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50例不稳定型心绞痛病人被随机分为治疗组(蝮蛇抗栓酶0.01U/kg,VD,1/d,n=25)和安慰组(n=25)。治疗组治疗后血浆6-K-PGF_(?)浓度明显增高(从38.52±11.08增至46.16±7.32,P<0.01),TXB_2及T/P 比值明显降低(分别从347.19±54.80降至309.79±84.45,从9.01±4.95降至6.71±11.53;P 分别<0.001,<0.01)。安慰组前后血浆6-K-PGF_(?)、TXB_2浓度及 T/P 比值无显著性差异(P 均>0.05)。治疗组与安慰组相比,血浆6-K-PGF_(?)浓度增高(46.16±7.32比37.78±8.16,P<0.05),TXB_2浓度及 T/P 比值降低(348.94±64.42比309.79±84.45,9.24±7.84比6.71±11.52;P 均<0.05)。这些结果揭示血浆6-K-PGF_(?)(PGI_2)浓度的增高、TXB_2(TXA_2)浓度及 T/P 比值的降低可能是蝮蛇抗栓酶治疗不稳定型心绞痛的重要机制之一。
Fifty patients with unstable angina were randomized into treatment group (viper antithrombin 0.01U / kg, VD, 1 / d, n = 25) and placebo group (n = 25). The concentration of 6-K-PGF_ (?) In the treatment group was significantly increased (from 38.52 ± 11.08 to 46.16 ± 7.32, P <0.01), and the TXB_2 and T / P ratios were significantly decreased from 347.19 ± 54.80 to 309.79 ± 84.45, from 9.01 ± 4.95 to 6.71 ± 11.53; P <0.001, <0.01, respectively). The concentration of 6-K-PGF_ (superscript TM), TXB_2 and the ratio of T / P had no significant difference before and after the stimulation group (all P> 0.05). Compared with the placebo group, the concentration of 6-K-PGF_ (4) increased (46.16 ± 7.32 vs 37.78 ± 8.16, P <0.05), TXB_2 and T / P ratio decreased in the treatment group (348.94 ± 64.42 vs. 309.79 ± 84.45, 9.24 ± 7.84 vs 6.71 ± 11.52, P <0.05). These results suggest that elevated concentrations of 6-K-PGF_ (?) (PGI_2), TXB_2 (TXA_2), and decreased T / P ratio may be one of the important mechanisms of vipers in the treatment of unstable angina pectoris.