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特异性放射免疫分析显示大鼠血小板与富血小板血浆(PRP)分别含NPY免疫活性物质90±16ng/10~7血小板与93±19ng/ml,大大高于普通血浆(1.2±0.1ng/ml)与贫血小板血浆(PPP)(1.7±0.3 ng/ml)中的含量(P<0.001)。血小板样品HPLC各馏分的NPY放免活性峰位与标准NPY的峰位相符。PRP经胶原最大程度聚集后,血小板内的NPY浓度降为34±5 ng/10~7血小板,而PPP中的NPY浓度则升高到26±4 ng/ml。1.6 ml PRP经胶原作用产生最大程度聚集,由此分离所得的PPP引起离体灌流大鼠尾动脉收缩,张力上升380±80 mg;上述PPP经NPY抗血清处理后引起尾动脉收缩的幅度显著减小(190±40 mg,P<0.001)。而1 nmol/L人工合成NPY并不引起血管收缩。结果表明大鼠血小板中含有大量NPY,在不可逆聚集时可以释放,释放的NPY可能参与血小板聚集时释放物质的缩血管效应。
Specific radioimmunoassay showed that rat platelets and platelet-rich plasma (PRP) contained 90 ± 16ng / 10 ~ 7 platelets and 93 ± 19ng / ml NPY immunoreactive substances, respectively, much higher than those of normal plasma (1.2 ± 0.1ng / ml) And platelet poor plasma (PPP) (1.7 ± 0.3 ng / ml) (P <0.001). Peak NPY activity of the HPLC fractions of the platelet samples was consistent with the peak position of the standard NPY. After PRP aggregated to the maximum extent, the concentration of NPY in platelets decreased to 34 ± 5 ng / 10 ~ 7 platelets, whereas the concentration of NPY in PPP increased to 26 ± 4 ng / ml. 1.6 ml of PRP generated by the maximum concentration of collagen accumulation, resulting from isolated PPP caused by isolated perfused rat tail artery contraction, tension increased 380 ± 80 mg; PPP by NPY antiserum caused by tail artery contraction amplitude was significantly reduced Small (190 ± 40 mg, P <0.001). However, 1 nmol / L synthetic NPY did not cause vasoconstriction. The results showed that rat platelets contain a large number of NPY, can be released in the irreversible aggregation, the release of NPY may be involved in platelet aggregation release vasoconstrictor effect.