性单位量与损伤程度及损伤后时间有关。     

Involvement of calcitonin gene-related peptide in the depressor effects of losartan and perindopril in rats

Previous investigations have indicated that calcitonin gene-related peptide (CGRP) plays an important role in the regulation of cardiovascular function, and that the development of hypertension may be related to the reduction of sensory vasodilator nerve actions. In the present study, we examined the effect of perindopril, an angiotensin-converting enzyme inhibitor, and losartan, an angiotensin II receptor antagonist, on the plasma level and synthesis of CGRP in 2 kidneys, 1-clip hypertensive rats (2K1C, Goldblatt). In the hypertension group, systolic blood pressure and mean artery pressure were raised, and the level of CGRP in plasma was slightly raised compared with control groups. Chronic treatment with losartan or perindopril significantly increased the plasma concentration of CGRP and the expression of CGRP mRNA in dorsal root ganglia in the 2K1C, Goldblatt hypertensive rats. These results suggest that the 2K1C, Goldblatt hypertensive model has a compensatory increase of sensory nerve actions, and that the depressor effects of perindopril or losartan may be related to stimulation of the synthesis and release of CGRP in the 2K1C, Goldblatt hypertensive rats.     

Transient receptor potential vanilloid 1 and transient receptor potential ankyrin 1 contribute to the progression of colonic inflammation in dextran sulfate sodium-induced colitis in mice: Links to calcitonin gene-related peptide and substance P

Transient receptor potential (TRP) vanilloid 1 (TRPV1) and TRP ankyrin 1 (TRPA1), which are non-selective cation channels, play important roles in the sensation of pain. This study investigated the roles of TRPV1 and TRPA1 in dextran sulfate sodium (DSS)-induced murine colitis. DSS (2%) administered for 7 days caused severe colitis that was significantly less severe in TRPV1-deficient (TRPV1KO) and TRPA1-deficient (TRPA1KO) mice than that in wild-type (WT) mice. Similar colitis attenuations were observed in TRPV1KO and TRPA1KO mice but not in WT mice that had been transplanted with bone marrow cells from WT, TRPA1KO, or TRPV1KO mice. DSS treatment upregulated calcitonin gene-relative peptide (CGRP)- and substance P (SP)-positive nerve fibers in the colonic mucosa of WT mice. TRPV1KO and TRPA1KO mice showed significant reductions in the DSS-induced upregulation of SP, but the DSS-induced upregulation of CGRP was not reduced. Sensory deafferentation evoked by pretreatment with high doses of capsaicin markedly exacerbated DSS-induced colitis with reductions in DSS-induced upregulation of SP- and CGRP-positive nerve fibers. These findings suggest that neuronal TRPV1 and TRPA1 contribute to the progression of colonic inflammation. While these responses may be mediated by the upregulation of SP-mediated deleterious mechanisms, CGRP may be associated with protective mechanisms.     

创伤愈合中降钙素基因相关肽对表皮干细胞迁移 趋化作用的研究

目的探讨创伤愈合中降钙素基因相关肽(CGRP)对表皮干细胞迁移、趋化作用的影响。方法将实验鼠随机分为CGRP组、P物质(SP)组、辣椒素组和对照组,4组均致背部全层皮肤缺损,CGRP组和SP组致伤当天开始创面给予CGRP和SP(1次/d),辣椒素组致伤前1周皮下预注射辣椒素,利用核标记物BrdU作为表皮干细胞的示踪剂,观察4组创面愈合速度和表皮干细胞的迁移特征。结果CGRP组与SP组的创面愈合速度最快,创缘BrdU阳性细胞率最高,峰值出现最早;辣椒素组愈合速度最慢,BrdU阳性细胞率最低,峰值出现晚;CGRP组和SP组除创缘外,在创面肉芽组织中也出现了BrdU阳性细胞,另2组未出现。结论CGRP能明显加速创面愈合速度,并具有诱导表皮干细胞向创缘集中和向创面肉芽组织中迁移的作用。     

Effects of capsaicin,tachykinins, calcitonin gene-related peptide and bradykinin in the pig iris sphincter muscle

Summary Capsaicin-sensitive sensory neurons of the rabbit iris, by releasing tachykinins, exert a major role in the control of pupil motility in response to various noxious stimuli. However, the contribution of sensory innervation to the regulation of iris smooth muscle tone in other mammals species is not known. We have studied the effects produced by electrical field stimulation, capsaicin, substance P, neurokinin A, calcitonin gene-related peptide (CGRP), and bradykinin in the isolated iris sphincter muscle of the pig.Capsaicin (10 M): a) contracted the isolated sphincter muscle and; b) released immunoreactivity for substance P (SP-LI) and CGRP (CGRP-LI) from this preparation. These two effects were no longer observed at the second exposure to the drug. Electrical field stimulation (10 Hz, 60 V, 0.5 ms for 5 s) produced a biphasic contractile response. The rapid component was inhibited by atropine (1 M), while the delayed response was blocked by previous exposure to capsaicin (10 M).Substance P and neurokinin A consistently produced contraction of the pig iris sphincter muscle, substance P being more potent than neurokinin A. CGRP induced a contractile response in more than 50% of the preparations. The tachykinin antagonist [D-Argl, D-Trp^7,9, Leu¹¹-substance P (3 M) blocked: a) the effect of substance P (1 nM); b) the delayed response to electrical field stimulation and; c) reduced by more than 50% response to capsaicin. Bradykinin (10 M) failed to release either SP-LI or CGRP-LI. The contractile response evoked by bradykinin was unaffected by in vitro pretreatment with capsaicin (10 M).The existence in the pig iris of capsaicin-sensitive sensory fibres releasing neuropeptides and thus regulating sphincter muscle tone is proposed. Send offprint requests to Dr. P. Geppetti at the above address     

降钙素基因相关肽在早期糖尿病肾病中的作用

目的通过检测降钙素基因相关肽(CGRP)在2型糖尿病及早期糖尿病肾病患者血中的含量及其与内生肌酐清除率(Ccr)之间的相关关系,探讨CGRP在糖尿病肾病中的变化及作用。方法选取健康对照组(NC)30名,2型糖尿病组(DM)30例,早期糖尿病肾病组(DN)30例为研究对象,采用放射免疫法测定CGRP,采用方差分析比较各组CGRP水平,采用直线相关分析CGRP与Ccr之间的关系。结果NC组CGRP水平为154.59pg/ml,DM组为249.86pg/ml,DN组为354.78pg/ml。DM组,DN组CGRP水平与NC组比较明显升高,差异有统计学意义(P<0.01)。CGRP与Ccr呈明显负相关(r=-0.52,P<0.01)。结论在糖尿病患者中,随Ccr的下降,CGRP升高,CGRP在糖尿病肾病早期,促进肾脏的高滤过。     

应激状态下大鼠颞颌关节内降钙素基因相关肽的变化

目的通过观察应激状态下髁突软骨细胞内降钙素基因相关肽(CGRP)的变化,探讨应激对颞下颌关节的可能致病机制。方法建立应激动物模型,运用RT-PCR技术检测对照组、应激组与药物对照组大鼠髁突软骨细胞CGRPmRNA表达。结果在第10天时应激组CGRPmRNA表达最高。药物对照组CGRPmRNA的表达也有升高。第20天时应激组CGRPmRNA与第10天时相比显著降低(P<0.05),但高于对照组(P<0.05)。药物对照组水平接近对照组(P>0.05)。30 d时应激组和药物对照组CGRP水平回落到对照组水平(P>0.05)。结论应激可能在TMD形成过程中起着重要作用。     

肺心病血浆内皮素-1与心钠素和降钙素基因相关肽水平的临床实验分析

目的:分析慢性肺源性心脏病(肺心病)患者血浆内皮素(ET-1)、心钠素(ANP)和降钙素基因相关肽(CGRP)水平的变化.方法:用放射免疫分析方法测定肺心病急性发作期和缓解期患者m浆圈r.1、ANP、CCRP含量,并行同步动脉血气分析.且与慢性阻塞性肺疾病(COPD)组比较.结果:肺心病患者血浆中ET-1和ANP含量升高,CGRP含量降低,尤其以急性期为著.其中ET-1和CGRP的变化不易随病情缓解而恢复,而ET-1的变化与ANP呈显著正相关(r=0.426,P＜0.05),与CGRP和PaO2呈显著负相关(r分别为-0.563、-0.739,P＜0.01).结论:肺心病血中ET-1与ANP、CGRP水平失衡长时间存在,可能是该病病情加重的一个重要体液因素.     

CGRP经鼻用药促进蛛网膜下腔出血后脑血供和VEGF表达

目的探讨经鼻给予降钙素基因相关肽(CGRP)对蛛网膜下腔出血(SAH)后脑血供和血管内皮生长因子(VEGF)表达的影响。方法将Wistar大鼠随机分入正常对照组、SAH组、经鼻生理盐水(NS)+SAH、经鼻CGRP+SAH组。用枕大池两次注入自体动脉血法制作SAH模型,CGRP和NS经鼻腔给予。用激光多普勒血流计检测皮层局部脑血流量(rCBF)动态变化;于第2次枕大池注血后3d,将大鼠处死取脑制作冰冻切片,用免疫荧光结合激光共聚焦显微镜检测大脑皮层VEGF蛋白表达。结果解剖学观察表明SAH模型制作成功。SAH组和经鼻NS+SAH组大鼠大脑皮层rCBF持续下降,经鼻CGRP+SAH组大脑皮层rCBF下降的程度较轻。第2次枕大池注血后3d,SAH组和经鼻NS+SAH组大鼠大脑皮层VEGF蛋白表达增多,经鼻CGRP+SAH组大鼠大脑皮层VEGF蛋白表达进一步增强。结论CGRP经鼻用药可缓解SAH脑血供下降,并促进血管新生。     

波依定治疗高血压患者后血压变异性及降钙素基因相关肽的变化

目的观察钙拮抗剂波依定对高血压患者降压效果,及对血压变异性和血浆降钙素基因相关肽(CGRP)的影响。方法60例原发性高血压患者,平均年龄(46±10.3)岁,男女各30例,为高血压组。30例健康人,平均年龄(45±10.8)岁,为对照组。高血压组治疗前采用放射免疫分析法直接测定血浆CGRP,用动态血压计测患者24h动态血压,通过计算机算出血压变异性。并给予波依定5～10mg/d治疗1个月后重复以上检查。对照组检查做1次。结果高血压患者血压变异性明显大于健康人(P<0.05)。血浆CGRP水平明显低于健康人(P<0.05)。血压变异性与CGRP呈负相关(P<0.05)。波依定具有明显降压作用。同时,明显降低患者血压变异性,尤其是24h收缩压变异性(P<0.01)。并提高患者血浆CGRP水平(P<0.05)。结论血压变异性增大、血浆CGRP水平降低是高血压患者的重要特征。钙拮抗剂波依定通过降低血压变异性,提高CGRP水平达到降压、改善高血压患者预后的目的。     

Importance of calcitonin gene-related peptide, adenosine and reactive oxygen species in cerebral autoregulation under normal and diseased conditions

1. Mechanisms regulating cerebral circulation, including autoregulation of cerebral blood flow (CBF), have been widely investigated. Vasodilators such as nitric oxide, prostacyclin, calcitonin gene-related peptide (CGRP) and K+ channel openers are well known to have important roles in the physiological and pathophysiological control of CBF autoregulation. In the present review, the focus is on the mechanism(s) of altered CBF autoregulation after traumatic brain injury and subarachnoid haemorrhage (SAH) and on the effect of adenovirus-mediated transfer of Cu/Zn superoxide dismutase (SOD)-1 in amelioration of impaired CBF autoregulation. 2. The roles of CGRP and adenosine are particularly emphasized, both being implicated in the autoregulatory vasodilation of the pial artery in response to hypotension. 3. After fluid percussion injury, production of NADPH oxidase-derived superoxide anion and activation of tyrosine kinase links the inhibition of K+ channels to impaired autoregulatory vasodilation in response to acute hypotension and alterations in CBF autoregulation in rat pial artery. 4. Subarachnoid haemorrhage during the acute stage causes an increase in NADPH oxidase-dependent superoxide formation in cerebral vessels in association with activated tyrosine phosphorylation-coupled increased expression of gp91phox mRNA and membrane translocation of Rac protein, thereby resulting in a significant reduction of autoregulatory vasodilation. 5. Fluid percussion injury and SAH-induced overproduction of superoxide anion in cerebral vessels contributes to the impairment of CBF autoregulation and administration of recombinant adenovirus-mediated transfer of the Cu/Zn SOD-1 gene effectively ameliorates the impairment of CBF autoregulation of the pial artery.