复方地龙汤对变态反应性哮喘的影响

目的：探讨复方地龙汤抗动物变态反应性哮喘的作用。方法：采用组胺喷雾致豚鼠哮喘法：致敏豚鼠离体气管平滑肌过敏性收缩实验法；离体气管片法：肺支气管灌流法进行试验。结果：复方地龙汤水煎液对喷入组胺致喘的豚鼠。能使其哮喘潜伏期延长（P〈0．01）；能使致敏豚鼠离体气管平滑肌过敏性收缩有非常显著的抑制作用（P〈0．01）；在抗组胺实验中，对给予组胺后的豚鼠离体气管片有非常显著的舒张作用（P〈0．01）；使肺支气管灌流速度加快，灌流量增加（P〈0．01）。结论：复方地龙汤求煎液对由各种过敏递质引起的哮喘．有显著的抑制作用。这可能是因为其对在体、离体气管平滑肌均有松弛作用．并拮抗组胺等过敏递质对气道的炎性反应和具有激动体内β-受体和免疫系统。从而发挥其作用的。     

硫酸寡糖对豚鼠气管平滑肌的作用

目的 观察硫酸寡糖对组胺(His)、乙酰胆碱(Ach)引起的正常豚鼠离体气管平滑肌收缩的影响、对卵白蛋白(OVA)致敏豚鼠离体气管平滑肌受到OVA攻击时引起收缩的影响及对吸入His引起的正常整体豚鼠哮喘的影响。方法 采用豚鼠离体气管片法、致敏豚鼠离体气管Schultz-Dale法和整体动物引喘法。结果 硫酸寡糖能显著抑制His引起的正常豚鼠离体气管平滑肌收缩,但对Ach引起的正常豚鼠离体气管平滑肌收缩无显著抑制作用;能显著抑制OVA诱发的致敏豚鼠离体气管平滑肌的收缩;能显著延长His引喘潜伏期,使抽搐动物数减少。结论 硫酸寡糖具有抗His、抗过敏和平喘作用。     

沙丁胺醇的抗过敏作用及酮替芬对其平喘效应的增强作用

目的　观察沙丁胺醇的抗过敏作用及酮替芬对沙丁胺醇平喘效应的增强作用。方法　用豚鼠离体气管实验法,组胺、乙酰胆碱引喘法,致敏豚鼠离体气管Ｓｃｈｕｌｔｚ Ｄａｌｅ 反应及支气管肺泡灌洗液中嗜酸粒细胞数测定法。结果　酮替芬可增强沙丁胺醇的松弛气道平滑肌作用和预防沙丁胺醇引起的β受体快速耐受性的产生;酮替芬还可增强沙丁胺醇抑制组胺、乙酰胆碱引起的豚鼠哮喘;沙丁胺醇和酮替芬对致敏豚鼠离体气管Ｓｃｈｕｌｔｚ Ｄａｌｅ 反应具有抑制作用,并能使过敏性哮喘迟发反应时豚鼠支气管肺泡灌洗液中嗜酸粒细胞数显著减少。结论　沙丁胺醇具有抗过敏作用,酮替芬可预防沙丁胺醇耐受性的产生和增强沙丁胺醇的平喘效应     

消咳喘片对豚鼠支气管平滑肌的影响

目的:研究消咳喘片(Xiaokechuan Tablets)对正常及致敏豚鼠支气管收缩的影响及平喘作用。方法:通过离体和整体实验,观察消咳喘片对以组胺和乙酰胆碱引起的正常豚鼠支气管的收缩和以卵蛋白诱发的致敏豚鼠支气管收缩的影响。结果:离体实验,消咳喘片52mg·L-1对组胺致正常豚鼠气管片的收缩具有对抗作用,对卵白蛋白所致的致敏豚鼠支气管平滑肌收缩有极显著的抑制作用(P<0．01)。对乙酰胆碱所致气管片收缩作用明显;整体实验,消咳喘片18mg·kg-1可显著延长卵白蛋白所致的致敏豚鼠呼吸困难,抽搐和跌倒的潜伏期(P<0．01)。结论:消咳喘片能拮抗组胺刺激引起的正常豚鼠和卵白蛋白引起的致敏豚鼠离体气管片的收缩,抑制致敏豚鼠哮喘的发生。     

吡布特罗胶囊对豚鼠支气管平滑肌的影响

目的:研究吡布特罗胶囊(PirbuteroI Capsules)对正常及致敏豚鼠支气管收缩的影响及平喘作用。方法:通过离体和整体实验,观察 Pributerol Capsules 对以组胺和乙酰胆碱引起正常豚鼠支气管的收缩和以卵白蛋白诱发的致敏豚鼠支气管收缩的影响。结果:离体实验,PirbuterolCapsules 52mg·L~(-1)对组胺致正常豚鼠气管片的收缩具有对抗作用,对卵白蛋白所致的致敏豚鼠支气管平滑肌收缩有极显著的抑制作用(P<0.01)。对乙酰胆碱所致气管片收缩作用明显;整体实验,Pirbuterol Capsules 18mg·kg~(-1)可显著延长卵白蛋白所致的致敏豚鼠呼吸困难,抽搐和跌倒的潜伏期(P<0.01)。结论:Pirbuterol Capsules 能拮抗组胺刺激引起的正常豚鼠和卵白蛋白引起的致敏豚鼠离体气管片的收缩,抑制致敏豚鼠哮喘的发生。     

紫癜灵合剂抗Ⅰ型变态反应的作用

目的:观察中药紫癜灵合剂抗Ⅰ型变态反应的作用,并初步探讨其抗Ⅰ型变态反应的作用机制。方法:豚鼠皮内注射抗卵白蛋白的抗血清(含IgG)诱导被动皮肤过敏反应,观察紫癜灵抗Ⅰ型变态反应的作用。以磷酸组胺兴奋的豚鼠离体回肠为模型,观察紫癜灵抗过敏介质组胺的作用。致敏豚鼠灌胃给紫癜灵合剂,观察紫癜灵对血清IgG抗体的影响。结果:紫癜灵呈剂量相关性地抑制豚鼠同种皮肤过敏反应,其中高、中剂量组(20,10g.kg-1)与模型对照组相比有显著差异(P<0.01或P<0.05);紫癜灵呈剂量相关性抑制磷酸组胺所致豚鼠离体回肠平滑肌收缩,与对照组相比有显著差异(P<0.01),高剂量组收缩抑制率可达92.26%;紫癜灵可以降低致敏豚鼠体内IgG抗体含量。结论:紫癜灵合剂具有显著的抗I型变态反应的作用,其机制可能与抑制体内组胺活性及减少IgG抗体的生成有关。     

止喘灵口服液治疗支气管哮喘的药效学研究

目的：根据止喘灵口服液宣肺定喘之功效，探讨其止喘的药理作用和机制。方法：采用喷雾致喘法制备哮喘模型，观察不同剂量止喘灵口服液的引喘潜伏期；体外实验观察止喘灵口服液对豚鼠离体气管和回肠平滑肌的收缩以及气管容积和肺支气管灌流量的影响。结果：止喘灵口服液能显延长乙酰胆碱组胺混合刺激所致豚鼠哮喘的引喘潜伏期，对抗乙酰胆碱或组胺对豚鼠离体支气管或回肠平滑肌有收缩作用，并可增加气管容积和离体肺支气管灌流量。结论：止喘灵口服液对胆碱能神经递质乙酰胆碱或肥大细胞炎性介质组胺所致的气道高反应性和通气障碍都有明显的对抗作用，缓解支气管平滑肌痉挛，改善肺通气功能，从而达到止咳平喘的效果。     

沙丁胺醇喷雾剂对致敏豚鼠和大鼠气管平滑肌痉挛的显效关系研究

目的:研究沙丁胺醇喷雾剂对过敏性支气管平滑肌痉挛的缓解作用。方法:采用离体气管法和肺溢流法观察沙丁胺醇喷雾剂对致敏豚鼠和大鼠的支气管平滑肌痉挛的缓解作用,采用整体动物药物引喘法观察沙丁胺醇喷雾剂对致敏豚鼠过敏性哮喘保护作用。结果:沙丁胺醇10-6molL、3×10-6molL、10-5molL剂量下,对致敏豚鼠离体气管平滑肌收缩有抑制作用;0.2mgkg、0.4mgkg、0.8mgkg沙丁胺醇对致敏麻醉大鼠肺溢流量具有抑制作用;该剂量下沙丁胺醇对致敏豚鼠过敏性哮喘有保护作用,均产生显著性差异。结论:沙丁胺醇喷雾剂对致敏豚鼠离体气管平滑肌有松弛作用,明显延长组织胺与乙酰胆碱致敏豚鼠引喘潜伏期,减少致敏麻醉大鼠的肺溢流量。     

蚯蚓总蛋白对豚鼠哮喘模型肺功能的影响

目的 研究蚯蚓总蛋白(Eisenia foetida protein,EP)对豚鼠哮喘模型支气管平滑肌收缩功能的影响,初步分析其作用机制.方法以新鲜赤子爱胜蚓为原料,经硫酸铵沉淀得到EP.采用经典的肺阻力(RL)和动态肺顺应性(Cdyn)指标评价EP对致敏豚鼠抗原攻击前后的肺功能变化;采用体外试验观察EP对豚鼠的离体气管平滑肌静息张力以及拮抗组胺、氨甲酰胆碱和白三烯引起的收缩反应.结果在整体试验中,EP10 g·kg-1(生药量,po)或EP5g·kg-1(生药量,im)预处理能明显抑制致敏豚鼠抗原攻击后引起的RL增加和Cdyn下降;在离体试验中,EP对离体豚鼠气管平滑肌静息张力无显著影响,对组胺或氨甲酰胆碱引起的气管平滑肌收缩反应无明显拮抗作用,但对白三烯D4引起的收缩反应呈现非常显著的拮抗作用(P<0.01).结论 EP抑制豚鼠哮喘模型肺功能下降可能与抗白三烯作用有关.     

硝普钠平作喘用的观察

确普钠能直接松驰豚鼠离体气管平滑肌;能非竞争性拮抗组胺引起的豚鼠离体肺条收缩;对组胺诱发的豚鼠肺条收缩有解痉作用;气雾吸入或吞下给药对豚鼠药物性哮喘有保护作用;气雾吸入对猪蛔虫蛋白抗原诱发的犬过敏性哮喘具有保护作用。确普钠能提高豚鼠离体气管平滑肌cAMP的含量,这可能是它平喘作用的机制。     

瘤果黑种草子挥发油平喘作用的研究

目的研究瘤果黑种草子挥发油平喘作用及其机制。方法采用整体动物喷雾致喘实验观察瘤果黑种草子挥发油的平喘作用;通过豚鼠肺支气管灌流法及离体回肠实验考察对气道平滑肌的舒张作用。结果低、高剂量(0.1和0.4mL·kg-1)瘤果黑种草子挥发油可明显延长小鼠哮喘反应的潜伏期,与对照组比较,差异具有统计学意义(P<0.01);低、中、高剂量(3,6和12μL·mL-1)挥发油明显增加豚鼠肺灌流量,降低豚鼠回肠平滑肌收缩张力,与对照组比较,差异具有统计学意义(P<0.01)。结论瘤果黑种草子挥发油具有一定的平喘作用,其作用机制可能与激动β2受体、拮抗M受体有关。     

辛夷挥发油的抗过敏实验研究

目的：研究辛夷挥发油的抗过敏作用。方法：采用磷酸组织胺（HA）、氯化乙醇胆碱（Ach）所致豚鼠离体回肠收缩实验，卵白蛋白（OA）引起的致敏豚鼠离体回肠实验及大鼠肥大细胞脱颗粒实验法。结果：辛夷挥发油能显著抑制HA、Ach引起的豚鼠离体回肠收缩，对致敏豚鼠离体回肠的过敏性收缩有较强的抑制作用，并能明显阻止大鼠肥大细胞脱颗粒。结论：辛夷挥发油具有较强的抗过敏作用。     

Effect of procaterol on the isolated airway smooth muscle and the release of anaphylactic chemical mediators from the isolated lung fragments.

The effects of an orally active and selective beta 2-stimulant, procaterol (OPC-2009) on the isolated pulmonary smooth muscle and the release of chemical mediators from the passively sensitized lung fragments were studied and compared with those of isoprenaline (isoproterenol) and salbutamol. Procaterol potently relaxed the isolated guinea pig trachea and lung parenchyma in a concentration-dependent fashion. The drug at a similar range of concentrations antagonized the contraction of the isolated guinea pig trachea and lung parenchyma or human bronchus induced by leukotriene (LT) D4. Salbutamol and isoprenaline also showed similar effects to those of procaterol on the above experiments, but the potencies were consistently weaker than that of procaterol. The release of either histamine or LTs from the passively sensitized human lung fragments was markedly and dose-dependently inhibited by both the 5 min and 15 h treatment with procaterol (10(-10)-10(-7) mol/l) before antigen challenge. Isoprenaline and salbutamol in 5 min treatment experiments showed similar potency as and less potency than procaterol, respectively, on the release of these mediators, but the inhibition potencies of these drugs, particularly isoprenaline, were remarkably reduced by 15 h treatment. From these results, procaterol, besides the existing use as a bronchodilator, is expected to be a potentially prophylactic drug for allergic asthma because of the strong inhibition of the anaphylactic mediator release.     

马布特罗对豚鼠支气管平滑肌松弛作用和平喘作用的影响

目的 :观察马布特罗对豚鼠的平喘作用和离体豚鼠支气管平滑肌的松弛作用。方法 :用 2 %氯化乙酰胆碱和 0 .1 %组胺等容积混合液喷雾诱发哮喘 ,观察马布特罗 (0 .0 6～ 1mg·kg-1)平喘作用的半数有效量(ED50 )及对引喘潜伏期的影响。用离体豚鼠肺支气管灌流法观察马布特罗 (1 0 -9,1 0 -7,1 0 -3 kg·L-1)对组胺 1 0 -4kg·L-1引起肺支气管灌流量减少的影响。结果 :马布特罗对致痉剂诱发豚鼠哮喘有明显抑制作用 ,减少哮喘诱发抽搐动物数 ,其ED50 为 0 .2mg·kg-1及 95 %可信限为 0 .0 8～0 .49mg·kg-1;马布特罗可剂量依赖性对抗组胺减少肺支气管灌流量作用 ,并显著缩短组胺灌流达固定流量时间。结论 :马布特罗对药物致豚鼠哮喘具有明显平喘作用 ,此作用与其松弛支气管平滑肌作用有关。     

Effect of AS-35 on agonist-induced contractions and the resting tonus of airway smooth muscles and the in vitro release of chemical mediators from passively sensitized lung fragments from humans and guinea pigs.

Effects of 9-[(4-acetyl-3-hydroxy-2-n-propylphenoxy)methyl]-3-(1H-tetrazol -5-yl)-4H-pyrido[1,2-alpha]pyrimidin-4-one (AS-35) on the resting tonus or contractions induced by agonists, such as leukotriene (LT) D4 and specific antigen of isolated guinea pig tracheas or human bronchi, and the in vitro anaphylactic release of histamine and LTs from human lung fragments were investigated and compared with the effects of FPL 55712 and disodium cromoglycate. AS-35 as well as FPL 55712 did not affect the contractions induced by acetylcholine and histamine of the isolated guinea pig trachea. However, the compound at relatively low concentrations obviously inhibited contractions induced by LTD4, and the antagonistic activity was stronger than that of FPL 55712. Treatment of the isolated human bronchus with AS-35 tended to induce the inhibition of both LTD4- and antigen-induced contractions and the relaxation of the resting tonus in a concentration-dependent manner. The inhibitory potency at 10(-6) g/ml was slightly stronger than that of FPL 55712, but this was not statistically significant. The anaphylactic release of histamine and LTs from the lung fragments appeared to be inhibited by the treatment with AS-35 5 min prior to the antigen challenge. From these results, it is suggested that AS-35 is effective against allergic asthma through antagonism towards peptide-LTs released anaphylactically in addition to inhibition of the chemical mediator release.     

Effects of the new antiallergic drug 11-oxo-11H-pyrido[2,1-b] quinazoline-2-carboxylic acid on type I allergic reactions

Antiallergic effects of the newly synthesized, quinazoline derivative 11-oxo-11H-pyrido[2,1-b]quinazoline-2-carboxylic acid (Sm 857) were investigated. The following results were obtained. 1. Anaphylactic and non-immunologic histamine and slow reacting substance of anaphylaxis (SRS-A) release from guinea pig lung fragments was dose-dependently inhibited by 10(-6)-10(-4) and 10(-7) -10(-4) g/ml of Sm 857, respectively. Similar inhibition of the mediator release by the compound was obtained from the experiments of passively sensitized monkey and human lung fragments by antigen. 2. Seven-day passive cutaneous anaphylaxis of guinea pigs was not inhibited at 1-20 mg/kg (i.v.) of Sm 857, but inhibited at 20-100 mg/kg (p.o.) in some experiments without dose dependency. 3. Cutaneous anaphylaxis and histamine-induced cutaneous reaction in guinea pigs were hardly affected by the treatment of 50 and 100 mg/kg (p.o.) of Sm 857. 4. Passive systemic anaphylaxis in guinea pigs was not inhibited at 50-200 mg/kg (p.o.) of Sm 857. 5. Arthus reaction in rabbits was slightly and dose-dependently enhanced at 50-200 mg/kg given twice p.o. 6. Sm 857 (10(-6)-10(-4) g/ml) exhibited antispasmogenic activity against histamine and leukotriene D4 in isolated human bronchi and guinea pig trachea, however, this activity is attributable to non-specific musculotropic smooth muscle relaxation. From these results it may be concluded that Sm 857 exerts preferential effect on the respiratory system and that it might be useful in allergic asthma.     

葛缕酮的气道扩张作用和呼吸道抗过敏作用

目的观察留兰香油中葛缕酮的气道扩张作用和对呼吸道介质的影响。方法用豚鼠药物引喘法、豚鼠离体气管片法、致敏豚鼠肺组织ＳＲＳ Ａ释放和拮抗ＳＲＳ Ａ、致敏豚鼠离体气管Ｓｃｈｕｌｔｚ Ｄａｌｅ反应法检测。结果葛缕酮对豚鼠药物性哮喘具有保护作用,灌胃给药延长５０％剂量为７６ｍｇ·ｋｇ－１,气雾给药为６３ｇ·Ｌ－１;对豚鼠离体气管有直接松弛作用,ｐＤ２值为４２７±００８,并有抗氨甲酰胆碱作用;能抑制致敏豚鼠肺组织ＳＲＳ Ａ的释放,ＩＣ５０为１８ｍｇ·Ｌ－１,拮抗ＳＲＳ Ａ收缩回肠的ＩＣ５０为２７ｍｇ·Ｌ－１,并能抑制致敏豚鼠离体气管的Ｓｃｈｕｌｔｚ Ｄａｌｅ反应。结论葛缕酮具有气道扩张作用和呼吸道抗过敏作用。