肾上腺髓质素对组胺诱发气道痉挛的作用

目的观察肾上腺髓质素（ＡＭ）对组胺诱发麻醉豚鼠气道痉挛的影响。方法实验分为生理盐水对照组、异丙肾上腺素０．０３μｇ／ｋｇ、０．３μｇ／ｋｇ、３μｇ／ｋｇ、３０μｇ／ｋｇ四个剂量组及ＡＭ０．０２μｇ／ｋｇ、０．２μｇ／ｋｇ、２μｇ／ｋｇ、２０μｇ／ｋｇ四个剂量组，每组豚鼠７只，戊巴比妥钠麻醉状态下，分别静脉注射生理盐水、不同剂量的异丙肾上腺素和ＡＭ，同时组胺（１０－４ｍｏｌ／Ｌ）雾化吸入，采用动物体描箱测定豚鼠气道阻力和肺顺应性。结果异丙肾上腺素０．３μｇ／ｋｇ、３μｇ／ｋｇ和３０μｇ／ｋｇ剂量下能明显拮抗组胺诱导的豚鼠气道阻力增加和肺顺应性降低（Ｐ＜０．０５）。ＡＭ２μｇ／ｋｇ、２０μｇ／ｋｇ剂量下能明显拮抗组胺诱导的气道阻力增加，０．２μｇ／ｋｇ、２μｇ／ｋｇ，２０μｇ／ｋｇ剂量下能明显拮抗组胺诱导的肺顺应性降低（Ｐ＜０．０５）。结论ＡＭ具有拮抗组胺诱发豚鼠气道痉挛的作用。     

气道组胺H2受体与哮喘发病机理关系的动物实验研究

报告（１）１０＾－６ｍｏｌ／Ｌ甲双咪胍能舒张预先用组胺诱发收缩的豚鼠气管螺旋条，用１０＾－６ｍｏｌ／Ｌ甲双咪胍预处理可使各浓度组胺诱发螺旋条最大收缩力降低、组胺累积剂量反应曲线右移。（２）地麻普利（３ｍｇ／ｋｇ）静脉注射对抗原激发引起的豚鼠肺功能降低有保护作用。提示组胺Ｈ２受体（Ｈ２Ｒ）参与气道平滑肌舒张，并通过抑制变态反应中炎性介质的释放而改善肺功能，从而在哮喘发病中起一定保护作用。     

兴安杜鹃挥发油抗气道变应性炎症的研究

目的 探讨兴安杜鹃挥发油对小鼠气道变应性炎症的治疗。方法 对昆明小鼠采用超声雾化吸入１％卵清蛋白生理盐水致敏，建立小鼠气道变应性炎症模型，检测并比较各组间肺组胺浓度及肺组织病理学变化。结果 治疗组模型组肺组胺浓度差异显著（Ｐ〈０．０５），肺组织病理学变化表明，治疗组模型组有明显恢复，与正常对照组接近。结论 兴安杜鹃挥发油具有明显的抗炎、平喘作用。     

哮喘气道炎症粘附机制的实验研究

目的评价细胞间粘附分子１（ＩＣＡＭ１）、Ｐ选择素在哮喘气道炎症粘附机制中的作用,进一步阐明哮喘的发病机理。方法用酶联免疫吸附试验、肺组织免疫组化检查和呼吸生理学方法系统观察正常组和哮喘组豚鼠各项指标。结果（１）哮喘组豚鼠肺潮气量、动态肺顺应性（Ｃｄｙｎ）和肺气道阻力与对照组比较差异有显著性（Ｐ＜０．０１及Ｐ＜０．０５）。（２）哮喘组豚鼠血浆和肺泡灌洗液（ＢＡＬＦ）可溶性ＩＣＡＭ１（ｓＩＣＡＭ１）、可溶性Ｐ选择素、血清和ＢＡＬＦ嗜酸粒细胞阳离子蛋白（ＥＣＰ）与对照组比较,差异有显著性（Ｐ＜０．０１）;ＢＡＬＦ中白细胞介素８（ＩＬ８）与对照组比较差异也有显著性（Ｐ＜０．０１）。（３）哮喘组豚鼠肺组织（气道上皮和血管内皮）ＩＣＡＭ１和ＩＬ８表达与对照组比较,差异有显著性（Ｐ＜０．０１）。结论ＩＣＡＭ１、Ｐ选择素、ＩＬ８、ＥＣＰ参与介导了哮喘气道炎症的粘附过程     

白细胞介素—8与豚鼠气道高反应性关系探讨

目的探讨白介素－８（ＩＬ－８）与哮喘气道高反应性（ＡＨＲ）产生的关系。方法经鼻腔给予豚鼠ＩＬ－８（０．５μｇ／ｋｇ或５μｇ／ｋｇ）３周，每周２次，在最后一次给予后２４小时，测定动物气道对吸入不同浓度组织胺（２５、５０、１００或２００μｇ／ｍｌ）的反应性；对支气管肺泡灌洗液（ＢＡＬＦ）中各种细胞成分计数；光镜下观察气道及肺组织的病理改变。结果豚鼠经ＩＬ－８处理后，其气道内压随吸入组织胺浓度的升高而增加，与对照组比较差异有显著性（Ｐ＜０．０５或０．０１）；ＢＡＬＦ中中性粒细胞数较对照组明显增多（Ｐ＜０．０１），而嗜酸性细胞减少（Ｐ＜０．０５）；气管、支气管粘膜及管壁周围有大量中性粒细胞浸润，对照组无此改变。结论ＩＬ－８能引起气道中性粒细胞炎症，同时伴有ＡＨＲ的产生，推测ＩＬ－８在哮喘ＡＨＲ的产生中起着重要作用。     

内源性一氧化氮在哮喘大鼠气道高反应性中的作用

目的　利用一氧化氮合成前体Ｌ精氨酸（ＬＡｒｇ） 和一氧化氮合酶抑制剂亚硝基Ｌ精氨酸甲酯（ＬＮＡＭＥ）研究内源性一氧化氮在哮喘大鼠气道高反应性中的作用,探讨支气管哮喘的发病机制。方法　用卵白蛋白作为致敏原制备哮喘大鼠模型,建立大鼠离体气管环张力的测定方法,并用ＬＡｒｇ、ＬＮＡＭＥ和ＬＡｒｇ＋ ＬＮＡＭＥ孵育离体气管环,观察气管环乙酰胆碱浓度反应曲线和最大收缩反应的变化,同时观察去上皮对哮喘大鼠气道反应性的影响。结果　哮喘大鼠（１０ 只） 离体气管环经ＬＮＡＭＥ１０５ ｍｏｌ／Ｌ孵育后对乙酰胆碱的最大收缩反应从孵育前（１２４±３９） ｍｇ 上升到（１８７ ±５３） ｍｇ,孵育前、后最大收缩反应比较差异具有显著性（ Ｐ＜ ０．０１）,浓度反应曲线上移,而ＬＡｒｇ 可以逆转ＬＮＡＭＥ的作用,单用ＬＡｒｇ ２×１０５ ｍｏｌ／Ｌ和ＬＡｒｇ１０３ ｍｏｌ／Ｌ孵育气管环,对哮喘大鼠气管环的最大收缩反应和浓度反应曲线与对照组比较,差异无显著性（ Ｐ＞ ０．０５） 。去上皮哮喘大鼠气管环的反应性与上皮完整气管环比较差异有显著性（ Ｐ＜ ０．００５） ,而ＬＡｒｇ、ＬＮＡＭＥ＋ ＬＡｒｇ 和ＬＮＡＭＥ孵育去上     

异丙肾上腺素超声负荷试验对二尖瓣球囊扩张术后疗效的评价

目的对２４例二尖瓣狭窄患者行球囊扩张术前后作异丙肾上腺素超声心动负荷试验，拟进一步评价经皮穿刺二尖瓣球囊扩张术的疗效。方法在患者安静休息的基础心率及应用异丙肾上腺素静脉点滴后不同心率状态下测定二尖瓣口面积（ＭＶＡ）、二尖瓣跨瓣压差（ＭＶＧ）及心排血量（ＣＯ）。结果二尖瓣球囊扩张使得静息状态下的瓣口面积（０．９１±０．２８升至１．８７±０．２３ｃｍ２，Ｐ＜０．０１），跨瓣压差（１２．５±６．３降至３．９±１．９ｍｍＨｇ，Ｐ＜０．０５），及心排血量（３．９３±１．４４升至４．７３±１．０１ｌ／ｍｉｎ，Ｐ＜０．０５）发生明显变化。在球囊扩张前做异丙肾上腺素试验时，虽然随着心率加快，跨瓣压差明显升高（Ｐ＜０．０１），但瓣口面积及心排血量并无显著改善（Ｐ＞０．０５）。但球囊扩张术后再做异丙肾上腺素试验时，随着心率加快，跨瓣压差升高，瓣口面积（从１．８５±０．４８升至２．３２±０．３６ｃｍ２，Ｐ＜０．０１）及心排血量（从４．４８±１．９８升至７．５５±１．９０Ｌ／ｍｉｎ，Ｐ＜０．０１）均明显进一步改善。结论异丙肾上腺素超声负荷试验能进一步评价二尖瓣球囊扩张术后的贮备功能，且该法安全、重复性强     

郁金对实验性高脂血症动物血脂含量的影响

以鹌鹑为实验动物，用高脂食饵法复制高脂血症模型，观察中药郁金对血脂的影响，并与“安妥明”进行对比。实验结果：郁金组、安妥明组血清胆固醇、甘油三脂含量均显著低于高脂对照组（Ｐ＜０．０１～０．０５）。郁金与安妥明组组间胆固醇、甘油三酯下降幅度差异无显著性（Ｐ＞０．０５），安妥明组实验动物头、背部出现圆形脱毛区，郁金组无这一现象发生，且郁金组血清低密度脂蛋白含量亦低于高脂对照组（Ｐ＜０．０５），同时血清中高密度脂蛋白含量也呈升高趋势，但差异无显著性（Ｐ＞０．０５）。提示郁金对血脂有调整作用，且可减轻高脂动物的体重     

强迫振荡肺功能测定新技术及临床研究

目的探讨强迫振荡肺功能测定在正常人、慢性阻塞性肺疾病、哮喘、肺纤维化等患者中气道阻力和相位角的变化规律以及哮喘患者吸入支气管舒张剂前、后肺功能的变化。方法使用德国Ｃｕｓｔｏｖｉｔｍ强迫振荡设备，测定各患者组气道阻力和相位角，然后分别和正常组进行统计学比较；哮喘患者吸入间羟舒喘宁前、后气道阻力改善率与一秒钟用力呼气容积（ＦＥＶ１）和流速容量（ＦＶ）曲线测定改善率比较。结果慢性阻塞性肺疾患和哮喘组气道阻力值与正常组比较差异有显著性（Ｐ＜０．０５）及显著频率依赖性（Ｐ＜０．０５）；各病种组相位角与正常组比较差异有显著性（Ｐ＜０．０５），且肺纤维化患者仅表现为相位角降低；哮喘患者吸入间羟舒喘宁后气道阻力改善率与ＦＥＶ１和ＦＶ曲线改善率比较差异有显著性（Ｐ＜０．０５）。结论强迫振荡法是一种简便、快速、无创性测定气道阻力与相位角的新方法，适用于重症慢性阻塞性肺疾病患者，且对哮喘的用药观察优于传统肺功能测定。     

体外循环时气道峰压与胸肺顺应性的变化

应用ＤＡＴＥＸＣａｐｎｏｍａｃＵｌｔｉｍａ－ＳＶ呼吸监测仪连续监测３０例病人体外循环对气道峰压及胸肺顺应性的影响。结果表明，潮气量在各阶段无明显改变，气道峰压于主动脉开放后５～３０分钟明显升高，与术前比较有高度显著性差异（Ｐ＜０．０１），而转流前、阻断前、停机时及术终，气道峰压与术前比较均无显著性差异（Ｐ＞０．０５）。胸肺顺应性降低与气道峰压升高呈相反的趋势（Ｐ＜０．０５），２０分钟时降低最甚，与术前比较有高度显著性差异（Ｐ＜０．０１）。本文就气道峰压与顺应性的改变进行了讨论。     

The protective role of epithelium-derived nitric oxide in isolated bovine trachea

Airway epithelial cells from bovine airways can release relaxant factors such as nitric oxide (NO) and prostaglandin E(2) and the removal of airway epithelium results in an increased responsiveness of smooth muscle to spasmogen stimuli. In this study, we assessed whether or not epithelial NO modulates the contractile response of bovine trachea in vitro.Cumulative concentration-response curves to acetylcholine (ACh), histamine (Hist) and 5-hydroxytryptamine (5-HT) were obtained in both intact and epithelium denuded tracheal strips in the presence of indomethacin (10 microM).In intact, but not in epithelium denuded strips, preincubation with the NO synthase inhibitor L-N((G))-Nitro-arginine methyl ester (L-NAME), but not with D-NAME, shifted to the left the concentration-response curve to ACh (pD(2) values in the absence and in the presence of L-NAME were 3.47+/-0.1 and 4.60+/-0.1, respectively; P<0.05) and to Hist (pD(2) in the absence and in the presence of L-NAME: 3.89+/-0.1 and 4.54+/-0.1, respectively; P<0.05). This effect was reversed by L-arginine (1mM), but not by D-arginine. The contractile response to 5-HT was not affected by L-NAME in either intact or epithelium denuded strips.These data suggest that NO is an epithelial relaxant factor modulating airway cholinergic and histaminergic contraction of bovine trachea and that the activation of the epithelial NO synthase is a mediator-specific process.     

Smooth muscle contraction and release of histamine and slow-reacting substance of anaphylaxis in pulmonary tissues isolated from guinea pigs passively sensitized with IgG1 or IgE antibodies

In previous studies, we have provided evidence that different Fc receptors mediate antigen-induced pulmonary smooth muscle contractile responses after passive sensitization of guinea pigs with IgG1 or IgE antibodies. In this study, we examined the relationship between contraction and release of histamine and slow-reacting substance of anaphylaxis (leukotrienes) in superfused trachea and parenchymal strips as well as mediator release from minced lung fragments after passive sensitization of guinea pigs with IgG1 or IgE antibodies. Guinea pigs were immunized to produce either IgG1 or IgG1 and IgE using oxazolone-guinea-pig albumin or oxazolone-Ascaris plus cyclophosphamide, respectively. The contaminating IgG1 in the IgE-rich serum was removed by passage over a protein A-Sepharose column. Normal guinea pigs were passively sensitized intraperitoneally or intravenously with injections of either IgG1 or IgE 1 or 2 days before in vitro studies. Superfused tissues were challenged with 10(-1) mg/ml antigen (oxazolone-human serum albumin conjugate), and contractions and histamine and leukotriene release were monitored at discrete time intervals thereafter. At equivalent levels of contraction, substantially more histamine and leukotrienes were released from tissues taken from IgG1-sensitized animals. The amounts of histamine released from lung parenchymal strips and trachea in the IgE-sensitized state were approximately 5 and 38%, respectively, of those released from corresponding tissues in the IgG1-sensitized state. The leukotriene release from tissues isolated from IgE-sensitized animals was less than 4% of that released from tissues in the IgG1-sensitized state. Similar differences in mediator release were seen in comparable studies on minced lung fragments.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hyperresponsiveness to autacoids and autonomic drugs in lung parenchymal strips from sensitized guinea pigs

The responsiveness of lung parenchymal strips isolated from actively sensitized guinea pigs to some selected autacoids (histamine, 5-hydroxytryptamine, bradykinin, and prostaglandins F2 alpha and l2) and autonomic drugs (acetylcholine, norepinephrine, methoxamine, and isoprenaline) was compared with that of strips from unsensitized animals. The concentration-response curves to the agonists, with the only exception of isoprenaline, in the sensitized group exhibited a left upward displacement (greater maximal effects and less effective concentration 50%) compared with those obtained in the unsensitized group. These results indicate the existence of a nonspecific increase in responsiveness of lung parenchymal strip isolated from sensitized animals.     

Tracheal responsiveness to both isoprenaline and beta2-adrenoreceptor blockade by propranolol in cigarette smoke exposed and sensitized guinea pigs

OBJECTIVE: Airway hyperresponsiveness is the main feature of asthma and also exists in cigarette smokers. In previous studies we have shown increased airway responsiveness to isoprenaline in asthmatic patients and smokers. In this study, tracheal responsiveness to isoprenaline and beta-adrenergic receptor blockade was investigated in animals exposed to cigarette smoke (AECS) with or without sensitization by ovalbumin (OA). METHODOLOGY: Guinea pigs were exposed to cigarette smoke over a 3-month period with or without sensitization by injection and inhalation of OA. Tracheal responses in AECS, AECS + sensitized and control animals (n = 7 for each group) to isoprenaline in the absence and presence of 20 nmol/L propranolol were measured and EC(50) was established. The propranolol blockade (concentration ratio minus one (CR-1)) was calculated (post-propranolol EC(50)/EC(50)) - 1. RESULTS: The tracheal response of AECS and AECS + sensitized guinea pigs to isoprenaline was significantly higher than that of control animals (EC(50): 4.24 +/- 0.54, 3.66 +/- 0.53 and 7.71 +/- 0.68.79 micromol for AECS, AECS + sensitized and control animals, respectively) (P < 0.001). There was no significant difference in EC(50) between AECS and AECS + sensitized. CR-1 was also significantly higher in the trachea of AECS and AECS + sensitized compared with controls (13.39 +/- 2.22 and 15.35 +/- 2.95 vs. 3.10 +/- 0.6, P < 0.05 in both cases). There was no significant difference in CR-1 between AECS and AECS + sensitized. There was a significant correlation between the tracheal response to isoprenaline (EC(50)) and CR-1 (r =-0.731, P < 0.001). There was no significant difference in tracheal maximum response to isoprenaline between the three groups of animals. CONCLUSIONS: The results of this study indicate an increased tracheal response to a beta(2)-adrenergic stimulating drug and enhanced beta(2)-adrenergic blockade by propranolol in both AECS and AECS + sensitized. These results suggest similar increase in airway responsiveness to beta(2)-adrenergic agonists and beta(2)-receptor blockade in AECS and AECS + sensitized guinea pigs.     

Hyperresponsiveness to tobacco dust extract in sensitized guinea pig trachea

The role of pre-existing airway inflammation in the pathogenesis of occupational airway disease is poorly understood. Previously we studied an extract of tobacco dust (TDE) and determined that it causes concentration dependent contractions of nonsensitized guinea pig trachea (GPT). In the present study animals were sensitized using Ovalbumin (OA) and subsequently challenged with an aerosol of 2.5% OA on day 21. A control group of nonsensitized GPs were divided into rings in which the epithelium was retained (EPI+) or removed (EPI-). Concentration related contractions of sensitized and nonsensitized GPTs were elicited with TDE. Sensitized GPTs demonstrated a greater contractile response to TDE than did nonsensitized GPTs. In nonsensitized animals the EPI- GPTs demonstrated a lesser response to TDE than did the EPI+. Similar findings were demonstrated in sensitized GPTs with and without epithelium. When epithelium was removed, sensitized and nonsensitized GPTs behaved similarly. Moreover, sensitized GPTs without epithelium and nonsensitized with epithelium responded similarly. These findings suggest that presensitization with an unrelated antigen enhances the response to an occupational agent and that in sensitized animals at least part of the enhanced response is mediated by the epithelial layer.     

Relationship between nonspecific airway hyperreactivity and antigen-induced contraction in an allergic animal model in vitro

Tracheal strips from actively sensitized guinea pigs exhibited an enhanced responsiveness (greater maximal effects; Emax) and sensitivity (smaller effective concentration 50%; pD2) to CaCl2 (in K(+)-depolarized tissues), KCl and histamine compared with that of strips from nonsensitized animals. A significant correlation was found between the magnitude of the contraction produced by bovine serum albumin (1 mg/ml) and the Emax and pD2 values of CaCl2, KCl and histamine in tracheal strips from sensitized guinea pigs. This indicates that specific and nonspecific challenges correlate in sensitized guinea pig trachea.     

Evidence for differential reflex regulation of cholinergic and noncholinergic parasympathetic nerves innervating the airways

The hypothesis that cholinergic and nonadrenergic, noncholinergic parasympathetic nerves innervating the airways are subject to differential reflex regulation was addressed. Pronounced contractile and relaxant parasympathetic reflex responses could be evoked by intravenous histamine, laryngeal mucosal application of capsaicin, inhaled capsaicin, or electrical stimulation of the vagal afferent nerves projecting to the esophagus and abdominal viscera. These data suggest that activation of multiple vagal afferent nerve subtypes can initiate both cholinergic and noncholinergic parasympathetic reflexes in the airways. Conversely, hypoxia or activation of the diving response from the nose evoked only cholinergic contractile reflexes. All contractile and relaxant responses evoked by these stimuli were absent in vagotomized animals or in animals pretreated with the ganglionic blocker trimethaphan, confirming their reflex and parasympathetic nature. The data indicate that cholinergic and noncholinergic parasympathetic nerves regulating airway caliber in guinea pigs are comprised of two distinct parasympathetic pathways that are subject to differential reflex regulation. This previously unrecognized complexity of autonomic regulation of airway caliber has potentially important implications for the mechanisms of airways hyperresponsiveness.     

Antigen-induced release of airway epithelium-derived inhibitory factor

The ability of guinea pig trachea to produce a vasoactive epithelium-derived inhibitory factor (EpDIF) in response to mast cell-derived mediators was assessed in a coaxial bioassay system. The mast cell degranulating agent compound 48/80 (10 micrograms/ml) and histamine caused reductions in phenylephrine-induced tone in endothelium-denuded rat aorta preparations mounted coaxially within epithelium-intact guinea pig tracheal tube tissue. Relaxation responses to histamine and to compound 48/80 (10 micrograms/ml) were markedly reduced in the presence of mepyramine (50 microM) or when the epithelium was removed from coaxially mounted guinea pig trachea, indicating that they were mediated via the release of EpDIF. Coaxial bioassay assemblies were also prepared using EpDIF donor tracheal tissue obtained from guinea pigs actively sensitized to ovalbumin. Subsequent challenge with ovalbumin (10(-7) to 10(-1) mg/ml) produced concentration-dependent relaxation mediated by EpDIF. Ovalbumin-induced relaxation responses were not inhibited in the presence of either mepyramine (20 and 100 microM) or SKF 104353-Z2 (10 microM) alone but were significantly reduced when both mepyramine (20 microM) and SKF 104353-Z2 (10 microM) were present. Antigen-induced relaxation was apparently mediated by EpDIF in response to mast cell-derived histamine and leukotrienes. Rat tracheal airway smooth muscle did not relax in response to EpDIF, suggesting selectivity of action on vascular smooth muscle. Vasoactive EpDIF may play a role in protecting against antigen-induced bronchoconstriction by regulating bronchial circulation flow.     

Histamine tachyphylaxis in human airway smooth muscle. The role of H2-receptors and the bronchial epithelium.

The role of airway epithelium and H2-receptors in the development of histamine tachyphylaxis was studied using human isolated bronchial smooth muscle strips obtained from 18 patients undergoing thoracotomy. In epithelium-intact strips, a 38% reduction in the maximal contractile response (Emax) (p less than 0.002) and a 2.14-fold increase in the EC50 (p less than 0.02; n = 18) was observed after three separate histamine cumulative concentration effect curves (CCEC). In contrast, significant differences were not seen for either Emax (p greater than 0.4; n = 10) or EC50 (p greater than 0.26; n = 10) in epithelium-denuded strips. In separate experiments, both intact and denuded muscle strips were treated with the H2-receptor antagonist ranitidine (60 microM), either 30 min prior to the first or 30 min prior to the second histamine CCEC. In epithelium-intact strips, pretreatment with ranitidine caused a 1.8-fold increase in Emax in the initial CCEC (p less than 0.02), and both ranitidine schedules prevented tachyphylaxis (n = 8). In epithelium-denuded preparations, ranitidine did not enhance the responsiveness to histamine beyond that seen in untreated epithelium-denuded strips (n = 6). These data suggest that histamine-induced tachyphylaxis occurs in human airway smooth muscle and is mediated, at least in part, via H2-receptors resident on airway epithelium. In vivo, this may function as a protective mechanism, but damage to the epithelium and loss of H2-receptors may be significant in the development of histamine bronchial hyperreactivity as seen in asthma.     

L-carnitine does not exert any in vitro relaxant effect in Guinea pig trachea,lung parenchyma and human bronchial tissue

The aim of the present study was to investigate the probable in vitro relaxant effect of carnitine in guinea pig trachea, guinea pig lung parenchymal strips, and human bronchial tissue. It was suggested by an in vivo study that carnitine pretreatment prevented the subclinic bronchospasm in children who underwent chronic hemodialysis. Tracheal and lung parenchymal preparations of 10 guinea pigs and 5 human bronchial tissues were prepared and mounted in 20-mL organ baths. In the first series of experiments, contractions to carbachol and histamine (10(-9) to 10(-3) M) were compared after the tissues were incubated with different concentrations of L-carnitine (10(-6) to 10(-4) M). pD(2) values were compared with analysis of variance (ANOVA) and P <.05 was considered as significant. In the second part of experiments, the inhibitory effect of L-carnitine (10(-9) to 10(-3) M) was investigated on the sustained contractions of preparations to carbachol (10(-6) M) and histamine (10(-5) M). In the first part of the study pD(2) values obtained with carbachol were 6.48 +/- 0.09, 5.42 +/- 0.05, and 6.48 +/- 0.02 for guinea pig trachea, guinea pig lung parenchymal strips, and human bronchial tissues, respectively. pD(2) values obtained with histamine were 5.34 +/- 0.10, 5.74 +/- 0.06, and 6.32 +/- 0.03 for guinea pig trachea, guinea pig lung parenchymal strips, and human bronchial tissues, respectively. No significant difference was observed between the pD(2) values before and after incubation with carnitine (P >.05). In the second part of the study, only 10(-4) M L-carnitine exerted an insignificant relaxant effect (6.16% +/- 1.22% on carbachol induced contractions and 4.48% +/- 0.85% on histamine induced contractions) in guinea pig trachea. Our results show that L-carnitine exerts no in vitro relaxant effect in guinea pig trachea, guinea pig lung parenchymal strips, and human bronchial preparations.