海群生对豚鼠离体气管条平滑肌收缩的影响

目的研究海群生（枸橼酸乙胺嗪,ＤＥＣ）对豚鼠离体气管条平滑肌收缩反应的影响及其作用机制。方法取气管条放入３７℃浴管的Ｋｒｅｂｓ溶液中,分别在浴液中加入药物,测定ＫＣＩ和５－羟色胺（５－ＨＴ）收缩气管条的作用和量效反应以及ＤＥＣ和维拉帕米对ＫＣｌ和５－ＨＴ作用的影响。结果ＤＥＣ能使ＫＣＩ或５－ＨＴ引起的气管条平滑肌收缩显著抑制,其ＩＣ５０值分别为５．０３ｍｍｏｌ·Ｌ－１和９．５４ｍｍｏｌ·Ｌ－１,与维拉帕米的作用相似。ＤＥＣ使ＫＣｌ和５－ＨＴ的量效曲线右移,最大反应降低,呈非竞争性拮抗,其ｐＤ２值分别为１．５５４和１．８５１,并对细胞内Ｃａ２＋释放和细胞外Ｃａ２＋内流引起的收缩有抑制作用。结论ＤＥＣ可抑制ＫＣｌ和５－ＨＴ引起的气管条平滑肌收缩,其机制可能是通过其钙拮抗作用所致。     

豚鼠离体气管平滑肌舒缩性压力测量法

离体气管平滑肌舒缩性的检测是许多相关实验研究所必须具备的方法。传统的检测方法主要包括有气管片法、气管环法、气管螺旋条法和气管容积法等[1～ 3] ,这些方法都分别具有操作复杂 ,灵敏度较低 ,记录曲线粗略 ,破坏气管完整性等不足 ,为克服上述缺点 ,本实验室试用测压法检测完整离体气管平滑肌舒缩功能 ,获得比较满意的结果。1　材料与方法动物用豚鼠 ,♀♂不拘 ,体重 3 5 0～ 4 5 0ｇ。击其后脑至昏 ,立即剖开颈部 ,取出 2～ 3ｃｍ完整气管段 ,放入充氧克氏液中 ,剥去外附组织 ,克氏液冲净管腔。取两根直径为 2 5～ 3 5ｍｍ的塑料管分…     

硝普钠在豚鼠离体气管螺旋条中的舒张作用

目的研究硝普钠(SNP)在豚鼠离体气管螺旋条中舒张作用的机制.方法在浴槽内加入硝普钠从10-7M至10-3M,观察气管螺旋条张力的变化,并检测浴槽中NO,气管螺旋条组织cAMP、cGMP的变化.结果加入硝普钠气管螺旋条张力下降,浴槽内NO增加,气管螺旋条组织cAMP、cGMP增加.结论硝普钠有舒张气管螺旋条的作用,推测是通过NO-cGMP系统发挥作用.     

鸭嘴花碱对豚鼠离体气管平滑肌收缩功能的影响

目的：研究鸭嘴花碱对组胺和乙酰胆碱所致气管收缩的抑制作用。方法：离体豚鼠气管条。结果：鸭嘴花碱能抑制氯化钾、乙酰胆碱、磷酸组胺所致气管平滑肌收缩，而且能使磷酸组胺、乙酰胆碱收缩气管平滑肌的量效曲线右移，并抑制最大效应，其作用为剂量依赖性。结论：鸭嘴花碱对气管平滑肌具有显著舒张作用。     

硝普钠在豚鼠离体气管螺旋条中的舒张作用

目的:研究硝普钠(SNP) 在豚鼠离体气管螺旋条中舒张作用的机制.方法:在浴槽内加入硝普钠从10-7M至10-3M,观察气管螺旋条张力的变化,并检测浴槽中NO,气管螺旋条组织cAMP、cGMP的变化.结果:加入硝普钠气管螺旋条张力下降,浴槽内NO增加,气管螺旋条组织cAMP、cGMP增加.结论:硝普钠有舒张气管螺旋条的作用,推测是通过NO-cGMP系统发挥作用.     

左旋沙丁胺醇抑制豚鼠气道平滑肌收缩的实验研究

目的评价左旋沙丁胺醇(R-Salbutamol,R-Sal)对组胺(histamine,His)诱发的豚鼠离体气管条和肺条收缩功能的影响。方法制备豚鼠离体气管条和肺条标本,以定量药理学方法测定10-8、10-7、10-6mol·L-1剂量的R-Sal孵育前后对His诱发的离体标本的收缩反应的舒张作用,并与10-6mol·L-1剂量的Sal进行比较。结果R-Sal可显著抑制His所引起的豚鼠离体气管和肺条的收缩反应,呈剂量依赖性,其作用强于Sal(P<0.01)。结论R-Sal对His诱发的豚鼠离体气管条和肺条的收缩反应具明显的舒张作用。     

硝普钠在豚鼠离体气管螺旋条中的舒张作用

目的：研究硝普钠（SNP）在豚鼠离体气管螺旋条中舒张作用的机制。方法：在浴槽内加入硝普钠从10^-7M至10^-3M,观察气管螺旋条张力的变化,并检测浴槽中NO,气管螺旋条组织cAMP、cGMP的变化。结果：加入硝普钠气管螺旋条张力下降,浴槽内NO增加,气管螺旋条组织cAMP、cGMP增加。结论：硝普钠有舒张气管螺旋条的作用,推测是通过NO-cGMP系统发挥作用。     

异甘草素对豚鼠离体气管平滑肌收缩功能的影响

异甘草素(isoliquiritigenin,ISL)是从甘草中提取出的一种黄酮类化合物.本文观察了ISL对豚鼠离体气管条张力的影响,旨在为其治疗支气管哮喘等呼吸道疾病提供实验依据.     

灯盏花素对离体豚鼠肺间质条平滑肌的松弛作用

目的:观察灯盏花素对豚鼠离体静息肺间质条的松弛作用及对组胺诱发的离体肺间质条平滑肌收缩的影响,并与溴化异丙托品及沙丁胺醇比较。方法:采用定量药理分析方法测定和记录灯盏花素、溴化异丙托品及沙丁胺醇孵育前后豚鼠肺间质条的影响。结果:灯盏花素、溴化异丙托品及沙丁胺醇对豚鼠离体肺间质条均产生了明显的松弛作用,并拮抗了组胺诱导的豚鼠肺间质条的收缩。结论:灯盏花素对离体豚鼠肺间质条有松弛作用,并能拮抗组胺诱导的肺间质条收缩,提示可用于临床治疗气道阻塞性疾病。     

Effect of Montelukast on bradykinin-induced contraction of isolated tracheal smooth muscle of guinea pig

Aim:

To explore the effect of montelukast on bradykinin-induced tracheal smooth muscle contraction of isolated guinea pig trachea.

Study Design:

To study the effect of bradykinin in the absence and in the presence of montelukast on the isolated tracheal smooth muscle of a guinea pig pretreated with indomethacin (10^-6M), phentolamine (10^-5M), and propranalol (10^-6M), to eliminate the effect of endogenous prostaglandins and catecholamines. The trachealis smooth muscle activity was recorded through the Isometric Force Displacement Transducer on a Four Channel Oscillograph. A cumulative dose-response relationship was demonstrated by adding successive doses of bradykinin on the tracheal strips, starting with 11 μg to 77 μg of 10^-4 concentration. A similar procedure was repeated in the presence of montelukast 0.5 μg/ml, which, was equal to approximate C_max achieved in vivo with a 10 mg oral dose of montelukast, and in the presence of 1 μg/ml of montelukast.

Statistical Analysis:

Data was expressed as mean ± standard error (SEM), and was analyzed using the SPSS version 15. A P value of less than 0.05 was considered significant.

Results:

Bradykinin produced a dose-dependent, reversible contraction of isolated tracheal smooth muscle. Montelukast significantly reduced the bradykinin-induced tracheal smooth muscle reactivity and shifted the bradykinin curve to the right and downwards, in the presence of both concentrations of montelukast. The mean magnitude of response achieved with 77 μg of bradykinin in the absence of montelukast was 39 mm ± 6.26, in the presence of 0.5 μg/ml of montelukast it was 24.17 mm ± 4.11, and in the presence of 1 μg/ml of montelukast it was 13 mm ± 2.6.

Conclusion:

It is concluded that montelukast significantly inhibits, in a dose-dependent manner, the bradykinin-induced contraction of the guinea pig tracheal smooth muscle, and alludes to an interaction between the bradykinin and leukotriene mediators.     

尼卡地平在异丙肾上腺素扩张气管中的作用

目的:探讨尼卡地平(Nic)对异丙肾上腺素(Iso)舒张气管的增强作用.方法:在豚鼠离体气管上观察Nic对Iso的增强作用,并与Nic对茶碱(Theo)和硝普钠(SNP)的作用进行比较.结果;(1)Nic能增强Iso豚鼠离体气管的舒张作用.此增强作用具剂量依赖性.表现在Iso量-效曲线随Nic剂量增高而逐渐左移;(2)Theo浓度大于Nic1000倍时,也增强Iso的作用;(3)相同条件下,SNP合用Nic或Theo后对SNP引起的气管舒张无增强作用.结论:Nic和Theo一样,可能通过抑制磷酸二酯酶而增高Iso对气管平滑肌的舒张作用.     

Relaxant effects of aflatoxins on isolated guinea pig trachea.

Dyspnea is one of the symptoms of acute aflatoxicosis. Contrary to expectations, we observed that naturally occurring aflatoxins (AF) AFB(1), AFB(2), AFG(1), and AFG(2) and their major metabolites AFM(1), AFM(2), AFP(1), AFQ(1), and AFG(2a) relaxed carbachol (C) precontracted guinea pig trachea to different degrees. The efficacies but not the potencies of AFB(1), AFB(2), AFG(1), and AFG(2) were similar to that of the beta-agonist, isoprenaline, whose activity was potentiated by the AF. Their mechanism of action is not clearly understood but several mechanistic indications were obtained with AFB(1): 1) its effect was not influenced by the beta-blocker, timolol, indicating that a direct interaction with beta(2)-adrenergic receptors was not involved. 2) AFB(1) potentiated PGE(1) and PGE(2), two relaxant prostaglandins, and its activity was reduced by indomethacin. 3) The cAMP level in the guinea pig trachea relaxed by AFB(1) increased, possibly due to inhibition of phosphodiesterase; direct interaction with PG receptors; and/or interaction with A(2) adenosinic receptors, suggested by the inhibitory activity of XAC, a specific antagonist. 4) Finally, since tetrodotoxin reduced the relaxant activity of AFB(1), it is speculated that this mycotoxin could stimulate inhibitory nonadrenergic, noncholinergic nerves (i-NANC). In conclusion, the symptoms of acute aflatoxicosis do not seem to be due to a direct activity on the tracheal muscle, but rather, to the well-known pro-inflammatory activity of the aflatoxins, which are capable of releasing arachidonic acid from cell membranes.     

黄体酮对离体豚鼠呼吸道平滑肌的作用

黄体酮能明显抑制由乙酰胆碱、组织胺和5—羟色胺所致的离体豚鼠气管、肺条平滑肌的收缩反应,对由5—羟色胺诱发的气管平滑肌依内钙释放引起的！相收缩有非常显著的抑制作用,并能抑制致敏豚鼠气管平滑肌schultZ—Dale反应.关键词黄体酮,维拉帕米,慢反应物质,呼吸道平滑肌     

Role of potassium channels in the relaxant effect of levosimendan in guinea pig tracheal preparations

We investigated both the effect of levosimendan and the role of various potassium channels in carbachol-precontracted tracheal preparations samples obtained from guinea pig. The tracheas were cut into 0.5 cm wide rings and suspended in a 20 ml organ bath. Isometric tension was continuously measured with an isometric force transducer connected to a computer-based data acquisition system. Levosimendan or cromakalim produced concentration-dependent relaxation responses in guinea pig tracheal rings precontracted by carbachol. Incubation of guinea pig tracheal rings with the ATP-dependent potassium channel (K_ATP) blocker glibenclamide for 30 min significantly inhibited the relaxant responses to both levosimendan and cromakalim. The large conductance Ca²⁺-activated potassium channel (BK_Ca) blocker iberiotoxin also caused a significant inhibition on relaxant responses to levosimendan. However, incubation of the tracheal rings with the voltage-dependent potassium channel blocker 4-aminopyridine for 10 min did not cause significant alterations on relaxant responses to levosimendan. The present findings suggested that the relaxant effect induced by levosimendan might be partially due to K_ATP and BKCa in isolated guinea pig tracheal rings.     

蒙药紫花高乌头醇提物对豚鼠离体气管平滑肌的作用及机制

目的观察蒙药紫花高乌头醇提物对豚鼠离体气管平滑肌张力的影响,探讨紫花高乌头醇提物的平喘机制。方法用离体气管环法观察紫花高乌头醇提物高、中、低3种不同剂量作用于由乙酰胆碱(Ach)预收缩的豚鼠离体气管平滑肌,观察其对平滑肌张力的影响及对Ach诱发的离体气管平滑肌收缩的量效曲线的影响。结果蒙药紫花高乌头醇提物可舒张由Ach诱发的豚鼠离体气管平滑肌收缩,且舒张作用随剂量增加而加强。紫花高乌头醇提物能使Ach诱发的豚鼠离体气管平滑肌收缩效应的量效曲线右移,最大效能降低。结论蒙药紫花高乌头醇提物对豚鼠离体气管平滑肌有舒张作用,可能与非竞争性拮抗Ach的收缩作用有关。     

绞股蓝总皂甙对豚鼠心肌氧自由基损伤的保护作用

用黄嘌呤—黄嘌呤氧化酶(X—XOD)诱发豚鼠心乳头肌氧自由基损伤,观察绞股蓝总皂甙(CPS)抗心肌氧化损伤的作用.结果示在X—XOD作用下,乳头肌收缩力先升高后降低,功能不应期缩短,兴奋性提高,肾上腺素诱发的自律性增加,心肌中超氧化物歧化酶活性降低,而脂质过氧化物丙二醛(MDA)含量升高.先给GPS 50mg·L~(-1),再给X—XOD,乳头肌收缩高峰推迟,并抑制其负性肌力作用,同时,逆转X—XOD所致的乳头肌不应期、兴奋性与自律性的改变.心肌组织中MDA含量均得以回复.提示,GPS对豚鼠心肌的氧化损伤具有保护作用.     

花椒毒酚对豚鼠离体心房肌生理特性的影响

目的 :研究花椒毒酚对豚鼠离体心肌生理特性的影响。方法 :采用豚鼠离体心房 ,测定花椒毒酚对豚鼠心房率 ,心肌收缩力 ,左心房的兴奋性的影响。结果 :在心肌收缩力的实验中 ,给花椒毒酚 2 0 ,4 0 ,80 μmol·L-115min后 ,左心房的收缩力分别为0 .85、0 .6 8、0 .4 8g ,与对照组比较 ,花椒毒酚明显抑制豚鼠左心房肌的收缩力 (P <0 .0 5 ) ,并呈浓度依赖性 ;在对心房率的实验中 ,给花椒毒酚 2 0 ,4 0 μmol·L-1,30min后 ,离体右心房的频率从90 .0次·min-1分别下降至 6 0 .2、38.7次·min-1,与对照组比较有显著的统计学意义 (P <0 .0 5 ) ;花椒毒酚对豚鼠左心房的功能性不应期和左心房兴奋性无明显影响。结论 :花椒毒酚可以降低心房自律性、抑制心房收缩力 ,其负性变频和负性变力效应可能与其抑制心肌细胞外钙内流和内钙释放有关。     

豚鼠气管平滑肌细胞钾离子通道动力学特性及对拮抗剂的敏感性

钾离子通道功能与细胞的兴奋性有关，在豚鼠支气管平滑肌细胞膜上，用膜片钳技术证实了一类电压依赖性钾通道的存在，该通道电导为７５±５ｐＳ，翻转电位为－７３±８ｍＶ．动力学特性显示，通道开放时程分布直方图符合双指数拟合．其中τ０２随去极化程度增大而增大．通道开放概率有明显的电压依赖性．该类通道可被四乙胺从膜的内，外侧面阻断，对４－氨基吡啶不敏感．可被铯离子阻断，通道活动与细胞内钙水平降低无关．提示钾离子通道特性在不同组织细胞上有差异．