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哮喘中的α-肾上腺素能反应。

Alpha-adrenergic responses in asthma.

作者信息

Davis P B, Paget G L, Turi V

出版信息

J Lab Clin Med. 1985 Feb;105(2):164-9.

PMID:2857756
Abstract

Medication-free subjects with asthma who had normal pulmonary function were evaluated for alpha 1-adrenergic sensitivity by determination of the dose of topical phenylephrine required for mydriasis and for alpha 2-adrenergic responsiveness by determination of the inhibition by norepinephrine of adenosine 3',5'-cyclic monophosphate synthesis in platelets. Asthmatic subjects required significantly lower concentrations of phenylephrine for mydriasis than normal individuals (1.20 +/- 0.38% vs. 1.53 +/- 0.57%, p less than 0.05), indicating increased sensitivity. However, platelet alpha 2-adrenergic responses were normal in these same asthmatic subjects, as were alpha 2-receptor number and antagonist affinity determined by Scatchard analysis of equilibrium binding of [3H]-yohimbine to platelet particulates. These data suggest that the autonomic aberrations associated with asthma do not extend to the alpha 2-adrenergic system of the platelet, and that the alpha 1-adrenergic hypersensitivity cannot be attributed to medication use or pulmonary dysfunction, but might be an intrinsic property of the disease.

摘要

对肺功能正常的无药物治疗史哮喘患者,通过测定散瞳所需的局部用去氧肾上腺素剂量来评估α1 - 肾上腺素能敏感性,并通过测定血小板中去甲肾上腺素对3',5'-环磷酸腺苷合成的抑制作用来评估α2 - 肾上腺素能反应性。哮喘患者散瞳所需的去氧肾上腺素浓度显著低于正常个体(1.20±0.38%对1.53±0.57%,p<0.05),表明敏感性增加。然而,这些哮喘患者的血小板α2 - 肾上腺素能反应正常,通过[3H]-育亨宾与血小板微粒平衡结合的Scatchard分析确定的α2 - 受体数量和拮抗剂亲和力也正常。这些数据表明,与哮喘相关的自主神经异常并不延伸至血小板的α2 - 肾上腺素能系统,且α1 - 肾上腺素能超敏反应不能归因于药物使用或肺功能障碍,而可能是该疾病的固有特性。

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