Buckner C K, Clayton D E, Ain-Shoka A A, Busse W W, Dick E C, Shult P
J Clin Invest. 1981 Feb;67(2):376-84. doi: 10.1172/JCI110045.
Guinea pigs, actively sensitized to ovalbumin, were inoculated by nasal insufflation with parainfluenza 3 or virus growth medium 4 d before performing in vitro pharmacological studies on tracheal and bronchial smooth muscle. In each airway segment, cumulative dose-response effects of ovalbumin were obtained in the absence and presence of a maximally effective concentration of a beta adrenergic receptor agonist, sulfonterol. Sulfonterol shifted the dose-response curve to the right and reduced the maximum smooth muscle contractile response to ovalbumin. Virus infection did not alter the dose-response effects of ovalbumin. However, the magnitude of the inhibitory effects of sulfonterol was smaller in segments taken from animals inoculated with virus. Blockade by virus infection of the inhibitory effect of sulfonterol was reversed when the concentrations of beta agonist were increased. Sulfonterol did not alter the dose-response effects of histamine at any of the concentrations that markedly antagonized the effects of ovalbumin. Virus infection did not alter the sensitivities to sulfonterol or papaverine in producing relaxation in either airway segment. The magnitude of relaxation produced by papaverine was significantly larger in bronchial rings taken from animals infected with virus for 4 d, but there was no alteration by virus of the dose-response effects of histamine or carbachol. In experiments measuring antigen-induced release of slow reacting substance of anaphylaxis and histamine from minced lung, virus infection did not alter the sensitivity or the maximum effects of ovalbumin. Also, the ability of sulfonterol to inhibit the release of slow reacting substance of anaphylaxis and histamine was not affected by virus infection.These results demonstrate that infection of guinea pigs with respiratory virus results in a selective blockade of the beta adrenergic-mediated inhibition of antigen-induced contraction of airway smooth muscle. The guinea pig may serve as a useful model in physiological studies of virus-induced asthma.
在对气管和支气管平滑肌进行体外药理学研究前4天，用鼻内注入法给已对卵清蛋白产生主动致敏的豚鼠接种副流感病毒3型或病毒生长培养基。在每个气道节段，分别在不存在和存在最大有效浓度的β肾上腺素能受体激动剂舒喘宁的情况下，获得卵清蛋白的累积剂量-反应效应。舒喘宁使剂量-反应曲线右移，并降低了平滑肌对卵清蛋白的最大收缩反应。病毒感染未改变卵清蛋白的剂量-反应效应。然而，在接种病毒的动物所取的节段中，舒喘宁的抑制作用强度较小。当β激动剂浓度增加时，病毒感染对舒喘宁抑制作用的阻断作用被逆转。在任何能明显拮抗卵清蛋白作用的浓度下，舒喘宁均未改变组胺的剂量-反应效应。病毒感染未改变任一气道节段对舒喘宁或罂粟碱产生舒张作用的敏感性。在感染病毒4天的动物所取的支气管环中，罂粟碱产生的舒张幅度明显更大，但病毒未改变组胺或卡巴胆碱的剂量-反应效应。在测量抗原诱导的过敏反应慢反应物质和组胺从肺匀浆中释放的实验中，病毒感染未改变卵清蛋白的敏感性或最大效应。此外，舒喘宁抑制过敏反应慢反应物质和组胺释放的能力不受病毒感染的影响。这些结果表明，呼吸道病毒感染豚鼠会导致β肾上腺素能介导的对抗原诱导的气道平滑肌收缩的抑制作用出现选择性阻断。豚鼠可作为病毒诱导哮喘生理学研究的有用模型。
