EFFECTS OF OUABAIN AND DIGOXIN ON THE GENE EXPRESSION OFSODIUM PUMP α-SUBUNIT ISOFORM IN AORTIC SMOOTH MUSCLE OF RATS

Objective To compare the effects or ouabain and digoxin on both the systolic blood pressure and sodium pump a-subunit isoforms gene expression in the aortic smooth muscle of rats. Methods Normal Sprague- Dawley rats were injected with ouabain (20μg·kg-1·d-l,i. p), digoxin (32 μg·kg-1·d-1, i. p)and normal saline once a day, respectively, and indirect systolic blood pressure was recorded once a week. Six weeks later,all the rats were killed and sodium pump α1-,α2-,and α3-subunit mRNA levels were detected in the aortic smooth muscle with reverse transcription polymerase chain reaction（RT-PCR） method. Results The systolic blood pressure of rats infused with ouabain increased significantly at the end of week 6 [l32. 6±9.0 mmHg （1 mmHg = 0. 133 kPa） vs 115. 7 ± 8. 2 mmHg, P <0.01],while no difference of blood pressure was found between digoxin group and NS group （P>0.05）. The expression or sodium pump α-subunit isoforms in aortic smooth muscle was regulated by either ouabain or digox- in:both ouabain and digoxin increased α1- and α3-subunit expression, α2-subunit decreased in digoxin group but un- changed in ouabain group. Conclusion These results suggest that both ouabain and digoxin could regulate sodium pump α-subunit isoform expression, which might be related to the physiological roles or endogenous ouabain and might be responsible for the difference between the pharmacological and toxicological effects or ouabain and digoxin, including their effects on blood pressure.

Effects of ouabain and digoxin on gene expression of sodium pump α-subunit isoforms in rat myocardium

Objective To compare the effects of ouabain and digoxin on the gene expression of sodium pump α-subunit isoforms in the myocardium of rats.Methods Normal Sprague-Dawley (SD) rats were injected with ouabain (20 μg· kg-1· d-1, i.p. ), digoxin (32 μg· kg-1· d-1, i.p. ) and normal saline (NS) once a day, respectively, and indirect systolic blood pressure was recorded once a week. Six weeks later, all of the rats were killed, and sodium pump α1-,α2-, and α3-subunit mRNA levels in the myocardium were detected with the reverse transcription polymerase chain reaction (RT-PCR) method.Results The systolic blood pressure of the rats infused with ouabain increased significantly at the end of week 6 ( 132.6 ± 9.0 mm Hg vs 115.7 ± 8.2 mm Hg, P ＜ 0.01 ), while no difference in blood pressure was found between the digoxin group and the NS group. The expression of sodium pump α-subunit isoforms in the ventricular myocardium was regulated by either ouabain or digoxin. Both ouabain and digoxin stimulated expression of the α3-isoform, whereas o2 was uncharcged in those two groups. α1-isoform expression decreased in the ouabain group and was unchanged in the digoxin group.Conclusions These results suggest that both ouabain and digoxin could regulate sodium pump α-subunit isoform expression, which might be related to the physiological roles of endogenous ouabain and might be responsible for the difference in the pharmacological and toxicological effects of ouabain and digoxin,including their effects on blood pressure.

Effects of Dingjifumai Decoction on Electrocardiogram and sodium potassium pump of rats with ventricular arrhythmia

Objective:To investigate the effect of Dingjifumai Decoction(DJFM)on Electrocardiogram(ECG)and sodium potassium pump in rats with ventricular arrhythmia.Methods:Forty healthy male SD rats(200±20g)were randomly divided into blank group,model group,Metoprolol group and DJFM group.Ten rats in each group were fed with normal diet and free drinking water.Each group was given gavage,and the amount of gavage in each group was calculated according to body weight.In the model group,0.001%Aconitine was injected into the tail vein at 30ug/kg.In the Metoprolol group,Metoprolol suspension was given according to the standard of 5.2mg/kg per day.In the DJFM group,DJFM was given at 17.6g/kg per day.After 2 weeks of administration,the biologic experiment system BL-420F was used to monitor the II lead ECG curve,and the ECG changes were observed and recorded.Then,the left ventricle of the rat was taken,and part of the heart tissue sodium potassium pump was detected.Results:(1)The effect of DJFM on ECG of rats with ventricular arrhythmia:After intravenous injection of aconitine,the incidence of Ventricular Premature beat(VP),Ventricular Tachycardia(VT),Ventricular Fibrillation(VF)in the model group was 100%,suggesting that the model building of rats with ventricular arrhythmia was successful.(2)VP,VT,and VF time:Compared with model group,DJFM group and Metoprolol group can significantly delay the VP,VT and VF,the difference was statistically significant(P<0.05).The effect of DJFM group and Metoprolol group on delaying the appearance of VP,VT and VF was the same,there was no significant difference(P>0.05).(3)The effect of DJFM on sodium potassium pump in rat ventricular arrhythmia heart tissues:Compared with the blank group,the sodium potassium pump value in the model group was significantly decreased,and the difference was statistically significant(P<0.05).Compared with the model group,the sodium potassium pump value of the tissues in the Metoprolol group and the DJFM group increased,and the difference was statistically significant(P<0.05).There was no significant difference in sodium potassium pump between the Metoprolol group and the DJFM group(P>0.05).Conclusion:1.The rat model of ventricular arrhythmia can be successfully prepared by intravenous injection of Aconitine.2.DJFM can prolong the occurrence time of cardiac arrhythmias caused by aconitine in rats,such as VP,VT,VF,et al.The mechanism may be related to fast Na^+channel,and it may prevent and control arrhythmias by inhibiting Na^+influx and reducing the fast response cellular self-discipline.3.DJFM can protect the myocardial tissue sodium potassium pump,which can protect the myocardial cells and improve the myocardial metabolism.

Drosophila models used to simulate human ATP1A1 gene mutations that cause Charcot-Marie-Tooth type 2 disease and refractory seizures

Certain amino acids changes in the human Na^(+)/K^(+)-ATPase pump,ATPase Na^(+)/K^(+)transporting subunit alpha 1(ATP1A1),cause Charcot-Marie-Tooth disease type 2(CMT2)disease and refractory seizures.To develop in vivo models to study the role of Na^(+)/K^(+)-ATPase in these diseases,we modified the Drosophila gene homolog,Atpα,to mimic the human ATP1A1 gene mutations that cause CMT2.Mutations located within the helical linker region of human ATP1A1(I592T,A597T,P600T,and D601F)were simultaneously introduced into endogenous Drosophila Atpαby CRISPR/Cas9-mediated genome editing,generating the Atpα^(TTTF)model.In addition,the same strategy was used to generate the corresponding single point mutations in flies(Atpα^(I571T),Atpα^(A576T),Atpα^(P579T),and Atpα^(D580F)).Moreover,a deletion mutation(Atpα^(mut))that causes premature termination of translation was generated as a positive control.Of these alleles,we found two that could be maintained as homozygotes(Atpα^(I571T)and Atpα^(P579T)).Three alleles(Atpα^(A576T),Atpα^(P579)and Atpα^(D580F))can form heterozygotes with the Atpαmut allele.We found that the Atpαallele carrying these CMT2-associated mutations showed differential phenotypes in Drosophila.Flies heterozygous for Atpα^(TTTF)mutations have motor performance defects,a reduced lifespan,seizures,and an abnormal neuronal morphology.These Drosophila models will provide a new platform for studying the function and regulation of the sodium-potassium pump.

艾司奥美拉唑钠持续泵入与静脉滴注给药方式在消化性溃疡合并出血患者中的应用效果

目的 比较艾司奥美拉唑钠持续泵入与静脉滴注给药方式在消化性溃疡合并出血患者中的应用效果。方法 选择2018年4月至2021年4月收治的90例消化性溃疡合并出血患者作为研究对象,按红绿双色球法将其分为对照组和研究组,各45例。对照组给予艾司奥美拉唑钠静脉滴注治疗,研究组给予艾司奥美拉唑钠持续泵入治疗。比较两组的治疗效果。结果 研究组的出血、呕血、黑便停止时间和腹痛缓解时间短于对照组(P<0.05)。研究组的治疗总有效率为95.56%,显著高于对照组的80.00%(P<0.05)。治疗后,研究组的纤维蛋白原、D-二聚体水平低于对照组,血小板计数(PLT)、红细胞比容(HCT)高于对照组(P<0.05)。治疗后,研究组的表皮生长因子(EGF)、前列腺素E2(PGE2)水平高于对照组,基质金属蛋白酶-2(MMP-2)、基质金属蛋白酶-3(MMP-3)水平低于对照组(P<0.05)。两组的不良反应总发生率比较,差异无统计学意义(P>0.05)。结论 相比于艾司奥美拉唑钠静脉滴注给药,持续泵入效果会更好,能够缩短消化性溃疡合并出血患者临床症状消失时间,提高治疗效果,改善凝血功能及血清指标。

七贤加压站管道供水次氯酸钠投加系统设计

结合济南市七贤加压站供水工艺对次氯酸钠投加系统展开研究。通过两种供水行业次氯酸钠投加方式的对比分析,分析七贤加压站新型节能供水工艺流程下次氯酸钠投加系统的新结构、新模式,达到自动控制调节余氯的目的,提升加压泵站次氯酸钠消毒的有效性,保证了系统管网末梢余氯值达到国标值,保障用户用水安全。

33 W quasi-continuous-wave narrow-band sodium D_(2a) laser by sum-frequency generation in LBO

We demonstrate an all-solid quasi-continuous-wave （QCW） narrow-band source tunable to sodium D2a line at 589.159 nm. The source is based on sum-frequency mixing between lasers at 1064 nm and 1319 nm in a LBO crystal. The 1064 nm and 1319 nm lasers are produced from two diode side-pumped Nd：YAG master oscillator power amplifier （MOPA） laser systems, respectively. A 33 W output of 589 nm laser is obtained with beam quality factor M^2 = 1.25, frequency stability better than ±0.2 GHz and linewidth less than 0.44 GHz. A prototype 589 nm laser system is assembled, and a sodium laser guided star has been successfully observed in the field test.

肿瘤坏死因子-α通过激活A549细胞Wnt/β-catenin通路降低肺泡液体清除功能

目的探讨炎症环境下Wnt/β-catenin通路对肺泡液体清除功能的影响。方法用不同浓度(10、40、80、160 ng·mL^(-1))肿瘤坏死因子-α(TNF-α)处理人肺泡上皮Ⅱ型细胞(A549)24 h,采用CCK-8法检测细胞存活率,酶联免疫吸附实验(ELISA)检测炎性因子白介素(IL)-1β、IL-18、IL-6表达水平,Western blot检测钠水转运蛋白上皮细胞钠通道β亚型(βENaC)、NA^(+)、K^(+)-ATP酶(NKA)和水通道蛋白(AQP)4的表达,综合实验结果选取TNF-α最佳干预浓度;然后A549分为control组、TNF-α40 ng·mL^(-1)组、Wnt通路抑制组(TNF-α+XAV939组),分别检测细胞存活率、凋亡率、炎性因子表达水平及β-连环蛋白(β-catenin)、细胞周期蛋白D1(Cyclin D1)、腺瘤息肉病基因蛋白(APC)、βENaC、NKA和AQP4的表达水平。结果自TNF-α的40 ng·mL^(-1)起,A549细胞存活率逐渐降低,炎性因子表达水平逐渐升高,钠水转运蛋白βENaC、NKA表达逐渐降低,AQP4表达逐渐升高(P<0.05),选出最佳干预浓度为TNF-α40 ng·mL^(-1);与control组相比,TNF-α40 ng·mL^(-1)组A549细胞存活率降低,凋亡率、炎性因子表达水平升高,βENaC、NKA、APC蛋白表达降低,AQP4、β-catenin、Cyclin D1蛋白表达升高(P均<0.05)。应用XAV939后,与TNF-α40 ng·mL^(-1)组相比,TNF-α+XAV939组A549细胞存活率升高,凋亡率、炎性因子表达水平降低,βENaC、NKA、APC蛋白表达升高,AQP4、β-catenin、Cyclin D1蛋白表达降低(P均<0.05)。结论TNF-α可通过激活A549细胞Wnt/β-catenin通路,使钠水转运蛋白βENaC、NKA表达减少,AQP4表达增加,降低肺泡液体清除功能。

钠钾泵抑制剂pNaKtide对糖尿病心肌病小鼠心脏损伤的作用

目的:探讨钠钾泵抑制剂pNaKtide对糖尿病心肌病小鼠心脏损伤的作用及机制。方法:自发性2型糖尿病心肌病(leptin基因敲除)db/db小鼠和野生wt小鼠各8只,分为4组:db/db组、db/db+pNaKtide组、wt组和wt+pNaKtide组,每组各4只。db/db+pNaKtide组和wt+pNaKtide组小鼠按10 mg/kg每周腹腔注射pNaKtide 1次,wt组和db/db组注射生理盐水,共8周。每周测量体重及小鼠尾动脉收缩压(SBP)。干预8周后检测小鼠血清甘油三酯及总胆固醇水平;HE和Masson染色评价心脏损伤和心肌纤维化程度,DHE染色观察活性氧(ROS)生成情况。结果:干预8周后db/db小鼠体重增加,pNaKtide干预后小鼠体重增加减少;db/db小鼠SBP升高,pNaKtide干预后降低(P<0.05)。db/db小鼠心肌细胞横截面积和纤维化面积百分比增大,pNaKtide干预后减小(P<0.05)。db/db小鼠血清甘油三酯及总胆固醇水平升高,pNaKtide干预后降低(P<0.05)。db/db小鼠产生大量ROS,pNaKtide干预后降低(P<0.05)。结论:抑制钠钾泵激活能有效改善糖尿病心肌病小鼠的心脏损伤,其机制可能与下调ROS生成,降低氧化应激水平有关。

头孢哌酮钠舒巴坦钠不同给药方式治疗老年绿脓杆菌肺炎的临床效果观察

目的观察头孢哌酮钠舒巴坦钠不同给药方式治疗老年绿脓杆菌肺炎(PAP)的效果。方法80例老年绿脓杆菌肺炎患者,根据头孢哌酮钠舒巴坦钠给药方式不同分成观察组和对照组,每组40例。对照组给予头孢哌酮钠舒巴坦钠静脉滴注治疗,观察组给予头孢哌酮钠舒巴坦钠静脉微量泵泵注治疗。比较两组患者的治疗效果、炎症反应指标[C反应蛋白(CRP)、肿瘤坏死因子-α(TNF-α)、白细胞介素(IL)-6、IL-8]、实验室指标[降钙素原(PCT)、D-二聚体(D-D)]与免疫功能指标[CD3^(+)、CD4^(+)/CD8^(+)、自然杀伤细胞(NK细胞)百分比]水平。结果观察组患者治疗总有效率97.50%高于对照组的82.50%,差异有统计学意义(P<0.05)。观察组患者CRP(7.07±3.96)mg/L、TNF-α(1.24±0.65)μg/L、IL-6(0.40±0.05)ng/L、IL-8(19.29±1.07)μg/L均低于对照组的(12.96±4.29)mg/L、(1.57±0.71)μg/L、(0.51±0.07)ng/L、(23.37±1.09)μg/L,差异有统计学意义(P<0.05)。观察组患者PCT(0.74±0.38)ng/ml、D-D(0.51±0.18)mg/L均低于对照组的(2.01±0.54)ng/ml、(0.72±0.23)mg/L,CD3^(+)(53.96±7.65)%、CD4^(+)/CD8^(+)(1.37±0.31)、NK细胞百分比(34.96±3.82)%均高于对照组的(50.87±7.12)%、(1.12±0.28)、(29.65±3.14)%,差异具有统计学意义(P<0.05)。结论通过持续静脉微量泵泵注头孢哌酮钠舒巴坦钠治疗老年绿脓杆菌肺炎,治疗效果更加优良,实验室各项指标都得到显著改善,值得临床广泛应用。

Development and Demonstration of Australian First Working Sodium Guide Star Laser

The Australian first working sodium guide star laser system has been designed and developed for various astronomical and space-related applications. A completely diode-pumped pulsed system was developed initially followed by a largely fiber-based continuous wave (CW) system operating at 589 nm achieved through a unique wavelength conversion scheme by combining 1342 and 1050 nm through a sum frequency generation process. For the CW system, single-mode laser beams at both 1342 and 1050 nm are achieved from fiber-based seed oscillators and fiber amplifiers. The output power of ~25 W at 1342 nm is achieved from a single frequency fiber Raman amplifier. Output power up to 70 W at 1050 nm is achieved from a Yb-doped fiber pre-amplifier followed by a Yb-doped fiber power amplifier. For the sum frequency generation process, optimum focusing parameters are evaluated and determined. The CW system has generated more than 20 W output power at 589 nm, a circularly polarised beam with a good beam quality, spectral linewidth ≤ 2 MHz, and the laser output locked on the sodium D2 line at 589.159 nm. The system has been successfully demonstrated at EOS Space Research Centre, Mt Stromlo, Canberra, and become the Australian first working sodium guide star laser system.

泮托拉唑钠合成工艺改进研究

泮托拉唑钠合成工艺改进,降低产品中杂质含量。以2-氯甲基-3,4-二甲氧基吡啶盐酸盐和5-二氟甲氧基-2-巯基-1H-苯并咪唑为起始物料,经缩合、氧化成盐、逆转化和成盐反应合成泮托拉唑钠的合成路线,产品总收率为67.3%,产品的总杂质在0.10%以下,产品结构经1HNMR、MS和IR验证。本改进工艺是适于工业化生产的经济环保的泮托拉唑钠合成工艺。

水飞蓟宾对利福平和异烟肼致肝损伤中胆汁酸转运体Ntcp与Bsep的影响

目的 初步探讨水飞蓟宾能否通过激动Nrf2/ARE信号通路,激活下游胆汁酸相关的转运体牛磺胆酸钠转运蛋白(Ntcp)及胆盐输出泵(Bsep)Bsep的表达,从而改善异烟肼/利福平(INH/RFP)INH/RFP引起的肝损伤。方法:选用SPF级ICR小鼠随机分成5组:对照组(CON组),模型组(IR组),水飞蓟宾干预组(SY50组,SY100组,SY200组),除对照组外,干预组及IR组根据体质量给予75 mg/kgINH+150 mg/kgRFP,对照组给予空白溶剂,干预组分别同时给予水飞蓟宾低剂量50 mg/kg(IR+SY50),中剂量100 mg/kg(IR+SY100)以及高剂量200 mg/kg(IR+SY200),连续灌胃给药14 d。第15天给予异氟烷吸入麻醉后摘眼球取血,离心后用于生化指标测定,取脏组织于10%福尔马林固定用于病理切片、HE染色;4%多聚甲醛固定用于目标蛋白免疫组化测定;Western blot测定目标蛋白Ntcp、Bsep及核Nrf2的表达。结果 与CON组相比,IR组均能够引起生化指标ALT、AST、TBil、DBil、ALP、TBA的显著变化,与IR组相比,低剂量的水飞蓟宾干预组ALT、Tbil、TBA降低明显,中剂量的水飞蓟宾能显著降低ALT、AST、Tbil、TBA,高剂量的水飞蓟宾能显著降低除ALP以外的所有指标,差异有统计学意义(P<0.05)。IR组Ntcp,Bsep蛋白表达均下调,而水飞蓟宾能显著上调这些蛋白的表达,IR组下调Nrf2核蛋白的表达,与水飞蓟宾合用后,Nrf2核蛋白的表达显著上调。结论 水飞蓟宾可能通过激活Nrf2入核,调控下游胆汁酸转运体Ntcp、Bsep的表达,治疗INH/RFP引起的肝损伤。

1例注射用奥美拉唑钠致过敏性休克病例的治疗分析

目的:探讨注射用奥美拉唑钠在临床应用过程中的药品不良反应,以提高其临床使用的合理性和安全性。方法:临床药师通过回顾性分析1例药物过敏性休克患者的临床资料,探究注射用奥美拉唑钠可能引起患者药物过敏性休克的原因。结果:注射用奥美拉唑钠可引起患者出现药物过敏性休克,引起药物过敏性休克的主要原因为超适应症用药。结论:临床在使用注射用奥美拉唑钠时,需详细询问患者过敏史,严格按照《质子泵抑制剂临床应用指导原则》适应症给药,遵守给药原则。

小型次氯酸钠发生器在二次供水站补氯消毒中的应用

为解决城市管网部分二次供水设备出水余氯不足问题,文章以小型次氯酸钠发生器作为补氯设备,研究次氯酸钠发生器在二次供水补氯中的应用,总结存在的问题并提出解决方案。项目采用有效氯产量为300 g/h的小型次氯酸钠发生器作为补氯设备,选用地下半密闭结构的二次供水站作为研究对象,研究次氯酸钠发生器在二次供水补氯过程中存在的安全、自控和效果问题。首先,本设备采用蜂窝陶瓷载体负载贵金属Pt催化剂催化去除氢气,解决了运行过程中副产物氢气可能存在的安全问题。结果表明,在预热温度为50℃的条件下,氢气去除率为100%,稳定运行后,氢气消解装置最终温度≤80℃。其次,在夏季高温天,二次供水站进水水温为36℃、余氯为0的条件下,设备开启高温运行模式,二次供水出水余氯为0.25~0.33 mg/L,末梢水余氯为0.09~0.16 mg/L,均满足消毒要求,同时制备的次氯酸钠溶液中副产物氯酸盐质量浓度为115~125 mg/L,投加到水体后并不会引起氯酸盐大幅波动。最后经过统计,小型次氯酸钠发生器每千克有效氯盐耗为4.5 kg,电耗为5 kw·h。

核电站一回路用机械密封

机械密封在各类核电站的一回路中有大量应用.核电站一回路用机械密封是核电站的关键部件之一,其性能好坏很大程度上决定着核电站能否长周期安全可靠运行.本文以几种具有代表性的核电站反应堆堆型为例,对其一回路用机械密封进行了介绍,这些反应堆分别以水、氦气和液态金属为冷却剂并跨越第二代到第四代核电技术.首先介绍了压水堆核主泵机械密封,分别叙述了美式风格的流体静压型核主泵密封及欧式风格的流体动压型核主泵密封的结构特点、工作原理和最新的基础研究状况;随后介绍了高温气冷堆氦气轮机/氦气风机干气密封的结构特点、使用要求及相应的针对性设计;最后介绍了钠冷快堆钠泵机械密封,包括1种惰性气体缓冲、油膜润滑的三级串联式机械密封和1种直接以液态金属润滑的螺旋槽式机械密封.

服地高辛后红细胞受体数目及活性的变化

本前瞻性研究以外周红细胞作为心肌细胞的模型,动态观察(40d)8例心衰患者应用地高辛维持量疗法之红细胞洋地黄受体的数目、活性和泵单位活性的变化规律,并与8例未服用地高辛的心衰患者作平行对照。结果显示服用地高辛第3d洋地黄受体的活性与数目明显降低(p<0.01),尔后同步上升,20d后达服药前水平;停药后受体的活性与数目一度下降,第10d恢复到原有水平;而泵单位活性不变;红细胞洋地黄受体的活性与数目间有良好的正相关关系(r=0.9361,p<0.01)。提示红细胞洋地黄受体恢复到治疗前水平是继发于受体数目的增加,可能是导致地高辛正性肌力作用减弱甚至消失,即出现耐受的机理。明显的耐受性在连续服用地高辛20d左右形成,停药10d左右又恢复正常。

高血压对大鼠脑基底动脉收缩和钠泵活性的影响

目的探讨高血压对大鼠脑血管收缩性的影响及其与钠泵活性的关系。方法取♂Wistar大鼠(WR)和自发性高血压大鼠(SHR)基底动脉环,通过Multi Myograph张力换能系统记录血管张力变化,比较两种大鼠离体脑动脉对KCl和5-羟色胺(5-HT)的收缩反应,分析高血压病变对脑血管收缩性和钠泵活性的影响。结果与WR基底动脉相比,SHR基底动脉的KCl和5-HT量效曲线明显右移,再复K+所致血管舒张作用减弱,提示高血压病变可明显降低脑血管钠泵活性及KCl和5-HT的收缩反应;哇巴因(Ouabain,OUA)浓度依赖性收缩SHR脑血管,其量效关系曲线可经两点结合模型进行最佳拟合,Kd分别为:1.7×10^(-8)mol·L^(-1)和1.6×10^(-5)mol·L^(-1),表明SHR脑基底动脉上存在高、低亲和力两种不同功能的钠泵。用5×10^(-7)mol·L^(-1)和10^(-4)mol·L^(-1)的OUA分别抑制高、低亲和力钠泵,仅能在SHR而非WR脑血管明显左移KCl和5-HT量效曲线,表明OUA可明显增强KCl和5-HT对脑血管的收缩作用,且OUA增强5-HT收缩SHR脑血管的作用呈明显的浓度依赖性(r=0.9393,P<0.05);在SHR脑血管,这两个浓度OUA对KCl量效曲线的左移幅度无明显差别,而对5-HT收缩量效曲线的左移幅度却有明显不同,提示仅高亲和力钠泵介导了SHR脑血管对KCl的收缩反应,而SHR脑血管对5-HT的收缩反应则由高、低亲和力两种钠泵共同参与。结论高血压病变可明显降低脑血管对血管收缩剂的反应性,其机制可能与高血压所致钠泵活性降低或钠泵对OUA敏感性增加有关。

补阳还五汤冲剂治疗缺血性中风的临床研究

缺血性中风患者服用补阳还五汤冲剂１０周，临床总有效率达８８．５％，其中愈显率占４２．３％；血液流变学指标有不同程度改善，红细胞钠泵活性提高，以重用黄芪的１号方疗效优于３号方。

抗哇巴因抗体及抗前海葱苷原A抗体的制备及其应用

为了探索内源性钠泵抑制因子在高血压发生中的作用，利用家兔免疫制备了抗哇巴因抗体及抗前海葱苷原Ａ 抗体，并对其特性进行了鉴定。利用该两种抗体和ＥＬＩＳＡ 法检测了高血压病人血浆及牛血清中哇巴因样及前海葱苷原Ａ 样钠泵抑制因子水平。检测结果发现原发性高血压病人血浆中存在哇巴因样物质水平（０．１３２±０．０２１ｍ ｏｌ／Ｌ）和前海葱苷原Ａ 样物质水平（０．１０２±ＤＦ８．８ｎｍ ｏｌ／Ｌ）；牛血清中哇巴因样物质的水平（１．６±０．２７ｎｍ ｏｌ／Ｌ）明显高于前海葱苷原Ａ 样物质水平（０．２２２±０．０８６ｎｍ ｏｌ／Ｌ）。证明内源性钠泵抑制因子哇巴因样及前海葱苷原Ａ 样物质在哺乳类动物血液里循环存在，是两种新的强心苷类固醇激素。