Long-term exposure to hand-transmitted vibration can lead to hand-arm vibration syndrome, one manifestation of which is impaired peripheral blood circulation in the arms. Altered expressions of prostacyclin I₂ (PGI₂) and thromboxane A₂ (TXA₂) in blood may be one of the important mechanisms of vibration-induced hand-arm vibration syndrome.

To reveal the effects of rat tail vibration on the expressions of PGI₂ and TXA₂ in plasma, and to establish the correlation between the change of rat plasma PGI₂ to TXA₂ ratio and rat tail vibration.

Fifty SPF-grade male SD rats were randomly divided into five groups: control group, 1 d exposure group, 3 d exposure group, 7 d exposure group, and 14 d exposure group, with 10 rats in each group. The rats were placed in rat immobilizes on a immobilization table, and the rats' tails were connected to a shaker and fixed with medical tape. There was no overlap between the immobilizes and between the rats' tails by no contact between the immobilization table and the shaker. The exposure dose was 125 Hz, 5.9 m·s⁻², 4 h·d⁻¹, and the vibration direction was linear vertical vibration. Abdominal aortic blood was taken at the end of vibration exposure, and the expressions of PGI₂, TXA₂, and their hydrolysates 6-keto-prostaglandin F_1α (6-keto-PGF_1α) and thromboxane B₂ (TXB₂) were measured by enzyme-linked immunosorbent assay, and the 6-keto-PGF_1α/TXB₂ values were calculated. Spearman rank correlation was used to analyze whether the expression of vascular factors correlated with the accumulated time of vibration.

The expression levels of plasma 6-keto-PGF_1α were (896.12±124.37), (1068.13±119.41), (1215.26±122.64), and (1317.94±106.54) ng·L⁻¹ in the 1 d, 3 d, 7 d, and 14 d groups of rats, respectively, which were higher than that in the control group, (830.60±109.47) ng·L⁻¹ (P<0.001). The PGI₂ expression levels were (86.49±2.40), (107.90±2.65), (114.02±2.16), and (126.95±1.94) ng·L⁻¹ in the 1 d, 3 d, 7 d, and 14 d groups of rats, respectively, all higher than (60.09±2.11) ng·L⁻¹ in the control group (P＜0.001). The expression levels of TXB₂ were (132.14±4.10), (145.52±4.09), (179.91±4.98), and (204.10±3.22) ng·L⁻¹ in the 1 d, 3 d, 7 d, and 14 d groups of rats, respectively, which were higher than that in the control group, (106.08±3.26) ng·L⁻¹ (P<0.001). The expression levels of plasma TXA₂ were (211.99±3.24), (236.33±3.88), and (245.45±4.23) ng·L⁻¹ in rats in the 3 d, 7 d, and 14 d groups, respectively, which were all elevated compared with (174.79±4.19) ng·L⁻¹ in the control group (P<0.001). Compared with the control group, the 6-keto-PGF_1α/TXB₂ values were decreased in the 7 d and 14 d groups (P<0.05). The 6-keto-PGF_1α, PGI₂, TXB₂, and TXA₂ expressions were positively correlated with vibration accumulation time (r=0.84, 0.84, 0.80, 0.84, P<0.001) and the 6-keto-PGF_1α/TXB₂ values were negatively correlated with vibration accumulation time (r=-0.24, P=0.003).

Local exposure of rat tail to vibration could increase the expressions of PGI₂ and TXA₂ in blood, and the elevated expressions show a dose-effect relationship with the duration of vibration exposure, but the PGI₂/TXA₂ tends to decrease with the accumulation of vibration exposure.