川芎提取物对神经刺激所致猪脑动脉反应的影响

目的 观察川芎提取物对神经刺激引起的猪脑动脉反应的作用及其与一氧化氮的关系.方法 采用离体去除内皮血管方法,测定脑动脉条的等容张力变化及药物的作用.结果 川芎提取物对电刺激或化学刺激引起的血管舒张反应具有增强作用,此作用不受酚妥拉明和哌唑嗪、心得安、阿托品、消炎痛的影响,但可被一氧化氮合酶抑制剂L-硝基精氨酸抑制,该抑制作用又可为一氧化氮供体L-精氨酸逆转.结论 川芎提取物对电刺激或化学刺激所致血管舒张反应的增强作用可能与一氧化氮有关.     

红花、三七提取物对神经刺激所致猪脑动脉反应的影响

目的观察红花、三七提取物对神经刺激引起的猪脑动脉反应的影响及其与一氧化氮的关系。方法采用离体去除内皮血管方法,测定脑动脉条的等容张力变化及药物的作用。结果红花、三七提取物对电刺激或化学刺激引起的血管舒张反应具有增强作用,此作用不受酚妥拉明和哌唑嗪、心得安、阿托品、消炎痛的影响,但可被一氧化氮合酶抑制剂L-硝基精氨酸抑制,该抑制作用又可为一氧化氮供体L-精氨酸逆转。结论红花、三七提取物对电刺激或化学刺激所致血管舒张反应的增强作用可能与一氧化氮有关。     

当归提取物对神经刺激所致猪脑动脉反应的影响

目的 观察当归提取物对神经刺激引起的猪脑动脉反应的作用及其与一氧化氮(NO)的关系.方法 采用离体去除内皮血管方法,测定脑动脉条的等容张力变化及药物的作用.结果 当归提取物对电刺激或化学刺激引起的血管舒张反应具有增强作用,此作用不受酚妥拉明和哌唑嗪、心得安、阿托品、消炎痛的影响,但可被NO合酶抑制剂L-硝基精氨酸抑制,该抑制作用又可为NO供体L-精氨酸逆转.结论 当归提取物对电刺激或化学刺激所致血管舒张反应的增强作用可能与NO有关.     

L-硝基精氨酸对神经刺激所致大鼠肠系膜动脉反应的影响

目的观察大鼠肠系膜动脉对神经刺激引起的反应及其与NO的关系。方法：采用离体去除内皮血管实验方法，测定肠系膜动脉条的等容张力变化。结果：电刺激和化学（烟碱）刺激明显引起大鼠肠系膜动脉收缩，L－硝基精氨酸（L－NA，NO合成抑制剂）明显增强上述收缩反应，此增强作用可被L一精氨酸（NO供体）取消。L－NA对刺激交感神经末梢去甲肾上腺素的释放及对去甲肾上腺素的血管收缩作用均无明显影响。动脉条用哌唑嗪处理并用PGF(2a)部分收缩后，电刺激和烟碱均可引起血管舒张，此舒张效应可被L－NA抑制，该抑制作用又可为L-精氨酸逆转。结论：电刺激和化学（烟碱）刺激引起的动脉舒张效应为NO所致，并提示在大鼠肠系股动脉可能有与NO有关的血管扩张神经存在。     

血管腔内,外给L—硝基精氨酸对电刺激所致肠系膜动脉灌注压？…

目的 比较血管腔内、外给硝基精氨酸对电刺激所致大鼠肠系膜动脉灌注压的影响。方法 应用灌流离体血管方法，测定肠系膜动脉灌注压变化。结果 电刺激引起大鼠肠系膜动脉灌注压明显升高，血管腔内、外给ＮＯ合酶抑制剂Ｌ－硝基精氨酸（Ｌ－ＮＡ）均明显增强上述灌注压升高反应，此增强作用可被ＮＯ供体－Ｌ精氨酸阻断。血管腔内、外给Ｌ－ＮＡ不改变基础灌注压而且对外源性去甲肾上腺素的作用也无明显影响。结论 静脉注射ＮＯ合酶     

家犬视网膜动脉舒张的神经源性一氧化氮机理

阐明在尼古丁所引起的家犬视网膜动脉舒张反应中所包含的神经源性一氧化氮（NO）作用机制. 利用离体除去内皮细胞的家犬视网膜动脉标本,观察其张力改变. 尼古丁引起前列腺素F_2α预收缩的家犬视网膜动脉舒张反应,其舒张反应被六甲铵和氧合血红蛋白所消除,但不受吲哚美辛,阿托品及塞吗洛尔的影响. NO合酶抑制剂左旋硝基精氨酸（L-NA）可消除尼古丁所致舒张反应并使其舒张转为收缩反应,而右旋硝基精氨酸无此作用. L-NA所致此抑制作用可被NO合成前体左旋精氨酸所复原,而不受右旋精氨酸的影响. 本研究表明家犬视网膜动脉上存在舒张血管神经,该神经通过释放NO神经递质引起该血管舒张反应.     

复方地黄提取物对链脲佐菌素诱导的糖尿病大鼠肠系膜动脉舒张功能的改善作用

目的:观察复方地黄三种不同提取物对链脲佐菌素(STZ)诱导的糖尿病(DM)大鼠肠系膜动脉舒张功能的影响。方法:以STZ(60mg·kg-1,i.p)诱导糖尿病大鼠模型,30d后分别用复方地黄95%乙醇提取物(107.8mg·kg-1),70%乙醇提取物(154.7mg·kg-1),水提取物(56.8mg·kg-1)i.g治疗,每天1次,连续30d,60d后分别记录在L-精氨酸(L-Arg),L-硝基精氨酸(L-NOArg,NLA)及吲哚美辛(indomethacin,Ind)存在或不存在时大鼠肠系膜血管舒张功能。结果:与正常组相比,模型组大鼠肠系膜动脉舒张反应减弱;NO基础释放较正常组的36.2%,NO诱导释放为正常组的22.3%,NO在内皮依赖性舒张中的比例为正常组的32.9%;95%、70%乙醇提取物组NO基础释放为正常组的62.0%、79.7%;NO诱导释放为正常组的51.4%、72.4%;NO在内皮依赖性舒张的比例为正常组的59.4%、79.2%。水提取物效果不明显。结论:糖尿病模型大鼠肠系膜动脉舒张功能异常,主要由NO介导;复方地黄提取物能够保护内皮细胞损伤,改善血管内皮细胞功能。     

越橘乙醇提取物诱导血管舒张的实验研究

目的探讨越橘乙醇提取物对血管内皮的舒张作用及其机制。方法以大鼠胸主动脉为标本,观察越橘提取物对去氧肾上腺素（PE）预收缩血管的舒张作用及其在血管内皮、平滑肌细胞中作用的机制。结果越橘提取物对由去氧肾上腺素（1．0×10^-5mol／L）引发的血管收缩具有浓度依赖性的松弛作用（P〈0．01）,去除血管内皮后舒张作用明显被抑制（P〈0．01）;在内皮完整的血管条中,舒张作用明显被一氧化氮合酶抑制剂L-N-硝基精氨酸甲酯（L—NAME）、亚甲蓝和鸟苷酸环化酶抑制剂（ODQ）所抑制（P〈0．01）,血管的舒张作用因维拉帕米浓度的增加而减弱,并且不受吲哚美辛、格列苯脲、四乙基铵、阿托品和普萘洛尔等药物的影响（P〈0．01）。结论越橘提取物具有明显舒张离体血管的作用,其松弛血管的作用是通过内皮依赖的一氧化氮-环鸟苷酸信号转导系统信号途径,还有可能涉及到L-Ca^2＋通道。     

血管腔内、外给L-硝基精氨酸对电刺激所致肠系膜动脉灌注压的影响

目的比较血管腔内、外给硝基精氨酸对电刺激所致大鼠肠系膜动脉灌注压的影响。方法应用灌流离体血管方法，测定肠系膜动脉灌注压变化。结果电刺激引起大鼠肠系膜动脉灌注压明显升高，血管腔内、外给ＮＯ合酶抑制剂Ｌ－硝基精氨酸（Ｌ－ＮＡ）均明显增强上述灌注压升高反应，此１９９８－０１－０８收稿，１９９８－０３－２０修回＊河北省自然科学基金资助课题，Ｎｏ３９４２５１作者简介：张建新，男，４４岁，医学博士（日本），研究员，药理研究室副主任增强作用可被ＮＯ供体－Ｌ精氨酸阻断。血管腔内、外给Ｌ－ＮＡ不改变基础灌注压而且对外源性去甲肾上腺素的作用也无明显影响。结论静脉注射ＮＯ合酶抑制剂不仅可直接作用于内皮，而且也可透过内皮、平滑肌作用于外周血管神经末梢，减少ＮＯ合成进而增强肾上腺素能神经刺激所致的收缩血管反应。     

L-精氨酸对糖尿病患者血管内皮功能的保护作用

目的研究L-精氨酸对糖尿病引起的血管内皮功能损伤的保护作用和意义。方法将60例糖尿病患者随机分为安慰剂对照组（n=30）和L-精氨酸治疗组（n=30）。L-精氨酸对照组给予口服精氨酸7g每天。两组治疗28d后再过7d的药物洗脱期。在治疗前和治疗后测定两组患者血浆一氧化氮（NO）、内皮素（ET）、血管性血友病因子（vWF）浓度及检测肱动脉血流介导的扩张反应（FMD）,并进行分析。结果L精氨酸治疗组较安慰剂对照组,血浆NO浓度升高,vWF和ET水平下降,差异有统计学意义（P〈0．05）。同时L精氨酸治疗的FMD较对照组明显升高（P〈0．05）。结论L-精氨酸可影响血管内皮活性物质,影响血管内皮的收缩舒张作用,从而对高血糖伴随的血管损伤有保护作用。     

静晕灵合剂的质量标准研究

目的建立静晕灵的质量标准。方法采用薄层色谱法对静晕灵合剂中的白术、当归、川芎、葛根、黄芩进行鉴别;采用高效液相色谱法测定芍药苷的含量。结果在薄层色谱中白术、当归、川芎、葛根均能检出;高效液相色谱法测得芍药苷在0.02～0.10mg.mL-1范围内呈良好的线性关系,r=09991。平均回收率为99.57%,RSD为0.37%(n=9)。结论该法简便,准确,专属性强,能有效控制静晕灵合剂的质量。     

Suppression by NG-nitro-L-arginine of relaxations induced by non-adrenergic, non-cholinergic nerve stimulation in dog duodenal longitudinal muscle.

In dog duodenal longitudinal muscle strips, transmural electrical stimulation (10 Hz, 15 sec) elicited a transient contraction, which was abolished by tetrodotoxin and atropine but potentiated by treatment with NG-nitro-L-arginine (L-NA), a nitric oxide (NO) synthesis inhibitor. The potentiation was reversed by L-arginine but not by its D-enantiomer. Acetylcholine-induced contractions were not influenced by L-NA. After treatment with atropine, the electrical neural stimulation relaxed the muscle strips partially contracted with bradykinin, the relaxation being abolished by tetrodotoxin and suppressed by L-, but not D-, NA. L-arginine reversed the L-NA-induced inhibition. Oxyhemoglobin abolished the relaxation caused by nerve stimulation and NO. The neurally-induced relaxation was not attenuated by adrenoceptor antagonists and indomethacin. It is concluded that electrical stimulation of non-adrenergic, non-cholinergic nerves relaxes dog duodenal smooth muscle, due possibly to NO produced upon neural excitation, and potentiation by L-NA of the contractile response to cholinergic nerve stimulation, would be derived from elimination of the neurally-induced relaxation.     

Involvement of nitric oxide in endothelium-dependent, phasic relaxation caused by histamine in monkey cerebral arteries.

Monkey cerebral artery strips partially contracted with prostaglandin F2 alpha responded to histamine with biphasic patterns of relaxation. The delayed and sustained relaxation was suppressed by cimetidine, whereas the phasic response was abolished by treatment with chlorpheniramine and NG-nitro-L-arginine (L-NA), a nitric oxide (NO) synthase inhibitor. The inhibition by L-NA was reversed by L-arginine. D-NA was without effect. Endothelium denudation abolished the phasic relaxation. We hypothesized that endothelium-dependent, phasic relaxations caused by histamine are mediated by NO that is released by H1-receptor stimulation, whereas the sustained relaxation is associated with the activation of H2-receptors in the smooth muscle of monkey cerebral arteries.     

Mechanisms underlying contraction and relaxation induced by nerve stimulation in monkey uterine arteries

We investigated the mechanisms of contractile and relaxant responses to nerve stimulation by electrical pulses and nicotine in isolated monkey uterine artery strips denuded of the endothelium. In the strips contracted with prostaglandin F(2alpha), transmural electrical stimulation (5 Hz, 40 s) produced a contraction which was partially attenuated by prazosin and abolished or reversed to a relaxation by additional treatment with alpha,beta-methylene ATP. The relaxation was abolished by N(G)-nitro-L-arginine (L-NA) and restored by L-arginine but not by D-arginine. Atropine, D-NA, aminophylline and suramin, an inhibitor of P(2Y) purinoceptors, were without effect. The neurogenic relaxation was abolished by 1H-(1,2, 4)oxadiazolo(4,3)quinoxalin-1-one (ODQ), an inhibitor of soluble guanylate cyclase. Nicotine (10(-4) mol/l) elicited contraction or relaxation of uterine arteries; the contraction was reversed by combined treatment with prazosin and alpha,beta-methylene ATP. Nicotine-induced relaxations were abolished by L-NA and restored by L-arginine. The relaxation induced by exogenously applied NO (acidified NaNO(2) solution) was not influenced by L-NA but abolished by ODQ. It is concluded that contractions induced by nerve stimulation are mediated by norepinephrine and ATP liberated from sympathetic nerves that stimulate alpha(1)-adrenoceptors and P(2x) purinoceptors, respectively. The neurogenic relaxation seems to be mediated exclusively by nitric oxide synthesized from L-arginine in perivascular nerves that activates guanylate cyclase and produces cyclic GMP in smooth muscle.     

HPLC测定丙戊酸钠注射液中丙戊酸钠的含量

目的建立测定丙戊酸钠注射液中丙戊酸钠含量的高效液相色谱法。方法采用ZORBAX Extent-C18（4.6 mm×250 mm,5 μm)色谱柱,甲醇-0.05 mol·L-1磷酸二氢钾缓冲液（80∶20）用10%磷酸调pH值至5.0±0.05为流动相,检测波长为210 nm。结果丙戊酸钠在0.932 2～9.322 3 mg·mL-1内浓度与峰面积呈良好的线性关系,r=0.999 9(n=6);平均回收率为100.37%,RSD为0.8%（n=9)。结论该方法准确可靠,重复性好,操作简便快速,可用于丙戊酸钠注射液中丙戊酸钠的含量测定。