高Cr镍基合金的高温内氧化和内氮化行为

通过对镍基合金进行不同温度的恒温氧化试验、横断面的组织形貌观察及微区成分分析,研究一种高Cr镍基合金在恒温氧化期间的氧化物分布特征、内氧化及内氮化行为。结果表明：该高Cr镍基合金在850、900、950和1 000℃空气中氧化100 h期间,合金表层发生元素的外氧化,且在外氧化膜中出现分层结构,由表及里各层中的主要氧化物分别为Al2O3、Cr2O3、NiCr2O4和NiAl2O4、Cr2O3、CrTaO4和Al2O3;合金在900℃以下为完全抗氧化级,900~1 000℃为抗氧化级。该合金在各温度的恒温氧化期间,均发生元素Al的内氧化和内氮化;与外氧化膜相邻的区域为元素Al的内氧化区,远离外氧化膜的基体内部形成元素Al的内氮化区;随恒温氧化温度的升高,内氧化区和内氮化区的深度增加,内氧化物和内氮化物的尺寸增大。其中,在内氧化物、内氮化物周围形成元素Al的贫化区,在贫化区内发生-′相的分解及贫乏。

NS163合金内氮化过程

在1050~1200℃温度范围内对NS163合金进行了内生氮化处理,通过氮化层深度随时间和温度的变化来表征氮化速率,并进行了NS163合金内生氮化过程的动力学分析。结果表明：氮化处理后获得了平行于表面的（Ti,Nb）N氮化物层,该氮化物有高温稳定、量大、细小和晶内弥散分布的特点;氮化层厚度与氮化时间之间满足抛物线关系;采用抛物线速率常K_p表征了不同温度的氮化速率,K_p随温度升高逐渐增大,二者满足Arrhenius型关系,表明内氮化过程受热激活过程控制;由此提出定量关系式来表达氮化层厚度与氮化时间和温度的关系。

4Cr14Ni14W2Mo 钢的内氮化动力学

本工作导出了紧靠氮化物层下方发生的内氮化过程的动力学方程,方程也可用于双层内氮化过程。按此方程所设计的方案在氨气介质中对4Cr14Ni14W_2Mo 钢进行氮化实验,得到与预期相一致的结果。较高的氮化温度和较高的氨气分解率可免除该钢种的氮化层剥落。

温度对高铬二代镍基单晶高温合金氧化行为的影响

采用不连续增重法研究了一种燃机用高Cr二代镍基单晶高温合金在1000℃和1100℃的氧化行为,采用XRD和SEM对样品的氧化层组织形貌进行表征,分析了氧化机理及温度对合金氧化行为的影响。研究表明,实验合金在1000℃的氧化动力学遵循抛物线规律,氧化500 h后仍具有较低的增重速率,外氧化层以Cr_(2)O_(3)为主,TiO_(2)呈团簇状分布在Cr_(2)O_(3)外侧,内部有少量颗粒状TiN,整个氧化层完整致密,合金抗氧化性能优异。温度升高至1100℃后,合金在氧化100 h后出现严重剥落,外氧化层疏松多孔,内氧化物呈网状向内部发展,内氮化物的数量明显增多,尺寸明显增大,合金抗氧化性能恶化。温度对合金氧化性能影响的机理为升温导致Cr_(2)O_(3)挥发速率增大,破坏了Cr_(2)O_(3)膜的致密性,增大了氧化膜的内应力,降低了氧化膜对氧、氮的抑制作用,合金的抗氧化性能降低。

NiCrAlY涂层对单晶镍基合金高温氧化行为的影响

通过对有无NiCrAlY涂层镍基单晶合金进行不同温度的恒温氧化动力学曲线测定及组织结构观察,研究了纳米晶NiCrAlY涂层对高Cr单晶镍基合金高温氧化行为的影响。结果表明:在高温氧化期间,无涂层试样发生明显的氧化、内氧化和内氮化,在表层为Al2O3、Cr2O3的混合氧化物,在次表层氧化物中富含元素Ta,而元素Al贫化,并在近基体区域存在内氧化物;随氧化温度升高,元素Al的贫化区尺寸增大,其中,富Ta相可抑制基体中元素Al向外扩散,延缓合金的氧化速率。合金在氧化初期增重迅速,而恒温氧化增重动力学曲线呈现起伏波动的原因,归结于表面氧化膜的形成与剥落。高Cr单晶合金经溅射NiCrAlY纳米晶涂层,可有效改善合金的抗氧化性能;有涂层试样在不同温度的恒温氧化动力学曲线仅在氧化初期有轻微增重而后趋于平稳,其形成的Al2O3氧化膜不发生明显的剥落,仅在基体近涂层/基体界面区域存在少量AlN内氮化物。

一种镍基合金在900和1000℃的高温氧化行为

采用X射线衍射(XRD),扫描电镜(SEM)及能谱(EDAX)等方法,研究了Cr5.0 Co8.0 Mo0.9W5.5 Ta7.4 Al6.0 Re4.2合金在900和1 000℃的氧化行为。结果表明,氧化动力学曲线遵循氧化初期氧化增重速率较快,氧化期间氧化动力学曲线呈波浪式变化,且呈现氧化温度越高波浪式越明显的特征。在900℃氧化300 h后合金表面氧化物膜分为3层,外层为Ni O、Ni2Cr2O4、Ni2Co O4和Cr Ta O4;中间层为平直的Al2O3层,内氧化层为Al2O3,氧化期间,分布在外层的Cr Ta O4抑制基体中Al向外扩散,并抑制氧化膜的生长,使氧化速度降低。1 000℃时合金表面的氧化物膜分为2层,外层为Ni O、Ni2Cr2O4、Ni2Co O4和Cr Ta O4;内氧化层为Al2O3。在900和1 000℃氧化期间,合金均发生元素Al的内氧化和内氮化,与外氧化膜相邻的区域为元素Al的内氧化区,远离外氧化膜的基体内部形成元素Al的内氮化区,随氧化温度升高,内氧化区和内氮化区的深度增加,内氧化物和内氮化物的尺寸增大。

Protective effects of icariin on human umbilical vein endothelial cell injured by angiotensin Ⅱ

To investigate the effects of icariin （ICA） on angiotensin Ⅱ（Ang Ⅱ）-induced injury in human umbilical vein endothelial cells line （ECV-304）. The ECV-304 cells were cultured in vitro. After 24 h incubating with icariin, the model of AngⅡ-induced injury in ECV-304 was established. The cell viability （MTT method）, Lactate dehydrogenase （LDH） release and Nitric oxide （NO） production in the medium, the capacity of scavenging superoxide anion radicals （O2^-） and hydroxyl radicals （.OH） were measured. The activities of superoxide dismutase （SOD）, total nitric oxide synthase （T-NOS）, inducible nitric oxide synthase （iNOS） and constitutive nitric oxide synthase （cNOS） in the cells were determined. Compared with the Ang Ⅱ-treated group, ICA can significantly raise the viability of EC, increase the activities of SOD, T-NOS and cNOS, increase the production of NO, enhance the capacity of scavenging superoxide anion radicals （ O2^- ） and hydroxyl radicals（.OH）, and lower LDH leakage and iNOS activity. The results suggest that ICA can protect endothelial cells （ECV-304） from Ang II-induced injury.

Association of Glu298Asp Polymorphism of the En-dothelial Nitric Oxide Synthase Gene with Essential Hypertension in Elderly People

Objective: To investigate the association of Glu298Asp polymorphism of theeNOS gene with essential hypertension in elderly people. Methods: Ninety-five cases of essentialhypertension were randomly chosen from outpatients and inpatients as the study group, and an equalnumber of sexes, age-matched healthy people as the control group. Their height, weight and bloodpressure were recorded and their fasting plasma lipid concentrations were measured. Glu298Asppolymorphism of the eNOS gene was measured using the methods of PCR and RFLP. Results: Theconstituent ratio of Genotype Glu/Asp in the study group (26.3%) was higher than that in the controlgroup (12.6%, x^2 = 5. 67, P<0.05), the allelic frequency of 298Asp in the study group (13.2%) wassignificantly higher than that in the control group (6.3%, x^2 = 5.06, P<0.05). Conclusion: Glu298Asp variant of the eNOS gene may be an independent predictor in essential hypertension.

Intestinal endotoxemia plays a central role in development of hepatopulmonary syndrome in a cirrhotic rat model induced by multiple pathogenic factors

AIM: To characterize the correlation between severity of hepatopulmonary syndrome (HPS) and degree of hepatic dysfunction,and to explore how intestinal endotoxemia (IETM) affects the development of HPS in cirrhotic rats. METHODS: Male Wister rats were fed with a diet containing maize flour,lard,cholesterol,and alcohol and injected subcutaneously with CCl4 oil solution every two days for 8 wk to induce typical cirrhosis and development of HPS. The animals were also given a nitric oxide (NO) production inhibitor,Nω-nitro-L-arginine methyl ester (L-NAME) intraperitoneally,and an iNOS inhibitor,aminoguanidine hydrochloride (AG) via gavage daily from the end of the 4th wk to the end of the 6th or 8th wk,or a HO-1 inhibitor,zinc protoporphyrin (ZnPP) intraperitoneally 12 h prior to killing. Blood,liver and lung tissues were sampled. RESULTS: Histological deterioration of the lung paralleled to that of the liver in the cirrhotic rats. The number of pulmonary capillaries was progressively increased from 6.1 ± 1.1 (count/filed) at the 4th wk to 14.5 ± 2.4 (count/filed) at the 8th wk in the cirrhotic rats. Increased pulmonary capillaries were associated with increased blood levels of lipopolysaccharide (LPS)(0.31 ± 0.08 EU/mL vs control 0.09 ± 0.03 EU/mL),alanine transferase (ALT,219.1 ± 17.4 U/L vs control 5.9 ± 2.2 U/L) and portal vein pressure. Compared with normal control animals,the number of total cells in bronchoalveolar lavage fluid (BALF) of the cirrhotic rats at the 8th wk was not changed,but the number of macrophages and the ratio of macrophages to total cells were increased by nearly 2-fold,protein expression of inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) started to increase significantly at the 4th wk,and reached its peak at the 8th wk in the lung of cirrhotic rats. The increase of iNOS expression appeared to be quicker than that of eNOS. NO2-/NO3-was also increased,which was correlated to the increase of iNOS (r = 0.7699,P < 0.0001) and eNOS (r = 0.5829,P < 0.002). mRNA expression of eNOS and iNOS was highly consistent with their protein expression. CONCLUSION: Progression and severity of HPS as indicated by both increased pulmonary capillaries and histological changes are closely associated with LPS levels and progression of hepatic dysfunction as indicated by increased levels of ALT and portal vein pressure. Intestinal endotoxemia plays a central role in the development of HPS in the cirrhotic rat model by inducing NO and/or CO.

Increased intestinal macromolecular permeability and urine nitrite excretion associated with liver cirrhosis with ascites

AIM： To determine intestinal permeability, the serum tumor necrosis factor （TNF）-α level and urine nitric oxide （NO） metabolites are altered in liver cirrhosis （LC） with or without ascites. METHODS： Fifty-three patients with LC and 26 healthy control subjects were enrolled in the study. The intestinal permeability value is expressed as the percentage of polyethylene glycol （PEG） 400 and 3350 retrieval in 8-h urine samples as determined by high performance liquid chromatography. Serum TNF-α concentrations and urine NO metabolites were determined using an enzyme-linked immunosorbent assay （ELISA） and Greiss reaction method, respectively. RESULTS： The intestinal permeability index wassignificantly higher in patients with LC with ascites than in healthy control subjects or patients with LC without ascites （0.88 ± 0.12 vs 0.52 ± 0.05 or 0.53 ± 0.03, P 〈 0.05） and correlated with urine nitrite excretion （r = 0.98）. Interestingly, the serum TNF-α concentration was significantly higher in LC without ascites than in control subjects or in LC with ascites （198.9 ± 55.8 pg/mL vs 40.9 ± 12.3 pg/mL or 32.1 ± 13.3 pg/mL, P 〈 0.05）. Urine nitrite excretion was significantly higher in LC with ascites than in the control subjects or in LC without ascites（ 1170.9± 28.7 μmol/L vs 903.1 ± 55.1 μmol/L or 956.7 ± 47.7 μmol/L, P 〈 0.05）. COMCLUSIOM： Increased intestinal macromolecular permeability and NO is probably of importance in the pathophysiology and progression of LC with ascites, but the serum TNF-α concentration was not related to LC with ascites.

Effect of IBD sera on expression of inducible and endothelial nitric oxide synthase in human umbilical vein endothelial cells

AIM： To study the expression of endothelial and inducible nitric oxide synthases （eNOS and iNOS） and their role in inflammatory bowel disease （IBD）. METHODS： We examined the effect of sera obtained from patients with active Crohn＇s disease （CD） and ulcerative colitis （UC） on the function and viability of human umbilical vein endothelial cells （HUVEC）. HUVECs were cultured for 0-48 h in the presence of a medium containing pooled serum of healthy controls, or serum from patients with active CD or UC. Expression of eNOS and iNOS was visualized by immunofluorescence, and quantified by the densitometry of Western blots. Proliferation activity was assessed by computerized image analyses of Ki-67 immunoreactive cells, and also tested in the presence of the NOS inhibitor, 10^-4 mol/L L-NAME. Apoptosis and necrosis was examined by the annexin-V-biotin method and by propidium iodide staining, respectively. RESULTS： In HUVEC immediately after exposure to UC, serum eNOS was markedly induced, reaching a peak at 12 h. In contrast, a decrease in eNOS was observed after incubation with CD sera and the eNOS level was minimal at 20 h compared to control （18%±16% vs 23%± 15% P〈0.01）. UC or CD serum caused a significant increase in iNOS compared to control （UC： 300%±21%; CD： 275% ± 27% vs 108% ± 14%, P〈0.01）. Apoptosis/necrosis characteristics did not differ significantly in either experiment. Increased proliferation activity was detected in the presence of CD serum or after treatment with L-NAME. Cultures showed tube-like formations after 24 h treatment with CD serum. CONCLUSION： IBD sera evoked changes in the ratio of eNOS/iNOS, whereas did not influence the viability of HUVEC. These involved down-regulation of eNOS and up-regulation of iNOS simultaneously, leading to increased proliferation activity and possibly a reduced antiinflammatory protection of endothelial cells.

Randomized controlled study of the safety and efficacy of nitrous oxide-sedated endoscopic ultrasound-guided fine needle aspiration for digestive tract diseases

AIM To evaluate the efficacy and safety of nitrous oxidesedated endoscopic ultrasound-guided fine needle aspiration. METHODS Enrolled patients were divided randomly into an experimental group(inhalation of nitrous oxide) and a control group(inhalation of pure oxygen) and heart rate, blood oxygen saturation, blood pressure, electrocardiogram(ECG) changes, and the occurrence of complications were monitored and recorded. All patients and physicians completed satisfaction questionnaires about the examination and scored the process using a visual analog scale. RESULTS There was no significant difference in heart rate, blood oxygen saturation, blood pressure, ECG changes, or complication rate between the two groups of patients(P > 0.05). However, patient and physician satisfaction were both significantly higher in the nitrous oxide compared with the control group(P < 0.05).CONCLUSION Nitrous oxide-sedation is a safe and effective option for patients undergoing endoscopic ultrasound-guided fine needle aspiration.

Expression and activity of inducible nitric oxide synthase and endothelial nitric oxide synthase correlate with ethanolinduced liver injury

AIM： To study the expression and activity of inducible nitric oxide synthase （iNOS） and endothelial nitric oxide synthase （eNOS） in rats with ethanol-induced liver injury and their relation with liver damage, activation of nuclear factor-KB （NF-κB） and tumor necrosis factor-α （TNF-α） expression in the liver. METHODS： Female Sprague-Dawley rats were given fish oil （0.5 mL） along with ethanol or isocaloric dextrose daily via gastrogavage for 4 or 6 wk. Liver injury was assessed using serum alanine aminotransferase （ALT） activity and pathological analysis. Liver malondialdehyde （MDA）, nitric oxide contents, iNOS and eNOS activity were determined. NF-κB p65, iNOS, eNOS and TNF-α protein or mRNA expression in the liver were detected by immunohistochemistry or reverse transcriptase-polymerase chain reaction （RT-PCR）. RESULTS： Chronic ethanol gavage for 4 wk caused steatosis, inflammation and necrosis in the liver, and elevated serum ALT activity. Prolonged ethanol administration （6 wk） enhanced the liver damage. These responses were accompanied with increased lipid peroxidation, NO contents, iNOS activity and reduced eNOS activity. NF-κB p65, iNOS and TNF-α protein or mRNA expression were markedly induced after chronic ethanol gavage, whereas eNOS mRNA expression remained unchanged. The enhanced iNOS activity and expression were positively correlated with the liver damage, especially the necro-inflammation, activation of NF-KB, and TNF-α mRNA expression. CONCLUSION： iNOS expression and activity are induced in the liver after chronic ethanol exposure in rats, which are correlated with the liver damage, especially the necro-inflammation, activation of NF-KB and TNF-α expression, eNOS activity is reduced, but its mRNA expression is not affected.

NITRIC OXIDE INHIBITS A RISE OF ATP-INTRODUCED CYTOSOLIC FREE Ca^(2+) CONCENTRATION AND RELEASE FROM INTRACELLULAR STORED Ca^(2+)

Object. The effects of ATP-introduced a rise in cytosolic free Ca2+ concentration and inhibition of nitric oxide were investigated. Method. Measurement of free Ca2+([Ca2+] i)of cultured rat tail arterial smooth muscle cells using Fura-2/AM dual excitation wavelength spectrofluorometer. Results. There are two components of [Ca2+] i can be evoked by ATP. One part is Ca2+ entry from Ca2+ channel and formed a plateau. The another part is a peak that released from Ca2+ store. Both of them can be inhibited by NO. Conclusion. The ATP induced [Ca2+] i rise that release Ca2+ from both Insp 3 and ryanochine receptors and Ca2+ entry through calcium channels. The inhibition of NO on ATP induced [Ca2+] i rise that was mediated by cGMP.

Expression of endothelial nitric oxide synthase and vascular endothelial growth factor in association with neovascularization in human primary astrocytoma

Objective: To investigate the relationship between the expression of endothelial nitric oxide synthase (eNOS), vascular endothelial growth factor (VEGF) and angiogenesis in primary astrocytoma. Methods: Thirty-seven primary astrocytomas and 4 astrocytic hyperplasia samples were collected and divided into three groups according to histological grade. The expression of eNOS, VEGF and factorⅧ related antigen (FⅧRAg) were assayed by immunohistochemistry. Microvascular density was assessed by FⅧRAg immunoreactivity. The intensity of immunoreactivity was graded according to the percentage of positive tumor cells. Results: No eNOS and VEGF were expressed in the astrocytes and vascular endothelium in astrocytic hyperplasia. The expression of eNOS or VEGF was light in low-grade astrocytoma and strong in glioblastoma. eNOS expression in astrocytoma was very positively correlated with VEGF. eNOS and VEGF expression in anaplastic astrocytoma was median in contrast to the low grade astrocytoma and glioblastoma. Lower microvascular density was found in low grade astrocytoma than that in higher grade malignant ones. The expressions of eNOS and VEGF were correlated with microvascular density and tumor malignancy. Conclusion: This finding suggests that eNOS and VEGF may have cooperative effect in tumor angiogenesis and play an important role in the pathogenesis of primary astrocytoma.

Changes of nitric oxide and endothelin, thromboxane A2 and prostaglandin in cirrhotic patients undergoing liver transplantation

AIM： To investigate the perioperative changes of nitric oxide （NO） and endothelin （ET）, thromboxane A2 （TXA2） and prostaglandin （PGI2） during liver transplantation in end-stage liver disease patients. METHODS： Twenty-seven patients with end-stage cirrhosis undergoing liver transplantation were enrolled in this prospective study. Blood samples were obtained from superior vena at five different surgical stages. Plasma concentrations of nitrate and nitrite were determined to reflect plasma NO levels. Plasma levels of ET-1, 6-keto-PGF1 alpha and thromboxane B2 （TXB2）, the latter two being stable metabolites of PGI2 and TXA2 respectively, were measured.RESULTS： The NO level decreased significantly after vascular cross-clamping and increased significantly at 30 rain after reperfusion. While the ET levels at 30 rain after clamping and after reperfusion were significantly elevated. The ratio of NO/ET decreased significantly at 30 rain after vascular cross-clamping and at the end of surgery. The PGI2 level and the TXA2 during liver transplantation were significantly higher than the baseline level, but the ratio of TXA2/PGI2 decreased significantly at 30 rain after clamping. CONCLUSION： NO/ET and TXA2/PGI2 change during liver transplantation. Although the precise mechanism remains unknown, they may play a role in the pathobiology of a variety of liver transplant-relevant processes.

Adrenomedullin in cirrhotic and non-cirrhotic portal hypertension

AIM:Adrenomedullin (ADM) is a potent vasodilator peptide. ADM and nitric oxide (NO) are produced in vascular endothelial cells.Increased ADM level has been linked to hyperdynamic circulation and arterial vasodilatation in cirrhotic portal hypertension (CPH).The role of ADM in non-cirrhotic portal hypertension (NCPH) is unknown,plasma ADM levels were studied in patients with NCPH,compensated and decompensated cirrhosis in order to determine its contribution to portal hypertension (PH) in these groups. METHODS:There were 4 groups of subjects.Group 1 consisted of 27 patients (F/M:12/15) with NCPH due to portal and/or splenic vein thrombosis (mean age:41±12 years),group 2 consisted of 14 patients (F/M:6/8) with compensated (Child-Pugh A) cirrhosis (mean age:46±4), group 3 consisted of 16 patients (F/M:6/10) with decompensated (Child-Pugh C) cirrhosis (mean age:47±12). Fourteen healthy subjects (F/M:6/8) (mean age:44±8) were used as controls in Group 4.ADM level was measured by ELISA.NO was determined as nitrite/nitrate level by chemoluminescence. RESULTS:ADM level in Group 1 (236±61.4 pg/mL) was significantly higher than that in group 2 (108.4±28.3 pg/mL) and group 4 (84.1±31.5 pg/mL) (both P<0.0001) but was lower than that in Group3 (324±93.7 pg/mL) (P=0.002).NO level in group 1 (27±1.4 μmol/L) was significantly higher than that in group 2 (19.8±2.8 μmol/L) and group 4 (16.9±1.6 μmol/L) but was lower than that in Group 3 (39±3.6 μmol/L) (for all three P<0.0001).A strong correlation was observed between ADM and NO levels (r=0.827,P<0.0001). CONCLUSION:Adrenomedullin and NO levels were high in both non-cirrhotic and cirrhotic portal hypertension and were closely correlated,Adrenomedullin and NO levels increased proportionally with the severity of cirrhosis,and were significantly higher than those in patients with NCPH. Portal hypertension plays an important role in the increase of ADM and NO.Parenchymal damage in cirrhosis may contribute to the increase in these parameters.

Cr含量对Ni-Fe-Cr-Al合金抗氧化性能的影响

用不连续称重法表征了Cr含量(质量分数)分别为20%、24%和28%的Ni-Fe-Cr-Al合金在1200℃空气中氧化后氧化膜的形貌和相组成,研究了这类合金的氧化行为。结果表明:这三种不同Cr含量的Ni-Fe-Cr-Al合金在1200℃氧化100 h后其氧化动力学曲线都符合抛物线规律,氧化速率相近,Cr含量的提高使其抗氧化性能有所提高。这三种Ni-Fe-Cr-Al合金在1200℃氧化1 h后生成的氧化膜均具有两层结构,外层由Cr_(2)O_(3)和少量尖晶石氧化物NiCr_(2)O_(4)组成,内层为Al_(2)O_(3)层;氧化100 h后氧化膜仍为两层结构,与氧化1 h的不同之处是外层主要由混合尖晶石和少量Cr_(2)O_(3)组成,混合尖晶石为NiCr_(2)O_(4)、NiFe_(2)O_(4),内层为连续Al_(2)O_(3)层。这三种合金在氧化过程中均出现明显的内氮化。Cr含量的提高对氧化1 h发生的内氮化有一定的抑制。随着氧化时间的延长(100 h)这三种合金的内氮化深度相近,提高Cr含量对内氮化影响不大。

INFLUENCE OF GINKGO BILOBA EXTRACT ON NITRIC OXIDE AND ENDOTHELIN-1 DURING CEREBRAL VASOSPASM IN RATS

Objective.To investigate the effects of Ginkgo biloba extracton cer ebral vasospasmafter subarachnoid hemorrhageand its influence on n itric oxideand endothelin-l .Methods.Noncraniotomy models of SAH in Wistar rats were used and animals were divided into sham-operated group ,SAH group,saline-treated group and EGb-treated group.Diameter of basilar a rtery was measured.Regional cerebral blood flow,NO and ET-1levels in blood,and calcium content in brain tissue within24hours after SAH were dete cted.Pathological examination of hippocampus CA1sub-field was also performed .Results.Sham operation did not alter the above parameters.Induction of SAH l ed to a marked spasm of basilar artery.rCBF decreased obviously and consecutive ly within24hours after SAH.Meanwhile NO level in serum decreased,ET-1level in plasma and calcium content in brain tissue significantly in-creased.Pyra midal cells in hippocampus CA1subfield were severely damaged.EGb significantly antago-nized the pathological alterations of the above parameters.Conclusion .Alterations of NO,and ET-1play an important role in the development of CV S after SAH.EGb exerts its protective effects on CVS by inhibitng the above pat hological alterations.

Extract of Meretrix meretrix Linnaeus induces angiogenesis in vitro and activates endothelial nitric oxide synthase

Meretrix meretrix Linnaeus has long been used as traditional Chinese medicine in oriental medicine.The angiogentic activity of the extract of M.meretrix was investigated in this study,using human umbilical vein endothelial cells(HUVECs).Extract of M.meretrix Linnaeus(AFG-25) was prepared with acetone and ethanol precipitation,and further separated by Sephadex G-25 column.The results show that AFG-25 promoted proliferation,migration,and capillary-like tube formation in HUVECs,and in the presence of eNOS inhibitor NMA,the tube formation induced by AFG-25 is inhibited significantly.Moreover,AFG25 could also promote the activation of endothelial nitric oxide synthase(eNOS) and the resultant elevation of nitric oxide(NO) production.The results suggested that M.meretrix contains active ingredients with angiogentic activity and eNOS/NO signal pathway is in part involved in the proangiogenesis effect induced by AFG-25.