Van Oosterhout A J, Nijkamp F P
Brain Res. 1984 Jun 8;302(2):277-80. doi: 10.1016/0006-8993(84)90240-3.
Bacterial endotoxin (E. coli O111:B4) induces, 4 days after intraperitoneal injection, a 30% reduction of guinea pig lung beta-adrenoceptor number (Bmax). No change in affinity (Kd) for the receptors occurred. Bilateral electrolytic lesions centered in the anterior hypothalamic nucleus prevent this reduction in Bmax and even reverse the reduction into a small increase in beta-adrenoceptor number. Since it is known from the literature data that anterior hypothalamic lesions as well as beta-adrenoceptor stimulants have an inhibitory influence on the immune system, the mechanism by which these lesions inhibit the reduction of beta-adrenoceptor sites after bacterial endotoxin and influence immune functions, may be related.
腹腔注射大肠杆菌O111:B4细菌内毒素4天后，豚鼠肺β-肾上腺素能受体数量（Bmax）减少30%。受体亲和力（Kd）未发生变化。以前下丘脑核为中心的双侧电解损伤可防止Bmax的这种减少，甚至使减少逆转，导致β-肾上腺素能受体数量略有增加。从文献数据可知，下丘脑前部损伤以及β-肾上腺素能受体兴奋剂对免疫系统有抑制作用，这些损伤抑制细菌内毒素后β-肾上腺素能受体位点减少并影响免疫功能的机制可能有关联。
