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采用低硒饲料饲养大鼠造成体内贫硒。１４周时测定血浆中脂质过氧化物（ＬＰＯ）、前列环素（ＰＧＩ２）和血栓素（ＴＸＡ２）的水平以及部分血液流变学指标。实验第３９周，测定血管组织一氧化氮合酶（ＮＯＳ）活性及一氧化氮（ＮＯ）水平。结果显示，低硒饲料组的血管ＮＯＳ活性、ＮＯ水平显著低于常规饲料的对照组；而在实验第１４周时，当低硒饲料组的血硒、血谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）活性显著下降、血浆ＬＰＯ水平明显上升的同时，其对应的血浆６－酮－ＰＧＦ１α水平也显著降低，但其ＴＸＢ２与对照组无显著差异。此外，随着大鼠体内的贫硒，其红细胞变形能力下降，但红细胞聚集指数和血沉方程Ｋ值提高。因此，硒不足可能会通过影响ＮＯＳ活性和ＰＧＩ２的合成以及红细胞特性而损害微循环功能。
The use of low-selenium feed rats selenium caused by the body. Plasma levels of lipid peroxide (LPO), prostacyclin (PGI2) and thromboxane (TXA2), and some hemorheologic parameters were measured at 14 weeks. At week 39, the activity of nitric oxide synthase (NOS) and the level of nitric oxide (NO) in blood vessels were measured. The results showed that the blood levels of NOS and NO in the low-selenium group were significantly lower than those in the control group. At the 14th week of the experiment, when selenium in the selenium-deficient group was lower than that in the control group, the blood levels of selenium and glutathione peroxidase GSH-Px) activity was significantly decreased, plasma LPO levels were significantly increased, while its corresponding plasma 6-keto-PGF1α levels were significantly lower, but the TXB2 and the control group no significant difference. In addition, with the selenium deficiency in rats, the erythrocyte deformability decreased, but the erythrocyte aggregation index and erythrocyte sedimentation rate K value increased. Therefore, insufficient selenium may impair microcirculation function by affecting NOS activity and PGI2 synthesis and erythrocyte properties.