山楂叶总黄酮对离体大鼠胸主动脉环功能的影响

目的 观察山楂叶总黄酮(HLF)对大鼠胸主动脉血管环的作用,并探讨其作用机制.方法 采用大鼠胸主动脉环张力测定法,观察HLF对高浓度KCl(6×10-2mol/L)和去甲肾上腺素(NE,1×10-6mol/L)预收缩的离体大鼠胸主动脉血管环作用;并观察左旋硝基精氨酸甲酯(L-NAME,1×10-5mol/L)和吲哚美辛(1×10-4mol/L)对其作用的影响.结果 HLF(5×10～50×10-3g/L)对高浓度氯化钾(KCl,6×10-2mol/L)预收缩的内皮完整或去内皮的血管环均无明显作用(P＞0.05);对去甲肾上腺素(NE,1×10-6mol/L)预收缩的血管环产生内皮依赖性的舒张作用(P＜0.01);HLF对NE预收缩血管的舒张作用能被L-NAME(1×10-5 mol/L)显著阻断(P＜0.01),而不能被吲哚美辛(1×10-4mol/L)阻断(P＞0.05).结论 HLF对胸主动脉血管有舒张作用,其机制可能是通过抑制受体操纵的钙通道(ROC)的激活而直接抑制细胞外钙内流降低细胞内Ca2+浓度而起作用的;HLF的内皮依赖性舒张作用可能与血管内皮一氧化氮(NO)合成有关.

Abstract：

Objective To investigate the effects and mechanisms of hawthorn leaf flavonoids (HLF) on isolated thoracic aorta in rats. Methods The tension of rat thoracic aorta tings was measured.The effects of HLF on the thoracic aorta preconstricted by potassium chloride ( KCl, 6 × 10-2 mol/L) and norepinephrine (NE, 1 × 10-6 mol/L), as well as the effects of L-nitro arginine methyl ester (L-NAME,1 × 10-5 mol/L) and indomethacin ( 1 × 10-4 mol/L) on the relaxation response of HLF were observed.Results HLF completely relaxed the constriction induced by NE ( 1 × 10 -6 mol/L) in endothelium-intact thoracic aorta ( P ＜ 0. 01 ), but had no effect on those preconstricted aorta rings by a high concentration of KCl (6 × 10-2 mol/L) in endothelium-intact and endothelium-denuded rat aorta (P ＞ 0. 05). The relaxation response of HLF was significantly inhibited by L-NAME (P ＜ 0. 01 ), but not by indomethacin (P ＞0. 05). Conclusion The vasorelaxation induced by HLF in rat aorta rings may involve the reduction of Ca2+ influx through the calcium channels operated by receptor (ROC). The endothelium-dependent relaxation of HLF may be related to the generation of nitric oxide (NO).     

咪达唑仑对大鼠离体主动脉的舒张作用

目的观察咪达唑仑对血管张力的直接影响,并探讨其作用机制.方法采用内皮完整和去内皮的大鼠离体主动脉环,首先观察咪达唑仑在3×10-6,10×10-6,30×10-6,100×10-6mol/L浓度时,对去氧肾上腺素(10-6mol/L)引起收缩的血管环等长张力的影响.然后观察咪达唑仑对经亚甲蓝(10-5mol/L)孵浴处理的内皮完整血管环和分别经过维拉帕米(5×10-6mol/L)和四乙胺(5×10-3mol/L)孵浴处理的去内皮血管环张力的影响.结果以上浓度的咪达唑仑对去内皮和内皮完整血管环均有舒张作用.去内皮血管环的舒张反应低于内皮完整血管环(P＜0.05).用亚甲蓝处理的内皮完整环的舒张反应与未经处理时比较无显著性差异(P＞0.05).四乙胺可增强咪达唑仑对去内皮血管环的舒张作用(P＜0.05).维拉帕米不影响咪达唑仑对去内皮血管环的舒张(P＞0.05).结论咪达唑仑对血管具有内皮依赖性和非内皮依赖性的舒张作用,其内皮依赖性的舒张反应与NO-sGC-cGMP途径无关.     

姜酚对家兔胸主动脉平滑肌的舒张作用及其机制

目的 观察姜酚(gingerol)对家兔胸主动脉平滑肌的舒张作用并探讨其作用机制.方法 制备离体内皮完整的和去内皮胸主动脉环肌条,悬挂于恒温浴槽中,并将其与张力-位移换能器相连记录血管环肌条张力的变化,所有标本分为内皮完整组和去内皮组.内皮完整组分为1×10-5 mol/L去甲肾上腺素(NE)+不同浓度gingerol组(1×10-8、1 ×10-7、1 ×10-6、1 ×10-5、1×10-4、1×10-3 mol/L,下同)、20 mmol/L KCl+不同浓度gingerol组、1×10-5 mol/L NE+左旋-硝基精氨酸甲脂(L-NAME)+不同浓度gingerol组、1×10-5 mol/L NE+吲哚美辛+不同浓度gingerol组、20 mmol/LKCl+ L-NAME+不同浓度gingerol组、20 mmol/L KCl+吲哚美辛+不同浓度gingerol组;去内皮组分为1×10-5 mol/L NE+不同浓度gingerol组、20 mmol/L KCl+不同浓度gingerol组.结果 (1)gingerol能抑制1×10-5 mol/L的NE或20 mmol/L的KCl引起的胸主动脉平滑肌收缩并呈剂量依赖性,另外,gingerol对内皮完整的胸主动脉的舒张作用较去内皮的胸主动脉明显增强(P＜0.05).(2)内皮完整的胸主动脉组,L-NAME能显著抑制gingerol对胸主动脉平滑肌的舒张作用(％,NE处理组:94.83±3.63比96.83±1.82、91.17 ±2.89比94.83±2.68、83.83±2.23比94.67±2.73、78.00±3.54比92.33±2.91、67.83±2.37比90.83±3.77、62.83±3.42比89.67±3.15;KCl处理组:90.33±8.33比98.17±7.56、80.83±7.24比96.83±7.28、70.83±7.57比92.17±7.31、67.83±7.68比89.83±7.23、62.83±7.49比90.33±8.87、57.33±8.32比87.67±8.97,P＜0.05).(3)内皮完整的胸主动脉组吲哚美辛能显著抑制gingerol对胸主动脉平滑肌的舒张作用(％,NE处理组:93.83±7.61比97.83±7.45、92.50±10.13比95.33±8.36、86.67±8.24比93.83±7.28、79.83±7.36比89.83±7.63、67.83±7.46比85.33±8.94、61.83 ±7.55比81.83 ±7.25;KC1处理组:90.17±7.77比96.17±7.31、79.67±8.65比91.33±8.62、72.17 ±7.48比85.67±8.76、70.83±7.78比83.17±7.79、56.83±7.62比77.83±7.29、54.17 ±7.68比74.83±7.34,P＜0.05).结论 gingerol对NE和KCl所诱发的收缩具有剂量依赖性的抑制作用,其机制可能与内皮产生的NO和前列环素有关.     

2型糖尿病对冠心病患者大隐静脉旁路血管内皮细胞的影响

目的 探讨2型糖尿病对冠心病患者大隐静脉血管内皮细胞的影响。方法 选取预行冠状动脉旁路移植术40例患者,其中冠心病合并2型糖尿病20例(试验组)及无糖尿病20例(对照组)。每例均取其大隐静脉旁路血管的远心端1 cm长的血管环,切成3段。分别观察血管内皮形态学的变化及采用器官管槽法,在37℃有氧条件下,检测苯肾上腺素(10-5 mol/L)引起的血管收缩反应、以及不同浓度(10-9～10-5 mol/L)的硝酸甘油、乙酰胆碱引起的血管舒张反应。结果 试验组大隐静脉超微结构受损程度较对照组严重。苯肾上腺素引发的预收缩强度和硝酸甘油引发的非内皮依赖性舒张反应两组差异无统计学意义(P＞0.05),但乙酰胆碱引发的内皮依赖性最大舒张反应,试验组明显低于对照组(P＜0.05)。结论 2型糖尿病会加重冠心病患者大隐静脉旁路血管内皮细胞的损害。     

维拉帕米对离体家兔阴茎海绵体平滑肌舒张作用的实验研究

为探讨维拉帕米(Verapami)舒张离体兔阴茎海绵体平滑肌的作用及其机制.本文将12只雄性新西兰大白兔(2.8～3.0kg),空气栓塞致死后迅速取出阴茎,去除阴茎皮肤、被膜及白膜,制成3 mm×3 mm×8mm长条形肌条.置于5mlKrebs 37℃恒温浴槽中,持续通以95%O2+5%CO2的混合气.用丝线将肌条连接于张力换能器,采用Powerlab生理记录仪记录收缩反应,平衡1 h,10μmol/L去氧肾上腺素(PE)预收缩,最大收缩张力为100%,处于收缩平台期后依次加入累积浓度为10-8～10-4M的Verapamil,观察舒张效应.另一组分别应用10-5 M和10-4M Verapamil预孵育20 min,然后加入累积浓度为10-8～10-4M的PE,记录浓度-效应曲线.结果均采用自身对照.     

七氟醚预先给药对血管紧张素Ⅱ诱发大鼠离体主动脉收缩反应的影响

目的观察七氟醚(SEV)预先给药对血管紧张素Ⅱ(AngⅡ)诱发大鼠离体主动脉收缩反应的影响。方法取雄性Wistar大鼠胸主动脉,制成4mm长的血管段,随机分为2组,正常组和去内膜组。实验分三部分进行。第一部分:两组均分为对照组和SEV组两个亚组,对照组不再进行任何处理,SEV组通入5.1%SEV,15min后给予不同浓度AngⅡ,每一血管段只随机接受一次单一剂量的AngⅡ刺激,测定血管收缩反应的峰值水平。第二部分:两组均将血管段先浸入含10-4mol/LN-硝基L-精氨酸甲酯(L-NAME)的KBS中15min,然后给予10-7mol/LAngⅡ,测定血管收缩反应的峰值。第三部分:将两组血管段先浸入通有不同浓度(0、1.7%、3.4%和5.1%)SEV的KBS中15min,然后给予10-7mol/LAngⅡ,观察SEV对AngⅡ诱发血管收缩反应的抑制效应。结果第一部分:与对照组比较,正常、去内膜组AngⅡ浓度分别在3×10-8-10-6mol/L和3×10-9-10-6mol/L时SEV组主动脉收缩反应降低(P<0.05或0.01);与正常组比较,去内膜组AngⅡ浓度在3×10-9-10-6mol/L时对照、SEV组主动脉收缩反应均升高(P<0.05或0.01)。第二部分:AngⅡ诱发的正常组血管段收缩反应由未经L-NAME处理的43%±5%增至经L-NAME处理的71%±6%(P<0.01);而去内膜组血管段收缩反应在未经和经L-NAME处理组无变化。第三部分:去内膜组在SEV浓度为0-5.1%时主动脉收缩反应均高于正常组(P<0.05);与SEV浓度为0时比较,正常组在SEV浓度为3.4%和5.1%时主动脉脉收缩反应降低,去内膜组在SEV浓度为1.7%-5.1%时主动脉收缩反应降低(P<0.05或0.01)。结论SEV能够抑制AngⅡ诱发的剂量依赖性大鼠离体主动脉收缩反应,去除血管内膜抑制作用加重;SEV还抑制AngⅡ刺激内膜释放NO所产生的血管舒张作用。     

茉莉花提取物的舒血管作用

目的 观察中药茉莉花提取物（EJs）对大鼠离体胸主动脉环的舒血管作用并探讨其作用机制。 方法 采用离体血管环灌流装置,观察EJs对苯肾上腺素（PE）或氯化钾（KCl）预收缩血管的影响。检测左旋硝基精氨酸甲酯（L-NAME）和氯化钡（BaCl2）,格列本脲（Gli）对0.5,1,2,4,8 g.L-1EJs舒血管作用的影响;观察EJs对氯化钙（CaCl2）及PE在无钙液中收缩影响;激光扫描共聚焦显微镜技术检测血管平滑肌细胞内钙浓度。结果 在内皮完整血管上,EJs依赖性地降低PE或KCl预收缩血管的张力,最大舒张幅度分别为（105.0±3.2）%,（78.0±6.5）%; L-NAME明显削弱对EJs的舒血管作用（P<0.01）,最大舒张幅度为（58.0±6.9）%;BaCl2,Gli均能明显削弱EJs的舒血管作用（P <0.01）,最大舒张幅度分别为（37.0±5.2）%,（78.0±10.0）%;在无钙环境下,EJs能抑制PE引起去内皮主动脉环短暂收缩（P <0.01）,最大收缩幅度（70.0±6.3）%,EJs能抑制0.5～8 mmol.L-1CaCl2引起的收缩（P <0.01）,血管收缩幅度降低（65.0±3.2）%。4,8 g.L-1Ejs钙Fmax/F0分别为（2.0±0.2）和（1.5±0.2）。结论 EJs 能够浓度依赖性舒张大鼠胸主动脉,其作用机制可能与促进一氧化氮释放、激活多个K＋通道,减少细胞内钙离子浓度有关。     

不同浓度丙泊酚通过缝隙连接通讯对舒张大鼠肠系膜动脉的影响

目的观察丙泊酚对SD大鼠肠系膜动脉的影响和对肠系膜动脉舒张作用是否与缝隙连接通讯相关。方法应用压力肌动图技术,在急性分离的SD大鼠肠系膜动脉2级血管上,观察1×10-7、3×10-7、1×10-6、3×10-6、1×10-5、3×10-5、1×10-4和3×10-4 mol/L丙泊酚对血管直径的影响,预孵育缝隙连接阻断剂18-β甘草次酸(18β-glycyrrhetinic acid,18β-GA)和2-aminoethoxydiphenylborate(2-APB)后,观察丙泊酚对血管直径的影响。结果给予1×10-7、3×10-7、1×10-6、3×10-6、1×10-5、3×10-5、1×10-4和3×10-4 mol/L的丙泊酚,使SD大鼠血管直径从(208.6±13.4)μm分别增加至(213.5±13.6)、(219.7±13.2)、(226.4±12.5)、(234.9±12.3)、(245.5±13.0)、(267.4±15.2)、(336.2±18.3)和(385.9±14.2)μm,1×10-4 mol/L的丙泊酚引起血管直径随着丙泊酚浓度增大而增加(P0.01)。分别预孵育18β-GA和2-APB后,1×10-4 mol/L的丙泊酚对大鼠肠系膜动脉舒张作用明显减弱(P0.01)。结论丙泊酚呈浓度依赖性舒张肠系膜动脉,其作用机制可能与缝隙连接通讯相关。     

维拉帕米对离体家兔阴茎海绵体平滑肌舒张作用的实验研究

目的　初步探讨维拉帕米 (VP)对离体兔阴茎海绵体平滑肌的舒张作用及其机制。方法　离体家兔阴茎海绵体平滑肌条实验方法 ,观察VP对阴茎海绵体平滑肌的舒张效应。结果　VP可舒张去氧肾上腺素 (PE)诱导的阴茎海绵体平滑肌收缩作用 ,最大舒张效应为 (4 6 .3± 2 .1) % (P <0 .0 1) ,且呈浓度依赖性。 10 -6mol·L-1,10 -5mol·L-1和 10 -4mol·L-1VP均可使PE引起的浓度 -效应曲线右移 ,最大收缩反应降低 ,10 -4mol·L-1VP拮抗作用更显著。结论　VP有明显的舒张阴茎海绵体平滑肌作用 ,并呈浓度依赖性。     

内源性一氧化碳对离体犬阴茎海绵体平滑肌的作用

目的:探讨内源性一氧化碳(CO)对离体犬阴茎海绵体平滑肌作用的影响。方法:利用水浴条件下阴茎海绵体肌条的张力测定技术,用CO合成的关键酶血红素氧合酶(HO)的诱导剂———氯高铁血红素诱导海绵体平滑肌生成内源性CO,观察CO对去氧肾上腺素(PE)诱导收缩的阴茎海绵体肌条作用的影响。结果:氯高铁血红素对10μmol/L PE诱导的肌条收缩具有浓度依赖性的松弛作用,10~100μmol/L氯高铁血红素对平滑肌肌条的松弛效应与空白对照相比明显升高(P<0.01)。用锌原卟啉-Ⅸ(ZnPP-Ⅸ)或亚甲蓝孵育处理后的肌条,氯高铁血红素的舒张作用明显减弱(P<0.01)。结论:内源性CO具有浓度依赖性松弛阴茎海绵体平滑肌的作用,其机制可能是通过CO环磷酸鸟苷途径作用所致。     

内皮素 - 1对离体动脉的收缩作用及舒张药物的对抗效应

目的　研究内皮素-1（Endothelin-1,ET-1）收缩血管的特性及显微血管外科常用舒张药物的对抗效应。方法　采用离体血管舒缩功能的实验技术比较ET-1与去甲肾上腺素（noradrenaline,NE）对离体动脉张力的影响,同时检测舒张药物对ET-1收缩血管的拮抗作用。结果　ET-1使离体大鼠颈总动脉环产生浓度依赖性的恒定收缩,ET-1与NE的半数有效浓度(medianeffectiveconcentration,EC     

6种中药提取物对离体新西兰白兔阴茎海绵体的松弛作用

目的:比较6种中药提取物(甲基莲心碱、粉防己碱、葛根素、灯盏花乙素、人参皂苷Rg1和人参皂苷Rb1)松弛离体新西兰白兔阴茎海绵体的作用。方法:采用离体新西兰白兔阴茎海绵体肌条张力记录法,观察6种中药提取物对去氧肾上腺素(PE)诱导收缩的阴茎海绵体肌条的松弛作用。结果:在(10-8~10-3)mol/L,甲基莲心碱、粉防己碱、葛根素和灯盏花乙素对PE诱导收缩的肌条具有浓度依赖性松弛作用,其IC50分别为4.60×10-6、3.73×10-5、8.03×10-4和3.33×10-3mol/L。而人参皂苷Rg1和人参皂苷Rb1对PE诱导收缩的肌条松弛作用较弱,终浓度为10-3mol/L时,仅分别松弛(16.32±13.36)%和(11.21±7.59)%。结论:6种中药提取物对离体新西兰白兔阴茎海绵体的松弛作用,甲基莲心碱最强。     

Relaxant effects of propofol on human omental arteries and veins

We have investigated the relaxant effects of propofol on smooth muscle tension in human omental arteries and veins to determine if endothelium- related mechanisms are involved. Isolated vessel segments were precontracted with endothelin-1 and propofol was added cumulatively (10(-7)-10(-4) mol litre-1). In both artery and vein segments, propofol induced relaxation, which was not dependent on an intact endothelium. Relaxation was reduced when the extracellular K+ concentration was increased and in the presence of tetraethylammonium chloride (TEA). In intact segments, N-nitro-L-arginine methyl ester (L-NAME), indomethacin, glibenclamide, 4-aminopyridine, clotrimazole and atropine did not affect the concentration-response curve of propofol. This indicates that propofol relaxes human omental arteries and veins in an endothelium independent manner, and that hyperpolarization caused by activation of the K+ channel, BKCa, may be involved.      

川芎嗪舒张离体兔阴茎海绵体平滑肌的作用及其机制的初步研究

目的 :探讨川芎嗪 (Chuanxiongzine ,Ligustrazine)对离体兔阴茎海绵体平滑肌条的舒张效应及其作用机制。　方法 :采用离体家兔阴茎海绵体肌条张力记录法 ,观察川芎嗪对去氧肾上腺素 (phenylephrine,PE)诱导收缩的阴茎海绵体肌条的舒张作用 ;应用亚硝基左旋精氨酸甲酯 (L NAME)、ODQ预处理和去除内皮 ,分别记录川芎嗪对阴茎海绵体肌的舒张作用。采用放射免疫法测定川芎嗪对阴茎海绵体平滑肌肌条中cGMP和cAMP含量的影响。　结果 :川芎嗪对阴茎海绵体平滑肌具有浓度依赖性舒张作用 ,其EC50 为 1 .5 8× 1 0 -4mol/L ,ODQ可部分抑制川芎嗪对肌条的舒张效应 (P <0 .0 5 ) ,而L NAME预处理和去除内皮对川芎嗪舒张肌条的效应没有影响 (P >0 .0 5 )。川芎嗪处理组阴茎海绵体平滑肌肌条中的cGMP和cAMP含量分别是对照组的 1 .5和 2 .3倍 ,差异有显著性 (P <0 .0 5 )。　结论 :川芎嗪对阴茎海绵体平滑肌具有浓度依赖性的舒张效应 ,其舒张作用机制与增加cGMP、cAMP浓度有关     

一氧化碳合成酶抑制剂对缺氧性肺血管收缩反应的影响

目的 观察内皮及内源性一氧化碳（CO）合成酶抑制剂（血红素氧化酶抑制剂ZnppIX)对大鼠缺氧性肺血管收缩反应的影响，探讨内源性CO在缺氧性肺血管收缩反应中的作用。方法 制备Wistar大鼠动脉环，观察内皮与缺氧性肺血管收缩反应的关系；并以一氧化氮合成酶抑制剂L－NAME为对照，观察ZnppIX对缺氧性肺血管收缩反应的影响。结果 缺氧可使去氧肾上腺素顶收缩的肺动脉环出现明显的收缩反应，去除内皮或血管环用L－NAME孵育后，缺氧性肺血管收缩反应受抑，而用ZnppIX及L－NAME共同孵育后，缺氧性肺血管收缩反应明显抑制或消除，与L－NAME组相比有显著性差异（P＜0．01）。L－NAME组的缺氧张力变化率与未孵育前相比也有显著性差异（P＜0．01）。结论 缺氧性肺血管收缩反应是内皮依赖性的，ZnppIX可抑制大鼠氧性肺血管收缩反应，内源性CO与NO一样参与了缺氧性血管收缩反应。     

Mechanism mediating nitric oxide-induced inhibition in human jejunal longitudinal smooth muscle

BACKGROUND: Enteric neurotransmission is a complex process involving multiple neurotransmitters, including nitric oxide (NO). Our aim was to evaluate the role and mechanism(s) of action of NO in normal human jejunal longitudinal smooth muscle. METHODS: Transmural strips of normal human jejunum obtained from subjects undergoing gastric bypass were studied in organ chambers. Effects of exogenous NO (7 x 10(-6) mol/L to 7 x 10(-5) mol/L) and electrical field stimulation (nonspecific release of endogenous neurotransmitters) on spontaneous contractile activity and on precontracted muscle strips (substance P, 10(-5) mol/L) were evaluated in the presence and absence of the competitive NO synthase inhibitor N(G)-amino-L-arginine (L-NNA, 10(-3) mol/L) and the specific soluble guanylyl cyclase inhibitor 1H-[1,2,4]-oxadiazaolo-[4,3-a]-quinoxalin-1-one (ODQ, 10(-5) mol/L and 10(-4) mol/L). RESULTS: Exogenous NO dose-dependently inhibited spontaneous contractility and relaxed precontracted smooth muscle strips. The effects of NO were markedly attenuated or completely inhibited in the presence of ODQ. Electric field stimulation under nonadrenergic, noncholinergic conditions also inhibited spontaneous contractility and relaxed precontracted smooth muscle strips; both of these effects were attenuated, but not completely inhibited, in the presence of both ODQ and L-NNA. CONCLUSIONS: NO is an endogenous inhibitory neurotransmitter in human jejunal longitudinal smooth muscle, acting at least in part via a mechanism mediated by guanylyl cyclase. Other (non-nitrergic) nonadrenergic, noncholinergic inhibitory neurotransmitters are likely active in this portion of the human gut.     

Relaxation mechanisms of neferine on the rabbit corpus cavernosum tissue in vitro

Aim： To investigate the relaxation mechanisms of neferine （Nef） on the rabbit corpus cavemosum tissue in vitro. Methods： Strips of rabbit corpus cavemosum were mounted in organ chambers. The effects of Nef were examined on isolated muscle strips precontracted with phenylephrine （PE） alone, in the presence of NW-nitro-L-arginine （LNNA, a nitric oxide synthase inhibitor）, 1-H-[ 1,2,4]oxadiazolo[4,3-tx]quinoxalin- 1-one （ODQ, a guanylyl cyclase inhibitor）, indomethacin （cyclooxygenase inhibitor）, tetraethylammonium （Ca^2＋ -activated K^＋ channel blocker）, 4-aminopiridine （4-AP ,voltage dependent K^＋ channel blocker） and glibenclamide （ATP sensitive K^＋channel blocker）. The effects of Nef on KCl-induced contraction of isolated muscle strips were also investigated. The procedure of calcium absencecalcium addition was designed to observe the effect of Nef on two components of the contractile responses to PE based on the source of Ca^2＋ （extracellular vs. intracellular）. Results： Corpus cavemosum strips relaxed in response to Nef （10-9-10-4 mol/L） in a concentration-dependent manner with an IC50 of 4.60 × 10^-6 mol/L. However, they were not affected by LNNA, ODQ, indomethacin or K^＋-channel blockers. Nef （10^-6 mol/L, 10^-5 mol/L） concentration dependently reduced the maximal contraction response of isolated strips induced by KC1 to 79.3% ± 5.5% and 61.5% ±3.2%, respectively （P 〈 0.01）. In the calcium absence-calcium addition procedure, Nef 10.5 mol/L inhibited both intracellular calcium-dependent and extracellular calcium-dependent contraction induced by PE （2 × 10^5 mol/L） （P 〈 0.05）. The inhibition ratios were 26.2% ± 5.4% and 48.3% ±7.6%, respectively. Conclusion： The results of the present study suggest that Nef possesses a relaxant effect on rabbit corpus cavemosum tissues, which is attributable to the inhibition of extracellular Ca^2＋ influx and the inhibition of release of intracellular stored Ca^2＋, but not mediated by the     

Stimulation of P2y purinoceptors induces, via nitric oxide production, endothelium-dependent relaxation of human isolated corpus cavernosum

PURPOSE: Endothelial P2y purinoceptor stimulation is known to induce vasodilatation mediated by NO release from endothelial cells. We examined the effect of a potent P2y agonist, adenosine-5'-O-(2-thiodiphosphate) (ADPbetaS), on human corporal cavernosal strips and its dependence on a functional endothelial lining. MATERIALS AND METHODS: The preparations mounted in isometric conditions were precontracted by noradrenaline (NA) at a concentration of 0.1 microM. Increasing concentrations of ADPbetaS from 1 microM to 100 microM were added in the presence and absence of a functional endothelium or in the presence and absence of an NO synthase inhibitor and a selective P2y antagonist. Acetylcholine (Ach)-induced relaxation was used in each experiment for control. RESULTS: In human precontracted corporal cavernosal strips with a functional endothelium (relaxed by acetylcholine) ADPbetaS induces a dose-dependent relaxation with maximal relaxation of 45.5+/-5.0% and an EC50 of 11.7 microM. The relaxant effect of ADPbetaS was reduced by 77.1+/-7.0% by reactive blue 2 (20 microM)(a P2y antagonist). L-NAME (L-Nitro Arginin Methyl Ester), an NO synthase inhibitor (100 microM), reduced Ach- and ADPbetaS- induced relaxations by 86.59+/-3.24% and 86.83+/-0.5% respectively. Ach- and ADPbetaS- induced relaxations were significantly inhibited after dislodging of the endothelial lining of the corporal cavernosal strips, 90.11+/-6.2% and 87.1+/-5% respectively. CONCLUSIONS: Human corporal cavernosal strips can be relaxed by stimulation of P2y purinoceptors via NO release. This relaxation is an endothelium-dependent mechanism. Purines may be implicated in physiological erection in man.     

载银珊瑚羟基磷灰石的抑菌活性与细胞毒性研究

目的 评价负载不同浓度银离子后的珊瑚羟基磷灰石(CHA)对大肠杆菌和金黄色葡萄球菌的抑菌效果与细胞毒性.方法 采用真空冷冻干燥法制备1×10-2～1×10-5 mol/L Ag+浓度的载银CHA(Ag-CHA),然后采用琼脂平板抑菌法评价Ag-CHA对大肠杆菌和金黄色葡萄球菌的抑菌效果,并测量24 h后的抑菌圈直径.采用甲基噻唑基四唑(MTT)法评价8×10-5mol/L的Ag-CHA在2、4、7d对L929小鼠成纤维细胞的毒性作用. 结果 载银浓度为1×10-2～8×10-5mol/L的Ag-CHA对大肠杆菌和金黄色葡萄球菌的抑菌圈直径均大于12 mm,有明显的抑菌作用;而载银浓度低于8×10-5mol/L的Ag-CHA无抑菌作用.载银浓度低于8×10-5mol/L的Ag-CHA对L929细胞无毒性作用;8×10-5mol/LAg-CHA浸提液作用细胞2、4、7 d后,细胞生长状态良好,相对增殖率均大于90%,毒性等级为0或1级.结论 最佳载银浓度为8×10-5mol/L,该条件下的Ag-CHA有良好的抑菌作用,且无细胞毒性.     

Exogenous hyaluronidase induces release of nitric oxide from the coronary endothelium

OBJECTIVE: Hyaluronidase, an endogenous enzyme that hydrolyzes mucopolysaccharides, has been shown to enhance myocardial protection when added to preservation solutions. In addition, hyaluronidase infusion reduces injury to ischemic myocardium. Endothelium-derived nitric oxide is an endogenous vasodilator that prevents leukocyte adhesion to the intima and inhibits platelet adhesion and aggregation in the coronary artery. Experiments were undertaken to determine whether the protective action of hyaluronidase could be mediated by the endogenous release of nitric oxide. METHODS: Segments of coronary artery, with and without endothelium, were placed in organ chambers (25 mL) to measure isometric force. Blood vessel segments were contracted with prostaglandin F(2)(alpha) (2 x 10(-6) mol/L) and exposed to hyaluronidase (3-15 units). RESULTS: Hyaluronidase induced vasodilation of arteries with intact endothelium but not of arteries without endothelium (n = 6, P<.05). Endothelium-dependent vasodilation to hyaluronidase was blocked by N(G)-monomethyl-L -arginine (10(-5) mol/L), an inhibitor of nitric oxide synthesis from L -arginine (n = 6, P<.05). Inhibition of vasodilation by N(G)-monomethyl-L -arginine was reversed by L -arginine (10(-4) mol/L) but not D -arginine (10(-4) mol/L; n = 6, each group). Vasodilation to hyaluronidase also was inhibited by hemoglobin (2 x 10(-6) mol/L), a scavenger of the nitric oxide radical (n = 6, P<.05). CONCLUSIONS: Hyaluronidase induces the release of nitric oxide from the coronary endothelium. Because nitric oxide, an endogenous vasodilator, inhibits leukocyte adhesion to the intima in addition to inhibiting platelet adhesion and aggregation, stimulated production of endothelium-derived nitric oxide by exogenous hyaluronidase could be the mechanism of the protective action of hyaluronidase infusion.