藻酸双酯钠对大鼠离体去内皮胸主动脉环的舒缩作用

目的:观察藻酸双酯钠(polysaccharide sulfate,PSS)对离体大鼠胸主动脉平滑肌舒缩的影响。方法:采用大鼠离体去内皮主动脉环灌流模型,观察不同浓度PSS(5×10-2～5×102 mg.L-1)对基础状态及氯化钾(KCl)、去氧肾上腺素(PE)等试剂的血管收缩效应的影响。结果:不同浓度PSS对基础状态、KCl或PE的去内皮血管环收缩效应无明显影响。PSS(5×102 mg.L-1)对内钙释放及外钙内流引起的血管收缩效应无明显影响。结论:在5×10-2～5×102 mg.L-1浓度范围内,PSS对离体血管平滑肌没有明显舒缩作用。     

苦碟子水提取液对大鼠离体胸主动脉环的舒张作用

目的研究苦碟子的内皮依赖性血管舒张作用,并探讨其可能机制。方法采用大鼠离体主动脉环灌流模型,观察累积浓度苦碟子对基础状态、去氧肾上腺素(PE)和氯化钾(KCl)预收缩的内皮完整血管环和去内皮血管环的舒张作用。结果苦碟子水提取液(苦碟子注射液,相当于含苦碟子原材料0.01～10g.L-1)对基础状态的内皮完整血管环和去内皮血管环的张力无影响。对PE预收缩的内皮完整血管环,苦碟子在累积浓度0.03～10g.L-1呈浓度依赖性舒张作用,分别用一氧化氮合酶抑制剂左旋硝基精氨酸甲酯(0.1mmol.L-1)和鸟苷酸环化酶抑制剂亚甲蓝(10μmol.L-1)预处理,此作用被抑制,用环氧合酶抑制剂吲哚美辛(10μmol.L-1)预处理亦被抑制。对KCl预收缩的内皮完整血管环和对PE或KCl预收缩的去内皮血管环,苦碟子在累积浓度0.01～10g.L-1无明显舒缩作用。结论苦碟子(0.03～10g.L-1)对主动脉具有内皮依赖性舒张作用。该作用可能是通过血管内皮细胞一氧化氮-鸟苷酸环化酶途径和血管内皮细胞环氧合酶途径介导的。     

异叶青兰总黄酮对离体大鼠胸主动脉环的舒张作用及其机制

探讨异叶青兰总黄酮(DHBF)对大鼠胸主动脉血管环张力的影响,并探讨其可能的作用机制,为新疆地方药材的开发和有效利用提供理论依据。采用离体血管灌流技术,通过生物信号采集和分析系统测定不同质量浓度的DHBF(0.015,0.030,0.060,0.120,0.240和0.360 mg/L)对大鼠胸主动脉环血管环张力的影响。结果显示：(1)不同质量浓度的DHBF对静息状态下血管环的张力无明显影响(P>0.05);(2)与对照组比较,DHBF对去甲肾上腺素预收缩的内皮完整组和去内皮组血管环均具有明显的舒张作用(P<0.05),且内皮完整组的舒张作用明显强于去内皮组(P<0.05);与对照组比较,DHBF对KCl预收缩的血管环有明显的舒张作用(P<0.05),且内皮完整组和去内皮组血管环的差异无统计学意义(P>0.05);(3)与对照组和去内皮组比较,DHBF+L-NAME组(DHBF+MB)组对血管环的舒张作用明显被抑制(P<0.05),并呈浓度依赖性。DHBF对NE及KCl预收缩的血管环有明显的舒张作用,这可能与抑制了胞内肌浆网钙释放和Ca^2+...     

新结构Rho激酶抑制剂对离体胸主动脉血管环舒张作用及机制研究

目的评价2个全新结构小分子Rho激酶抑制剂J35242和J35243对离体大鼠胸主动脉血管环的舒张作用,并探讨其作用机制。方法利用离体大鼠胸主动脉血管环模型,分别用高浓度KCl和去甲肾上腺素(norepinephrine,NE)预刺激,评价化合物的舒张血管活性;通过各种工具药干预,观察化合物舒张血管作用的内皮相关机制、钾通道相关机制和钙离子相关机制。结果 J35242和J35243可以剂量依赖性舒张高浓度KCl和NE预收缩的血管环,并呈现一定的内皮依赖性;L-NAME和亚甲蓝可在一定程度上影响其舒张作用;化合物还明显抑制由细胞内钙释放和外钙内流引起的血管收缩,说明其可能通过阻断钙离子通道发挥舒张血管作用;另外两个化合物可能不是通过开放钾离子通道发挥舒张血管作用。结论 J35242和J35243在体外具有一定的舒张血管作用,并且J35242的作用要强于J35243,其机制可能依赖于血管内皮功能,另外可能与抑制平滑肌细胞钙离子通道,降低细胞内钙离子浓度相关。     

四乙酰葛根素对离体大鼠胸主动脉环作用初步研究

目的 观察四乙酰葛根素(Tp)对离体大鼠胸主动脉环的作用以及作用机制。方法 采用大鼠离体胸主动脉环灌流装置,观测四乙酰葛根素对重酒石酸去甲肾上腺素(NA)和氯化钾(KCl)预收缩主动脉环张力的影响。结果 四乙酰葛根素对去甲肾上腺素预收缩主动脉环有明显的舒张作用,与空白对照相比,具有显著性差异(P<0.01);由KCl引起主动脉环预收缩,Tp与空白对照相比,具有统计学差异(P<0.01),对内皮完整血管环的舒张作用明显强于去内皮血管环(P<0.01);Tp对NA在无钙液及正常钙液所致离体血管环收缩的舒张作用不明显(P>0.05)。结论 四乙酰葛根素的舒血管作用与受体依赖性钙通道和电压依赖性钙通道均有关,并且其舒血管作用可能与内皮有一定关系。     

四乙酰葛根素对离体大鼠胸主动脉环作用初步研究

目的观察四乙酰葛根素（Tp）对离体大鼠胸主动脉环的作用以及作用机制。方法采用大鼠离体胸主动脉环灌流装置,观测四乙酰葛根素对重酒石酸去甲肾上腺素（NA）和氯化钾（Kcl）预收缩主动脉环张力的影响。结果四乙酰葛根素对去甲肾上腺素预收缩主动脉环有明显的舒张作用,与空白对照相比,具有显著性差异（P〈0．01）;由KCl引起主动脉环预收缩,Tp与空白对照相比,具有统计学差异（P〈0．01）,对内皮完整血管环的舒张作用明显强于去内皮血管环（P〈0．01）;Tp对NA在无钙液及正常钙液所致离体血管环收缩的舒张作用不明显（P〉O．05）。结论四乙酰葛根素的舒血管作用与受体依赖性钙通道和电压依赖性钙通道均有关,并且其舒血管作用可能与内皮有一定关系。     

牛膝总皂苷对大鼠离体胸主动脉环舒张作用的机制研究

目的研究牛膝总皂苷(ABS)对大鼠离体胸主动脉血管环舒张作用及其作用机制。方法采用累积加药法,通过观察ABS对去甲肾上腺素(NE)和KCl预收缩的血管环张力的影响,并观察几种抑制剂对其作用的影响。结果 ABS对NE预收缩的内皮完整和去内皮血管环均有舒张作用,L-硝基精氨酸甲酯(L-NAME)、亚甲蓝(MB)、吲哚美辛(INDO)能显著减弱ABS诱导的血管环舒张作用;钾离子通道阻滞剂对ABS的舒血管效应有明显抑制作用(P<0.05);ABS对KCl预收缩的血管环有良好的舒张作用。结论 ABS的舒血管作用与NO介导途径有关,同时与钾离子通道的开放及血管平滑肌细胞上受体依赖性钙通道和电压依赖性钙通道有关。     

维药唇香草醇提物对大鼠离体胸主动脉血管环的舒张作用

目的:研究唇香草醇提物(EEZ)对大鼠离体胸主动脉血管环的舒张作用。方法:制备大鼠离体胸主动脉血管环。试验设内皮完整组与内皮去除组,以去氧肾上腺素(PE)预收缩血管环后逐步累积加入100、300、500、700、900、1 100 mg/L EEZ,绘制浓度-张力曲线并计算最大舒张率(Emax)、半数有效浓度(EC50)。试验只设血管环内皮去除组,在无钙或无钙高钾液中以EC50的EEZ预处理血管环后逐步分别累积加入0.4、0.8、1.2、1.6、2.0、2.4 mmol/L Ca Cl2,绘制钙浓度-张力曲线;以EC50的EEZ预处理血管环后加入1μmol/L PE记录收缩张力并计算血管收缩百分率。结果:EEZ对PE预收缩的血管环具有浓度依赖性和平滑肌依赖性的舒张作用;内皮完整组与内皮去除组Emax分别为(58.18±16.23)%与(73.54±17.21)%,EEZ的EC50为773.27 mg/L。在无钙高钾液中,EEZ可以明显引起钙离子收缩曲线右移;在无钙液中,EEZ对PE引起的血管收缩具有抑制作用。结论:EEZ具有血管舒张作用,其机制可能是通过抑制电压依赖性钙通道(VDCCs)的方式来抑制外钙内流和胞质内钙释放,从而干扰胞质内钙离子平衡。     

鸟苷对大鼠胸主动脉血管环的舒张作用及机制

目的研究鸟苷对大鼠离体血管环的影响,并探讨其可能的作用机制。方法分离SD大鼠胸主血管环,分成去内皮组和内皮完整组,采用离体血管环实验方法,经生物信号采集与分析系统测定血管环张力的变化,观察鸟苷的舒血管作用并探讨不同抑制剂对鸟苷舒张大鼠离体血管环作用的影响。结果鸟苷(10-9～10-5 mol.L-1)对基础状态下或KCl预收缩血管环的张力无影响;对PE预收缩的血管环有内皮依赖性舒张作用;环氧合酶抑制剂吲哚美辛孵育对鸟苷的舒张作用无明显影响;一氧化氮合酶抑制剂L-NAME或鸟苷酸环化酶抑制剂亚甲蓝可阻断鸟苷的血管舒张作用。结论鸟苷对大鼠离体胸主动脉有浓度依赖性舒张作用,其舒张作用可能与NO-GC-cGMP途径相关。     

依那普利对大鼠离体胸主动脉的舒张作用及其机制

目的：观察依那普利对血管的直接作用，并探讨其机制。方法：采用Powerlab生物信号采集系统记录依那普利对去甲肾上腺素（NE）和KCl预收缩的离体大鼠胸主动脉环舒张作用，观察左旋硝基精氨酸甲酯（L—NAME，10^-4mol／L）和吲哚关辛（10^-8mol／L）对其作用的影响。结果：在内皮完整的大鼠离体胸主动脉环，依那普利（10^-9～10^-4mol／L）对NE（10^-5mol／L）或KCl（20mmol／L）引起的收缩具有浓度依赖性的舒张作用。去内皮后，依那普利的舒血管作用显著减弱。在内皮完整的血管环，L—NAME（10^-4mol／L）和吲哚美辛（10^-8mol／L）对依那普利的舒血管作用具有明显的抑制作用。结论：依那普利对大鼠离体胸主动脉环具有浓度依赖性的舒张作用，此作用具有内皮依赖性，与内皮产生的NO和前列环素（PGI2）有关。     

Effects of a vasorelaxing factor liberated by the rat isolated atria on rat aortic rings with and without endothelium

In 1993, Illanes et al. described a vasoactive factor, the auricular vasorelaxing factor (AVF), by controlled distension of rat isolated atria. This factor produces vasodilation, antagonizing the vasoconstrictor action of phenylephrine. We now report assays by using isolated rat aortic rings and norepinephrine as a vasoconstrictor. Isolated thoraxic aortic rings were mechanically deprived of endothelium and subjected to the effects of increasing, cumulative concentrations of 6.6 x 10(-11) M to 6.6 x 10(-7) M norepinephrine. AVF significantly decreases the constrictor effect of norepinephrine assayed afterward, shifting the vasoconstrictor dose-response relation to the right. The effect was the same in rat aortic rings with or without endothelium. Subjecting aortic rings to control vehicle samples did not alter the dose-response curve to norepinephrine. We conclude that AVF antagonizes the norepinephrine vasoconstrictor effect in rat isolated aortic rings and that the mechanism of this vasorelaxing effect is independent of any contribution from the endothelial cells.     

麝香保心丸对大鼠离体主动脉环的药理作用

目的：研究麝香保心丸的舒张血管作用及可能的机制。方法：将离体大鼠动脉环随机分成正常组，去内皮组２组（共为６对动脉环，组内比较用自身对照，组间比较用配对对照）。用去甲肾上腺素诱导动脉环收缩后，加入麝香保心丸，记录反应。结果：麝香保心丸对正常组，去内皮组动脉环均有舒张作用（Ｐ＜０．０１），其效应呈剂量依赖；且其对正常组的舒张作用较去内皮组强（Ｐ＜０．０１）。结论：麝香保心丸具有舒张血管的效应，其机制可能有直接及内皮依赖的舒张血管２种作用。     

Studies in the rat on the haemodynamic overshoot response to withdrawal of guanfacine or clonidine treatment

1. Normal rats were injected intramuscularly twice daily for either 3 days or 3 weeks with guanfacine (0.1 or 1.0 mg/kg), clonidine (0.01 or 0.1 mg/kg) or 0.9% saline. All were anaesthetized at various times before or after the last injection, and their arterial pressures and heart rates were monitored via a carotid artery catheter. 2. Overshoots in systolic and diastolic pressure and heart rate, reaching peak values as soon as 16 h after the last injection, occurred in all rats withdrawn from guanfacine or clonidine treatment, but in no control rats. 3. Post-withdrawal blood pressures and heart rates of rats which had received the low dose of guanfacine or clonidine were as great as those of rats which had received the ten-fold greater dosage. Moreover, withdrawal responses were as great in rats which had been treated for only 3 days as in those treated for 3 weeks. 4. The dosages and duration of treatments used in these experiments thus did not influence the magnitude of the haemodynamic overshoots provoked by withdrawal of guanfacine or clonidine. However, all groups of rats from which guanfacine was withheld exhibited significantly greater peak overshoots in systolic and diastolic pressure than did those withdrawn from clonidine treatment.     

Peroxynitrite-induced relaxation in isolated rat aortic rings and mechanisms of action

The present study was designed to evaluate the effects of peroxynitrite (ONOO-), the product of superoxide and nitric oxide, on isolated segments of rat aorta. In the absence of any vasoactive agent, ONOO- (from 10(-8) to 10(-4) M) failed to alter the basal tension. In phenylephrine (PE; 5 x 10(-7) M)-precontracted rat aortic rings (RAR), ONOO- elicited concentration-dependent relaxation at concentrations of from 10(-8) to 10(-4) M. The effective concentrations producing approximately 50% of maximal relaxation (ED50) to ONOO- were 1.84 x 10(-5) M and 1.96 x 10(-5) M in intact and denuded RAR, respectively (P > 0.05). No significant differences in the relaxation responses were found between RAR with or without endothelium (P > 0.05). The presence of either 5 microM methylene blue (MB) or 5 microM 1H-[1,2,4]oxadiazolo-[4,3-alpha]quinoxalin-1-one (ODQ) significantly inhibited the relaxations induced by ONOO-. Sildenafil (10(-7) M), on the other hand, significantly potentiated the ONOO--induced relaxations. Tetraethylammonium chloride (T-2265) significantly decreased the ONOO--induced relaxations in a concentration-dependent manner. However, ONOO- had no effect on RAR precontracted by high KCL (40 mM, n = 6, P > 0.05). Addition of calyculin A also significantly decreased the ONOO--induced relaxation in a dose-dependent manner. Furthermore, ONOO- significantly inhibited calcium-induced contractions of K+-depolarized aortic rings in a concentration-related manner. Lastly, a variety of other pharmacological agents and antagonists including L-NMMA, L-arginine, indomethacin, atropine, naloxone, diphenhydramine, cimetine, glibenclamide, haloperidol, superoxide dismutase (SOD), and catalase did not influence the relaxant effects of ONOO- on RAR. Our new results suggest that ONOO--triggered relaxation on rat aortic rings is mediated by elevation of cGMP levels, membrane hyperpolarization via K+-channel activation, activation of myosin phosphatase activity, and interference with calcium movement and cellular membrane Ca2+ entry.     

黄芪甲苷对正常大鼠离体血管功能的影响

目的观察黄芪甲苷对血管功能的影响并探讨其作用机制。方法采用大鼠离体主动脉环灌流模型,观察黄芪甲苷对血管环收缩和舒张功能的影响。结果黄芪甲苷能够浓度依赖性舒张血管。一氧化氮合酶抑制剂、鸟苷酸环化酶及环加氧酶抑制剂可抑制黄芪甲苷诱导的血管舒张作用。黄芪甲苷能够抑制苯肾上腺、KC l和CaC l2引起的血管收缩。结论黄芪甲苷具有内皮依赖性的舒张血管作用,此作用主要通过NO-cGMP途径发挥作用。黄芪甲苷抑制血管收缩主要通过拮抗外钙内流实现。     

Effects of lysophosphatidylcholine and endothelium on isolated rabbit aortic ring contraction by serotonin

在离体兔胸主动脉环模型上观察溶血性磷脂酰胆碱（ＬＰＣ）促血管收缩作用的机理以及血管内皮对ＬＰＣ促血管收缩作用的影响．１０μｍｏｌ·Ｌ－１ＬＰＣ预温育３０ｍｉｎ可显著增强兔胸主动脉环对５－羟色胺（５－ＨＴ）的收缩反应,使０．１μｍｏｌ·Ｌ－１５－ＨＴ诱导的峰值张力增加到约２．５倍,ＥＣ５０降低,收缩曲线左移．而蛋白激酶Ｃ（ＰＫＣ）抑制剂显形孢菌素（ｓｔａｕｒｏｓｐｏｒｉｎｅ,１００ｎｍｏｌ·Ｌ－１）能抑制ＬＰＣ的促血管收缩作用,ＥＣ５０恢复;去除血管内皮或加入１００μｍｏｌ·Ｌ－１左旋单甲基精氨酸（Ｌ－ＮＭＭＡ）预处理均可显著增强ＬＰＣ的促血管收缩作用,Ｌ－ＮＭＭＡ的作用更强（Ｐ＜０．００１）．结果提示,ＬＰＣ可能通过ＰＫＣ途径促进５－ＨＴ介导的血管收缩,血管内皮可能在其中起调控作用．     

Mechanisms underlying vasorelaxant action of astragaloside IV in isolated rat aortic rings

1. Astragaloside IV is a component from the widely used traditional Chinese herb Astragalus membranaceus and its effect on rat aortic ring contraction and relaxation were investigated. 2. The aorta from male Sprague-Dawley rats was isolated in an organ bath and ring tension was recorded with or without endothelium. Cumulative effects of astragaloside IV on vessel contraction and relaxation were observed in the presence of various antagonists related to vessel activity. 3. Astragaloside IV showed concentration-dependent inhibition of vessel contraction induced by phenylephrine and potassium chloride. The amount of calcium released from intracellular stores sensitive to phenylephrine was also markedly reduced by astragaloside IV. There was dose-dependent vasorelaxation in endothelium-intact rings, which was partly inhibited by pre-incubation with nitric oxide (NO) synthase (NOS) Nomega-nitro-L-arginine methyl ester and guanylate cyclase inhibitor, 1H-[1,2,4] oxadiazolo [4,3-alpha] quinoxalin-1-one. Astragaloside IV also induced a significant increase in aortic tissue content of guanosine 3",5"-cyclic monophosphate (cGMP) both in vivo and in vitro. Endothelial NOS inhibitor Nomega-nitro-L-arginine prevented vasodilatation, whereas neuronal NOS inhibitor 7-nitroindazole did not show significant influence on the vessel relaxation of astragaloside IV. 4. In conclusion, astragaloside IV inhibited vessel contraction through blocking calcium influx and intracellular calcium release. The endothelium-dependent vessel dilation of astragaloside IV was attributed mainly to the endothelium-dependent NO-cGMP pathway.     

神经肽Y对离体兔脑血管的作用及其内皮依赖关系

神经肽Y对离体兔脑基底动脉的作用表现在:(1)直接收缩;(2)增强组胺的收缩效应;(3)抑制乙酰胆碱和腺苷的舒张效应。作用(1)和(3)不依赖于血管内皮的存在,而作用(2)依赖血管内皮,其机理可能是由于神经肽Y对血管内皮舒张因子(EDRF)的释放或作用具有抑制性影响。     

氯化汞对离体兔动脉环的作用

氯化汞(HgCl2)是环境中重要的污染物之一，其对心血管系统的毒性作用机制尚不十分清楚，有研究表明，HgCl2可引起离体灌流心脏的等容收缩压下降，心房、心室率下降，及各类心律失常，有研究指出，小剂量HgCl2能引起大鼠离体乳头肌收缩力增加，可能与肌浆网钙释放有关。马欣等研究表明，HgCl2对心     

Effect of endothelium on phenylephrine-induced contraction in the rat isolated aortic strips

Phenylephrine tested on the isolated endothelium intact rat aortic strips elicited an enhanced response in the second assay when compared with the response obtained in the first trial. Removal of the endothelium and the pretreatment of the strips in the endothelium with methylene blue almost completely prevented the enhanced response to phenylephrine in the second assay. Pretreatment of the strips with lysine acetyl salicylate failed to abolish the potentiated response to phenylephrine in the second test. These data were taken as an evidence that the basal production or release of endothelium-derived relaxing factor(s) but not cyclooxygenase products of arachidonic acid from the endothelium of the rat aorta can influence the contractile effect of phenylephrine and the enhanced response to this alpha-adrenoceptor agonist in the second assay is probably due to the recuded production or release of these endogenously occurring endothelium-originated substance(s).