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用受体结合实验测定大鼠脾脏淋巴细胞β-受体Bmax和Kd。5×10~9个SRBC ip大鼠后,d1 Bmax比对照组明显升高,d2达峰值,以后逐渐下降,d6降至对照水平。+d1-+d3 β-受体Bmax与72h后血清IgM量高度正相关(r=0.86),ipl.8 mg/kg普萘洛尔后,+d2 Bmax和+d5血清IgM量平行降低。在体外诱生抗体中,10μmol/LNE显著提高诱生的IgM量。可被1μmoI/L普萘洛尔阻断。上述结果表明:(1)SRBC致敏上行调节大鼠脾脏淋巴细胞β-受体密度;(2)脾脏淋巴细胞β-受体Bmax的上行调节可能促进其IgM的合成;(3)NE促进脾淋巴细胞IgM合成通过β-受体介导。
Receptor binding assay was used to determine the β-receptor Bmax and Kd of spleen lymphocytes in rats. After 5 × 10 ~ 9 SRBC ip rats, d1 Bmax was significantly higher than the control group, d2 peaked, then decreased gradually, d6 dropped to the control level. The level of IgM + d1- + d3β-receptor was positively correlated with serum IgM after 72h (r = 0.86). After ipl. 8 mg / kg of propranolol, the levels of IgM in + d2 Bmax and + d5 decreased in parallel. Among in vitro induced antibodies, 10μmol / LNE significantly increased the amount of induced IgM. Can be 1μmoI / L propranolol block. The above results indicate that: (1) upregulation of SRBC sensitization regulates the density of β-adrenoceptors in rat splenic lymphocytes; (2) upregulation of β-adrenergic Bmax in splenic lymphocytes may promote the synthesis of IgM; (3) Lymphocyte IgM synthesis is mediated by β-receptors.