炎症介质与β-肾上腺素能受体功能
Inflammatory mediators and beta-adrenoceptor function.
作者信息
Raaijmakers J A, Beneker C, van Geffen E C, Meisters T M, Pover P
机构信息
Department of Pulmonary Disease, State University Hospital, Utrecht, The Netherlands.
出版信息
Agents Actions. 1989 Jan;26(1-2):45-7. doi: 10.1007/BF02126558.
In this study the, in vitro, influence of arachidonic acid metabolites on human beta-adrenoceptors was investigated. Incubation of normal human pulmonary membranes with PAF, LTB4 and LTC4 affected pulmonary beta-adrenoceptor properties, as was shown in radioligand binding studies. The same mediators were able to induce a decreased lymphocyte cAMP synthesis. It is concluded that beta-adrenoceptor deficiencies, that can be demonstrated in peripheral lung tissue of COLD patients, may result from pathological processes such as inflammation.
在本研究中，对花生四烯酸代谢产物在体外对人β-肾上腺素能受体的影响进行了研究。如放射性配体结合研究所显示，用血小板活化因子（PAF）、白三烯B4（LTB4）和白三烯C4（LTC4）孵育正常人肺膜会影响肺β-肾上腺素能受体特性。相同的介质能够诱导淋巴细胞环磷酸腺苷（cAMP）合成减少。得出的结论是，在慢性阻塞性肺病（COLD）患者外周肺组织中可证实的β-肾上腺素能受体缺陷可能是由炎症等病理过程导致的。
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