哌替啶的舒血管作用及其机制

目的:探讨哌替啶扩张血管导致低血压的机制.方法:制备大鼠离体主动脉环,记录血管环张力,观察哌替啶对高钾和苯肾上腺素(PhE)预收缩血管的作用.结果:哌替啶不影响血管的静止张力,但可对高钾和PhE诱导的收缩产生非内皮依赖的舒张作用,并呈剂量-反应关系.哌替啶既不影响咖啡因诱导的血管收缩,也不改变钌红作用后对高钾诱导收缩的抑制作用.在无钙条件下,哌替啶仍能抑制PhE的收缩,也抑制后续加入钙后引发的收缩.结论:哌替啶对高钾和PhE诱导的血管收缩有舒张作用,机制可能与其阻断细胞膜钙通道和抑制IP3敏感钙池的钙释放有关.     

桑叶乙酸乙酯提取物的血管作用及其机制

目的:探讨桑叶乙酸乙酯提取物对离体大鼠胸主动脉环收缩张力的作用及其机制。方法:采用生物信号采集系统记录灌流胸主动脉环张力变化。结果:①桑叶乙酸乙酯提取物(0.25~32.0 g/L)对苯肾上腺素(PE,1-0 6m o l/L)和KC l(6×1-0 2m o l/L)预收缩的内皮完整和去内皮的血管环均有舒张作用,且呈浓度依赖性;②EC50(KC l 6 g/L,PE 6.4 g/L)的桑叶乙酸乙酯提取物可使CaC l2量效曲线下移,最大反应降低;③经钙通道阻断剂维拉帕米预处理的去内皮血管,桑叶乙酸乙酯提取物可加强PE引起的血管收缩,与ryanod ine受体阻断剂钌红共孵育可取消维拉帕米的上述作用,而IP3受体阻断剂肝素则不能取消其作用。结论:桑叶乙酸乙酯提取物对血管呈非内皮依赖性的双重作用,其舒张效应大于收缩效应。桑叶乙酸乙酯提取物产生的血管舒张作用可能是通过抑制电压依从性钙通道和受体依从性钙通道减少Ca2 内流入血管平滑肌细胞所致;其收缩作用可能是通过激活内质网ryanod ine受体,引起内质网内Ca2 释放引起的。     

Effects of Total Alkaloids in Buxus microphylla Leaves on Aorta Smooth Muscle of Rats and Their Mechanisms

Objective To investigate the effects of total alkaloids in Buxus microphylla leaves (ABML) on isolated rats thoracic aorta rings, and then to explore the possible mechanisms underlying the effects. Methods Thoracic aortas of Wistar rats were isolated, removed, and mounted onto an organ bath. The effects of ABML at different concentration on the contraction of isolated thoracic aorta rings (with and without endothelium) precontracted with KCl or PE were observed with organ bath technique. Dose-effect curves of CaCl2 were recorded by organ bath technique. The concentration of intracellular Ca2+ ([Ca2+]i) increased by PE, KCI, and caffeine in the presence of ABML was determined using Ca2+ sensitive fluorescence indicator Fura-2/AM loaded thoracic aorta vascular smooth muscle (VSM) cells of rats. Results In aorta rings precontracted with PE and KCl, ABML produced concentration- dependent relaxation in both intact and denuded endothelium ring groups. There was no difference in the inhibition of contraction between the intact and denuded endothelium ring groups at the same concentration. Exposure of isolated thoracic aorta rings to ABML led to a significant reduction in the contracting response induced by CaCl2, and shifted the cumulative concentration-response curves to right. ABML could significantly inhibit the extracellular Ca2+ influx induced by PE and KCl under [Ca2+]0 of 1.5 mmol/L, with inhibitory ratios of 40.2% and 49.9%, respectively. In the case of Ca2+-free, ABML could significantly inhibit the intracellular Ca2+ release induced by PE, with inhibitory ratio of 72.4%. Conclusion ABML relaxes thoracic aorta VSM cells by suppressing influx of extracellular Ca2+ via voltage-dependent Ca2+ channel and receptor-operated Ca2+ channel.     

Effect of propofol on vascular reactivity in thoracic aortas from rats with endotoxemia

BackgroundThis study examined the effect of propofol on thoracic aortas isolated from endotoxic rats to assess endothelium-dependent and -independent relaxant responses.MethodsAdult male Wistar rats were assigned randomly to one of two groups, a saline control group or an experimental group treated with lipopolysaccharide (LPS, 10 mg/kg intravenously). At 6 hours after saline or LPS infusion, the thoracic aorta was excised and cut into 3-mm rings. Aortic rings with or without endothelium were suspended in organ baths for isometric tension recording.ResultsBoth norepinephrine (NE)-induced vascular contraction and acetylcholine-induced vasodilation were attenuated in aortasfrom LPS-treated rats. Furthermore, preincubation with propofol caused a rightward shift in the NE concentration–response curve for aortasfrom LPS-treated rats compared to sham controls. The slow and sustained, but not the initial fast, contractile response to NE was significantly suppressed by propofol in LPS-treated aortas. In addition, vascular relaxation induced by propofol in LPS-treated aortas was partially suppressed by inhibitors of either nitric oxide (NO) synthase or soluble guanylate cyclase, but not bypotassium channel inhibitors.ConclusionThese data suggest that propofol reduces the sensitivity to NE in aortic rings from endotoxic rats. This appears to be caused by (i) blockade of the extracellular calcium influx rather than a reduction in intracellular calcium release and (ii) an increased response to, at least in part, NO–cGMP in rat aortas.     

血凝酶对大鼠离体胸主动脉环收缩作用的影响

目的:研究血凝酶(Reptilase,RTA)对离体大鼠胸主动脉的收缩作用与机制。方法:制备离体大鼠胸主动脉环,经生物信号采集与分析系统测定血管环的张力变化。分有内皮组和去内皮组,采用累计加药法,观察血凝酶对去氧肾上腺素(PE)和氯化钾(KCl)预收缩的胸主动脉环收缩张力的影响。结果:血凝酶对PE预收缩的胸主动脉环产生浓度依赖性的收缩作用,对内皮完整PE预收缩血管环组显著高于去内皮组;而对KCl预收缩的胸主动脉环张力无显著影响;在内皮完整的血管,预孵内皮素转化酶抑制剂磷阿米酮(phosphoramidone,5×10-6mmol/L,PAMD)后,血凝酶对PE预收缩张力明显低于未孵育组(P<0.01);在去内皮的血管环上,应用EDTA(3mmol/L)螯合细胞外Ca2+或LaCl3(100μmol/L)后,可明显阻断血凝酶对PE预收缩作用(P<0.01)。结论:血凝酶对PE预收缩的胸主动脉环的收缩作用呈浓度依赖性,其机制可能为有内皮细胞途径参与,促进内皮素释放,对PE缩血管产生协同效应;还可能与血管平滑肌上有受体操纵性钙通道(receptor-operated calcium chan-nel,ROCC)[1]参与,增加血管平滑肌钙内流有关。     

山莨菪碱对正常及自发性高血压大鼠离体血管舒张功能的影响

目的:观察山莨菪碱对离体正常(Wistar)大鼠及自发性高血压大鼠(spontaneously hypertensive rats,SHR)腹主动脉舒张作用的影响,并探讨其可能的作用机制。方法:采用大鼠离体腹主动脉环(长度为4~5 mm的血管)灌流技术,观察山莨菪碱对正常大鼠及SHR血管舒张功能的影响,并观察苯肾上腺素(phenylephrine,PE)、左旋硝基精氨酸甲酯(L-NAME)预处理对山莨菪碱作用的影响。结果:山莨菪碱对PE预收缩的正常大鼠内皮完整和去内皮血管的舒张作用差异显著(P<0.05);对PE预收缩的SHR内皮完整及去内皮血管环,山莨菪碱均具有显著舒张作用,呈剂量-效应关系,最大舒张率分别为(78.6±6.9)%和(65.76±11.39)%,无统计学差异。用NOS抑制剂L-NAME预处理正常大鼠内皮完整的血管环,可显著地抑制山莨菪碱诱导的舒张作用(P<0.05)。山莨菪碱对SHR血管的舒张作用能够被L-NAME抑制,抑制前后最大舒张率分别为61%和11.9%(P<0.01)。结论:山莨菪碱可能通过内皮和平滑肌2条途径发挥舒张大鼠离体腹主动脉的作用。     

腹膜炎休克大鼠离体主动脉对去甲肾上腺素反应性降低的可能机理

应用不同拮抗剂分析导致腹膜炎休克大鼠离体主动脉环对ＮＥ反应性内皮依赖性降低的可能因素。结果表明，内皮功能完整的血管环经甲基蓝、阿托品、山莨菪碱（６５４－２）、消炎痛、心得安等预处理后，对ＮＥ的浓度效应曲线均左移，最大收缩有不同程度的升高；去内皮血管环经心得安处理后也可见到类似变化。与此相反，内皮功能完整与去内皮血管经育亨宾预处理后，对ＮＥ的浓度效应曲线均较各自对照右移，最大收缩降低。提示导致休克大鼠离体主动脉对ＮＥ的反应性内皮依赖性降低的因素可能是多方面的，其中通过ｃＧＭＰ引起血管平滑肌舒张可能是相当重要的机理之一。     

银杏叶水提取物对大鼠离体胸主动脉环的舒张作用

[目的]探讨银杏叶水提取物对大鼠离体胸主动脉环的舒张作用及其机制.[方法]建立大鼠离体主动脉环灌流模型,观察银杏叶水提取物对分别经1μmol/L苯肾上腺素及5-HT预收缩的内皮完整血管环和去内皮血管环的舒张作用,并观察左旋硝基精氨酸甲酯（L-NAME）及亚甲蓝预处理对银杏叶水提取物的舒张血管作用的影响.[结果]银杏叶水提取物对大鼠离体内皮完整的胸主动脉环具有浓度依赖性的舒张作用;L-NAME和亚甲蓝预处理可明显抑制银杏叶水提取物的舒张作用.[结论]银杏叶水提取物对大鼠离体胸主动脉环具有内皮依赖性舒张血管作用,其可能机制是通过血管内皮细胞鸟苷酸环化酶途径介导.     

茶提取物预防离体大鼠血管对硝酸甘油耐受作用的研究

目的探讨茶提取物茶多酚和茶黄素预防离体大鼠血管对硝酸甘油耐受的作用。方法用硝酸甘油30μM预孵90min的方法诱导大鼠离体胸主动脉环对硝酸甘油产生耐受,用苯肾上腺素预收缩血管,通过organbath的方法观察茶提取物茶多酚和茶黄素处理与否对硝酸甘油舒张血管作用的影响。结果硝酸甘油预孵使血管对硝酸甘油的舒张反应显著减弱,pD2由对照组的8.21±0.09降低为耐受组的6.86±0.20（P〈0.05）;茶多酚和茶黄素预处理均使硝酸甘油耐受血管的舒张反应明显增强,pD2值分别为7.76±0.11和7.97±0.13,与耐受组相比均P〈0.05;各组Emax无显著变化。结论茶多酚和茶黄素预处理可预防离体大鼠血管发生硝酸甘油耐受。     

Endothelium-dependent inhibition of the contractile response is decreased in aorta from aged and spontaneously hypertensive rats

BACKGROUND: Stimulation of vascular 5-hydroxytryptamine-2C (5-HT(2c)) receptors produces contraction in rat aorta. We investigated the effect of aging on endothelium-dependent inhibition of contractile responses in thoracic aorta from normotensive Wistar Kyoto (WKY) and spontaneously hypertensive rats (SHR). METHODS: Endothelium-intact and denuded aortic rings were prepared from young (7-9 weeks old) and senescent (65-70 weeks old) WKY and SHR rats. Changes in isometric tension elicited by 5-HT, in the absence or in the presence of N(G)-nitro-L-arginine methyl ester (L-NAME) or indomethacin were recorded. RESULTS: In aorta from WKY and SHR, 5-HT elicited concentration-dependent contractions, which were increased by endothelium removal. The ability of endothelium to depress contractile response to 5-HT was found to be reduced in vessels from senescent animals, mainly in SHR. L-NAME increased the sensitivity and maximal effect to 5-HT in endothelium-intact but not in denuded aortic rings from young WKY rats. The effect of L-NAME was lower in young SHR compared with age-matched WKY rats, but it did not modify the response to 5-HT in senescent rats. Indomethacin did not affect contraction in arteries from young WKY or in denuded aortic rings from young SHR and aged WKY. In contrast, the inhibitor attenuated the response in endothelium-intact vessels from young SHR and aged WKY, and this effect was more marked in arteries with and without endothelium from senescent SHR. Thus, inhibition of cyclooxygenases by indomethacin revealed an enhanced endothelium-dependent modulation of contraction in senescent and hypertensive rats. CONCLUSIONS: Results indicate that hypertension and aging decrease the negative modulator role of endothelium, in 5-HT-induced vasoconstriction in aorta from WKY and SHR. Data also point out that endothelial dysfunction involves an increased formation of vasoconstrictor prostanoids, which counteract nitric oxide effects. In addition, SHR endothelium releases contractile prostanoids at an early stage of hypertension, whereas in old SHR vascular smooth muscle also releases prostanoids, which contribute to 5-HT-induced contraction.     

槲皮素对大鼠血管平滑肌肌张力的影响

[目的]观察槲皮素对血管平滑肌肌张力的影响并初步探讨其机制。[方法]Wistar大鼠,取胸主动脉,制成血管环,采用离体血管环灌流法,观察不同浓度的槲皮素对血管平滑肌肌张力的影响。[结果]对于内皮完整的血管环,低浓度（≤10-5mol.L-1）槲皮素可明显抑制去甲肾上腺素或氯化钾引起的血管收缩,且在一定浓度范围内呈剂量依赖性;对于去内皮的血管环,抑制作用则不明显;高浓度（〉10-5mol.L-1）槲皮素,无论是对于内皮完整的还是去内皮的血管环,均可使血管收缩,其收缩作用可被异博定阻断。[结论]槲皮素在低浓度时,对于非内皮损伤所致的高血压具有一定的降压作用;同时槲皮素可激活血管平滑肌L-型钙通道,因此高浓度则表现出相反作用。     

Effects of nitric oxide donors on non-pregnant and pregnant rat uterine and aortic smooth muscle

OBJECTIVE: To compare the effects of nitric oxide (NO) donors, diethylamine/nitric oxide (DEA/NO) and nitroglycerin (NTG), on isolated uterine and aortic tissues from non-pregnant, mid and late pregnant rats. METHODS: The uterus and thoracic aorta were obtained from non-pregnant (estrous cycle) and pregnant Sprague-Dawley rats on day 14 and day 21. The uterine and aortic rings were incubated in organ chambers filled with Krebs-Henseleit solution bubbled with 5% CO2 in air for isometric tension recordings. Cumulative concentration-response relationships to DEA/NO and NTG were obtained in the aortic rings contracted with phenylephrine and in spontaneously contracting uterine rings. RESULTS: The sensitivity and the maximal inhibitory effects of DEA/NO did not differ in aortic tissues of any group. DEA/NO-induced Maximal inhibition of spontaneous contractions of uterine tissues from mid-pregnant rats was greater (although not significantly) than in the tissues from non-pregnant animals (with similar sensitivity), but it was significantly depressed in tissues from late pregnant rats. The sensitivity to and maximal inhibitory effects of NTG were less in aortic tissues from late pregnant versus mid-pregnant and non-pregnant rats. In uterine tissues from late pregnant rats the effect of NTG was negligible. The inhibitory action of both NO donors was much more pronounced in aortic versus uterine tissues. CONCLUSIONS: Uterine smooth muscle is less sensitive than vascular smooth muscle to NO. Uterine smooth muscle from late pregnant animals demonstrates refractoriness to both DEA/NO and NTG, while vascular smooth muscle from late pregnant animals demonstrates refractoriness to NTG, but not to DEA/NO.     

黄芪舒张血管平滑肌的作用及机制

目的:探讨黄芪对血管平滑肌的舒张作用及其机制.方法:采用大鼠离体胸主动脉环灌流模型.在去除血管环内皮后,观察累积浓度黄芪对基础状态(基础组)、苯肾上腺素(PE)预收缩(苯肾上腺素组)、氯化钾预收缩(氯化钾组)的血管环的作用和黄芪对经无钙液(无钙液组)、无钙液加肝素(肝素组)、普萘洛尔(普萘洛尔组)预处理后的血管环的作用.结果:在血管内皮被去除后,黄芪对基础状态或氯化钾预收缩的血管环无影响;当黄芪浓度累积达(10-1、3×10-1、100、3×100)g/L时,对PE(3×10-7mol/L)预收缩的血管环产生剂量依赖性舒张作用(P<0.05).经无钙液预处理后,黄芪(3×100 g/L)对血管环的舒张作用未被阻断;但经无钙液加肝素预处理后,该作用被显著抑制(P<0.01);而普萘洛尔预处理不影响黄芪对PE预收缩血管环的舒张作用.结论:黄芪对去除内皮的血管具有舒张作用.其机制可能与阻断血管平滑肌细胞内质网上的三磷酸肌醇敏感的钙离子通道,抑制内钙的释放有关.     

应用干扰素-α减弱大鼠血管内皮依赖性的舒张作用

目的 :研究急、慢性干扰素 - α(IFN- α)处理对离体大鼠胸主动脉环的影响及其可能机制。方法 :用离体血管灌流方法 ,测定离体主动脉环张力。结果 :IFN- α(10、10 0、10 0 0、10 0 0 0 U/ ml)对苯肾上腺素 (PE,10 -6mol/ L)预收缩的内皮完整血管环产生浓度依赖性的舒张作用 ,分别降低为对照的 (90 .1± 0 .91) %、(6 5 .1± 5 .2 1) %、(39.5± 8.2 2 ) %、(35 .3± 8.2 7) %。去除内皮后 IFN- α的舒张作用被取消。用一氧化氮合酶 (NOS)抑制剂 L- NAME(10 -4mol/ L)、鸟苷酸环化酶抑制剂亚甲蓝 (10 -5mol/ L)和诱导型 NOS抑制剂 AMG(10 -4mol/ L)预处理后 ,10 0 U/ mlIFN- α引起的血管舒张作用被阻断 ,其血管舒张幅度分别为对照的 (97.2± 5 .34) %、(95 .1± 6 .2 5 ) %、(93.7±8.82 ) %。用 IFN- α10 0 0 0 U/ ml预处理 2 h对 Ach引起的内皮依赖性主动脉环的舒张作用无显著影响 ,用IFN- α10 0万 U/ d腹腔注射 5 d后的 SD大鼠的主动脉环对 Ach引起的内皮细胞依赖性舒张作用明显降低。结论 :IFN- α可能通过诱导 i NOS合成或增强 i NOS其活性产生内皮依赖的血管舒张作用 ,慢性 IFN-α处理可能损害了血管内皮的功能或使 NO- s GC信号途径的效能降低。     

槲皮素与芦丁对离体大鼠主动脉环的舒张作用及机制

目的:比较研究槲皮素与芦丁对离体大鼠胸主动脉环的作用及其可能的途径。方法:采用累积加药法,检测槲皮素和芦丁对去氧肾上腺素(pheny lephrine,PE)预收缩的胸主动脉环张力的影响。结果:槲皮素对离体大鼠内皮完整和去内皮的胸主动脉环均有浓度依赖性的舒张作用,而芦丁对PE预收缩血管的舒张作用是内皮依赖性的。槲皮素和芦丁对内皮完整的胸主动脉环的最大舒张反应分别为(77.20±6.11)%和(44.28±7.48)%,但两者对内皮完整的胸主动脉环最大舒张的半数有效浓度无明显差异。用一氧化氮合酶抑制剂L-NAM E(0.1 mm o l/L)预处理后,可阻断芦丁诱导的舒张血管作用,但不能阻断槲皮素引起的舒张血管作用;用鸟苷酸环化酶抑制剂亚甲蓝(10μm o l/L)预处理后,两者的血管舒张作用均被阻断。用环氧合酶抑制剂吲哚美辛(10μm o l/L)预处理后可减弱槲皮素诱导的舒张血管作用,但不能阻断芦丁引起的舒张血管作用。结论:槲皮素的舒血管作用强于芦丁,槲皮素可能是通过鸟苷酸环化酶和环氧合酶途径产生非内皮依赖性的血管舒张作用,而芦丁可能是通过NO-鸟苷酸环化酶途径产生内皮依赖性的血管舒张作用。     

TRPV4在高血压小鼠胸主动脉舒张中的作用

目的:研究瞬时受体电位香草素亚型4（transient receptor potential vanilloid type 4,TRPV4）在高血压小鼠胸主动脉舒张中的作用,并探讨其作用机制。方法:分离小鼠胸主动脉,取其离体胸主动脉血管环进行血管张力测试,以1 μmol/L盐酸苯肾上腺素预收缩血管,分别观察对照组与TRPV4抑制剂HC067064处理组在乙酰胆碱（ACh）和GSK1016790A介导下血管张力变化,野生型与TRPV4基因敲除（TRPV4-/-）小鼠在ACh和GSK1016790A介导下血管张力变化;对于普通饮食组和高盐饮食组小鼠胸主动脉环进行血管张力测试,检测GSK1016970A舒张血管的张力变化。结果:HC067064组在ACh和GSK1016790A引起的动脉舒张反应明显低于对照组（P<0.05）;TRPV4-/-小鼠胸主动脉环在ACh和GSK1016790A引起的动脉舒张反应亦低于野生型小鼠（P<0.05）;高盐饮食组GSK1016790A引起的动脉舒张反应低于普通饮食组（P<0.05）。结论:TRPV4参与了小鼠胸主动脉的舒张作用,此作用是通过刺激TRPV4通道开放,促进内皮细胞外钙离子内流进入胞内,经过一系列信号转导,继而舒张血管;但是在病理模型,如高盐饮食下,TRPV4在胸主动脉中的舒张作用会被抑制。     

醋柳黄酮对大鼠离体主动脉环的舒张作用及机制研究

目的:探讨醋柳黄酮(TFH)对大鼠离体胸主动脉环的舒张作用及其与内皮的关系.方法:采用离体血管环技术制备大鼠胸主动脉环,并置于灌流槽中.使用累积加药法,检测TFH对去甲肾上腺素(NE)预收缩的胸主动脉环张力的影响,并分为去内皮组及非去内皮组,对TFH扩血管作用对照研究.结果:TFH对离体大鼠内皮完整和去内皮的胸主动脉环均呈剂量(浓度为0.02g/L;0.04g/L;0.06g/L)依赖性扩血管作用,THF在0.02g/L;0.04g/L的浓度对内皮完整的主动脉环较去内皮主动脉环舒张血管作用更强,有统计学差异(P＜0.05),在0.06g/L的浓度两组均为完全舒张,最大舒张反应均为100%.结论:THF呈剂量依赖性扩血管作用,其舒张血管作用在小剂量呈内皮依赖性,而大剂量呈非内皮依赖性.     

催产素舒张血管的作用及其机制

目的观察催产素（OT）的血管舒张作用并探讨其可能机制。方法采用大鼠离体血管功能实验装置,描记张力变化,血管按随机数表分组,每组6枚血管环,分别保留或去除内皮,各阻断剂预处理30min之后做OT舒张曲线。结果 OT不能舒张苯肾上腺素（PE）预收缩的内皮完整非孕大鼠血管环。而OT（0.1U-3.2U）浓度依赖性地舒张苯肾上腺素（PE）预收缩的内皮完整或去除内皮的大鼠胸主动脉环。一氧化氮合成酶抑制剂亚硝基左旋精氨酸甲酯（L-NAME）可抑制PE诱导的血管舒张作用（P〈0.01）;环氧合酶抑制剂吲哚美辛（Indo）对PE诱导的血管舒张作用无影响。钾通道阻断剂四乙胺（TEA）3mmol/L预处理可减弱OT对内皮完好血管的舒张效应。OT对PE诱导的血管舒张作用与Ca2＋浓度无关。结论 OT具有舒张孕鼠血管作用,其机制与NO-cGMP途径和血管平滑肌钾通道有关。     

硫化氢对家兔肠系膜动脉血管环张力调节研究

目的:观察硫化氢(H2S)对家兔肠系膜血管环张力的调节作用,及其可能的作用机制。方法:应用离体血管环张力测定技术,用金属钩将3mm左右的动脉环悬置于含K-H液的离体器官浴槽中,观察硫化氢在血管环张力的作用,由计算机生物信号采集处理系统进行记录分析,检测血管环张力的变化,制作浓度反应曲线。结果:(1)外源性的NaHS(H2S的供体)可以剂量依赖性地舒张由氯化钾(KCL)预收缩的肠系膜动脉血管环。(2)用ATP敏感性钾通道(KA T P)通道阻断剂格列苯脲(Gli)、钙通道的开放剂1,4-二氢-2,6-二甲基-5-硝基-4-(2-[三氟甲基]苯基)吡啶-3-羧酸甲酯(Bay K8644)、NO合酶的抑制剂左旋硝基精氨酸甲酯(L-NAME)和环氧合酶阻断剂吲哚美辛预处理以及去除血管内皮后,H2S的舒张效应均被显著抑制,浓度反应曲线均明显右移。(3)给予鸟苷酸环化酶的抑制剂1H-(1,2,4)恶二唑(4,3-α)喹喔啉-1-酮(ODQ)预处理后,对H2S的舒张作用没有显著改变。结论:H2S在50～800μmol/L之间浓度依赖性的舒张家兔肠系膜动脉,部分是通过开放KA T P通道和关闭L型钙通道实现的,但与3ˊ,5ˊ-环一磷酸鸟苷(cGMP)途径无关。此作用是内皮依赖性的,且与一氧化氮(NO)和前列环素(PGI2)具有协同作用。     

川芎提取物对大鼠离体胸主动脉血管环的作用及其机制

目的研究川芎提取物对离体大鼠胸主动脉血管环的作用及其作用机制。方法制取Wistar大鼠胸主动脉血管外,经生物信号采集与分析系统测定血管环张力的变化。结果川芎提取物对血管环具有明显的直接舒张作用;能明显减小苯肾上腺素(PE)对血管环引起的收缩幅度;此舒张作用可被一氧化氮合酶抑制剂L-硝基精氨酸抑制。结论川芎提取物对血管环具有明显的直接舒张作用并能抑制PE对血管环所引起的收缩作用。该作用机制可能与NO有关。