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本实验应用了单独染镉和β－肾上腺素能受体阻断剂与镉联合作用两种动物模型，探讨了不同剂量镉对大鼠脾细胞β－肾上腺素能受体密度的影响，同时检测了Ｔ淋巴细胞亚群（ＣＤ＋４，ＣＤ＋８，ＣＤ＋４／ＣＤ＋８）和Ｔ淋巴细胞的增殖功能。结果表明镉可刺激并使脾细胞膜上的β－受体密度增加，镉对Ｔ细胞的免疫毒性表现为抑制Ｔ淋巴细胞的增殖功能，改变Ｔ细胞亚群的分型；而在β－受体被阻断后，镉的这种免疫毒性作用减轻：Ｔ淋巴细胞增殖功能不再受影响，Ｔ细胞亚群所受的影响也减少。因此，β－肾上腺素能受体机制可能是镉的细胞免疫毒性机制的一个重要部分。
In this study, two kinds of animal models of cadmium and β-adrenergic receptor blockers combined with cadmium were applied to investigate the effect of different doses of cadmium on the β-adrenergic receptor density of splenocytes in rats. Simultaneous detection T lymphocyte subsets (CD + 4, CD + 8, CD + 4 / CD + 8) and T lymphocyte proliferation. The results showed that cadmium could stimulate and increase the density of β-receptor on the spleen cell membrane. The immunotoxicity of cadmium to T cells was to inhibit the proliferation of T lymphocytes and change the type of T cell subsets. Blocked, this immunosuppressive effect of cadmium diminishes: T-lymphocyte proliferation is no longer affected and T-cell subsets are less affected. Thus, β-adrenergic receptor mechanisms may be an important part of the cellular immunotoxic mechanism of cadmium.