摘要
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 in rat neuropeptide Y (NPY) immuno--re-activities (IR) in platelets and platelet rich plasma (PRP) were respectively 90±16ng/10~7 platelets and 93±19 ng/ml. Both values were much greater than those in theplasma (1.2±0.1 ng/ml, P<0.001) and platelet poor plasma (PPP) (1.7±0.3ng/ml, P<0.001). The NPY--IR in rat platelets eluted at the same position as authen-tic NPY on reverse phase HPLC. The NPY-IR in the platelets prepared from the PRPaggregated maximally by collagen reduced to 34±5 ng/ 10~7 platelets, while the NPY-IR in the PPP prepared from the same PRP increased to 26±4 ng/ml. PPP 1.6 mlprepared from the aggregated PRP induced contraction of isolated rat caudal arterieswith the maximal tension of 380±80 mg; while the maximal contraction induced by1.6 ml of the same PPP pretreated with NPY anti--serum was only 190±40 mg (P<0.001). Authentic NPY 1 nmol/L did not cause any contraction. The results indicatethat rat platelets contain a high concentration of NPY, which can be released during ir-reversible platelet aggregation. The NPY released can potentiate vasoconstriction re-sponses induced by co--released substances during platelet aggregation.
出处
《生理学报》
CAS
CSCD
北大核心
1993年第4期400-404,共5页
Acta Physiologica Sinica
基金
国家自然科学基金
关键词
神经肽Y
血小板
血管
收缩
neuropeptide Y
platelet
blood vessel
vasocontraction
platelet aggregation
