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脾脏参与内毒素诱导的豚鼠呼吸道和淋巴细胞β-肾上腺素能系统的恶化。

Involvement of the spleen in the endotoxin-induced deterioration of the respiratory airway and lymphocyte beta-adrenergic systems of the guinea pig.

作者信息

Van Oosterhout A J, Folkerts G, Ten Have G A, Nijkamp F P

机构信息

Department of Pharmacology, University of Utrecht, The Netherlands.

出版信息

Eur J Pharmacol. 1988 Mar 15;147(3):421-9. doi: 10.1016/0014-2999(88)90177-x.

DOI:10.1016/0014-2999(88)90177-x
PMID:2837397
Abstract

The beta-adrenergic binding sites on splenic lymphocyte membranes of the guinea pig were characterized with the radio-ligand [125I]cyanopindolol and showed a maximal number of binding sites (Bmax) of 125 fmol/mg protein and an affinity (Kd) of 170 pM. The potency of various beta-adrenoceptor antagonists to compete for [125I]cyanopindolol binding suggested that the receptor is of the beta 2 subtype. Endotoxin (1 mg/kg) induced a 35% decrease in the number of beta-adrenergic binding sites on lymphocytes, 4 days after i.p. administration. The reduction in the number of beta-adrenoceptors on the lymphocytes was accompanied by a 30% decrease in the relaxation of isolated guinea pig tracheal spirals to isoprenaline and a 20% reduction in the number of beta-adrenergic binding sites in peripheral lung tissue. The endotoxin-induced deterioration of the beta-adrenergic system in the respiratory airways was completely prevented by splenectomy. It is concluded that the spleen, and or cells or products derived from the spleen, are involved in the changes of the beta-adrenergic system in the respiratory airways and lymphocytes.

摘要

采用放射性配体[125I]氰基吲哚洛尔对豚鼠脾淋巴细胞膜上的β-肾上腺素能结合位点进行了表征,结果显示其最大结合位点数(Bmax)为125 fmol/mg蛋白,亲和力(Kd)为170 pM。多种β-肾上腺素能受体拮抗剂竞争[125I]氰基吲哚洛尔结合的能力表明该受体为β2亚型。腹腔注射内毒素(1 mg/kg)4天后,淋巴细胞上β-肾上腺素能结合位点的数量减少了35%。淋巴细胞上β-肾上腺素能受体数量的减少伴随着离体豚鼠气管螺旋条对异丙肾上腺素舒张反应降低30%以及外周肺组织中β-肾上腺素能结合位点数量减少20%。脾切除可完全预防内毒素诱导的呼吸道β-肾上腺素能系统的恶化。结论是脾脏以及源自脾脏的细胞或产物参与了呼吸道和淋巴细胞中β-肾上腺素能系统的变化。

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