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许多资料表明,支气管哮喘患者长期使用拟交感神经类药物,可导致β-肾上腺素能受体的阻滞,使病情加重,发生喘息状态,甚至引起患者死亡。支气管痉挛的根本原因是肾上腺素能系统的机能障碍,即β-受体感受性降低和α-受体感受性升高。拟交感神经类药物可刺激β_2-受体,使细胞内环一磷酸腺苷(cAMP)含量升高,引起支气管扩张、血管通透性降低及组织胺和5-羟色胺的释放抑制,因此使哮喘缓解。支气管哮喘患者,由于Adenilayclaza先天或后天的缺乏,表现为β受体对拟交感神经类药物的感受性降低,因而迫使患者必须经常使用这些药物以缓解哮喘发作。
Many sources indicate that long-term use of sympathomimetic drugs in patients with bronchial asthma can lead to β-adrenergic receptor blockade, exacerbations, wheezing and even patient death. The underlying cause of bronchospasm is dysfunction of the adrenergic system, ie, decreased β-receptor sensitivity and increased α-receptor sensitivity. Sympathomimetic drugs can stimulate the β 2 -receptors and increase the content of intracellular cyclic AMP, causing bronchiectasis, decreasing vascular permeability and inhibiting the release of histamine and serotonin, thus making asthma ease. Patients with bronchial asthma, due to a congenital or acquired deficiency of Adenilayclaza, exhibit reduced susceptibility of the beta receptors to sympathomimetic drugs, thereby forcing patients to frequently use these medications to alleviate asthma attacks.