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近些年来不断报道α-受体和β-受体在哮喘发病中的作用,提出了哮喘发病的β-受体阻断和α-受体功能亢进的假说。最近,P.J.Barnes 等发现实验性哮喘动物肺中α-受体增加,β-受体减少,进一步支持上述假说。实验性哮喘动物模型系用卵蛋白致敏豚鼠后,再用卵蛋白反复攻击所造成,均有喘、咳、呼吸困难、青紫和气道高敏性等症状。取这种豚鼠和正常豚鼠的肺制备匀浆,用放射标记结合分析法测定肺匀浆中的α-受体和β-受体的数量及它们的比例。还测定肺匀浆中腺苷酸环化酶的活性,以确定β-受体对β-受体激动剂的敏感性。结果发现,实验性哮喘动物肺匀浆中α-受体数量为对照动物的两倍(P<0.001),β-受体数量则低于对照动物(P<0.05)。在实验性哮喘动物肺匀浆中,α:β受体结合部位的比例为1:12,在对照动物则为1:30。
In recent years, the role of a-receptors and β-receptors in the pathogenesis of asthma has been continuously reported, and the hypothesis of β-blocker and α-receptor hyperactivity in asthma has been proposed. More recently, P. J. Barnes et al. Found that in experimental asthma animals, increased α-receptors and decreased β-receptors in the lung further support this hypothesis. Animal models of experimental asthma with ovalbumin sensitized guinea pigs, and then repeated attacks caused by ovalbumin, are asthma, cough, dyspnea, bruising and airway hyperresponsiveness and other symptoms. Hams of this guinea pig and normal guinea pig were homogenized and radiolabeled binding assays were used to determine the amount and their proportion of alpha-receptors and beta-receptors in the lung homogenate. The adenylate cyclase activity in the lung homogenate was also assayed to determine the sensitivity of the beta-receptor to the beta-agonist. The results showed that the amount of α-receptor in the lung homogenate of experimental asthma animals was twice as that of the control animals (P <0.001) and the number of β-receptors was lower than that of the control animals (P <0.05). In experimental asthma animal lung homogenates, the ratio of α: β receptor binding sites was 1:12 in the control animals and 1:30 in the control animals.