Mitchell R W, Ndukwu I M, Leff A R, Padrid P A
Department of Medicine, Physiologic and Pharmacologic Sciences, University of Chicago, IL 60637, USA.
Am J Vet Res. 1997 Jun;58(6):672-6.
To determine the effect of in vivo antigen sensitization (Ascaris suum) of cats on tracheal smooth muscle (TSM) and bronchial smooth muscle (BSM) muscarinic reactivity in vitro.
Healthy domestic shorthair cats of either sex.
Cats were sensitized and were long-term antigen (or sham) challenge exposed for 6 weeks by aerosolization with soluble Ascaris suum. Tracheal and BSM preparations were obtained and stimulated in vitro by electrical field stimulation (EFS), acetylcholine (ACh, a muscarinic agonist), and physostigmine (an AChase inhibitor). Responses were compared with responses of comparable tissues from sham antigen challenge-exposed cats.
Tracheal and BSM from sensitized, compared with sham-sensitized (control), cats had greater isometric contraction (expressed as percentage of the response observed for isotonic, 63 mM KCl-elicited contraction [% KCl]) in response to endogenous (EFS) and exogenous muscarinic receptor activation (ACh). Contractions in response to EFS by TSM from control cats were 74% KCl vs 97% KCl for antigen-sensitized TSM (P < 0.04). Muscarinic responses were augmented comparably by in vivo sensitization; TSM from control cats contracted to 190% KCl vs 230% KCl (P < 0.03) for TSM from immune-sensitized cats. Physostigmine augmented responses of all tissues to ACh so that TSM from control (290% KCl) and antigen-sensitized (257% KCl) cats were similar. Responses of BSM from antigen-sensitized cats had similar augmentation of contractile response to EFS and ACh.
Long-term in vivo antigen sensitization increases numbers of muscarinic receptors on airway smooth muscle or decreases the availability or activity of AChase in cats.
Modulation of muscarinic receptors may be useful for treatment of asthmatic cats with in vivo airway hyperreactivity.
确定猫体内抗原致敏（猪蛔虫）对气管平滑肌（TSM）和支气管平滑肌（BSM）体外毒蕈碱反应性的影响。
健康的家养短毛猫，雌雄不限。
猫经致敏后，通过雾化可溶性猪蛔虫抗原进行为期6周的长期抗原（或假抗原）激发暴露。获取气管和BSM标本，体外用电场刺激（EFS）、乙酰胆碱（ACh，一种毒蕈碱激动剂）和毒扁豆碱（一种乙酰胆碱酯酶抑制剂）进行刺激。将反应与来自接受假抗原激发暴露猫的相应组织的反应进行比较。
与假致敏（对照）猫相比，致敏猫的气管和BSM对内源性（EFS）和外源性毒蕈碱受体激活（ACh）的等长收缩更大（以等张、63 mM KCl诱发收缩所观察到反应的百分比表示 [% KCl]）。对照猫TSM对EFS的收缩为74% KCl，而抗原致敏TSM为97% KCl（P < 0.）。体内致敏使毒蕈碱反应同等增强；对照猫TSM收缩至190% KCl，而免疫致敏猫的TSM为230% KCl（P < 0.03）。毒扁豆碱增强了所有组织对ACh的反应，因此对照（290% KCl）和抗原致敏（257% KCl）猫的TSM相似。抗原致敏猫的BSM对EFS和ACh的收缩反应有类似的增强。
长期体内抗原致敏增加了猫气道平滑肌上毒蕈碱受体的数量，或降低了乙酰胆碱酯酶的可用性或活性。
调节毒蕈碱受体可能有助于治疗体内气道高反应性的哮喘猫。
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