Medcalf R L, Iwanov V, Moulds R F
Clin Exp Pharmacol Physiol. 1983 Sep-Oct;10(5):567-75. doi: 10.1111/j.1440-1681.1983.tb00225.x.
The supernatant solutions obtained after aggregation or sonication of washed human platelets were superfused over preparations of human isolated digital arteries using a small volume bioassay method. The agents released from the platelets caused strong contractions of the artery strips. Platelet aggregation induced by 10 micrograms/ml collagen or by 100 micrograms/ml heat aggregated IgG, released 31.5% and 38.5% respectively, of the contractile activity produced by sonication of the platelets. The quantitative contractile effect of supernatants from platelets aggregated by 50 micrograms/ml IgG was significantly less than that for 100 micrograms/ml HA IgG. Similarly, the maximum contractile effect of supernatants from platelets aggregated by 300 ng/ml collagen was significantly less than that for 1 microgram/ml collagen. This suggests that the concentration of contractile agents released from platelets depends on the concentration of aggregating stimulus. Comparison with concentration-effect curves for exogenous serotonin suggests that if the contractility of the platelet supernatant occurring after sonication of platelets is solely due to serotonin, then it is present in a concentration of approximately 3.3 X 10(-6) mol/l (6.6 nmol per 10(9) platelets). It is suggested from this study that in certain clinical situations characterized by hypertension, and in which circulating immune complexes have been found, in vivo platelet activation by immune complexes may be releasing sufficient concentrations of serotonin to constrict peripheral blood vessels and contribute to the hypertension.
使用小容量生物测定法,将洗涤后的人血小板聚集或超声处理后获得的上清液灌注到分离的人手指动脉制剂上。血小板释放的物质引起动脉条强烈收缩。由10微克/毫升胶原蛋白或100微克/毫升热聚集IgG诱导的血小板聚集,分别释放出由血小板超声处理产生的收缩活性的31.5%和38.5%。50微克/毫升IgG聚集的血小板上清液的定量收缩作用明显小于100微克/毫升热聚集IgG的作用。同样,300纳克/毫升胶原蛋白聚集的血小板上清液的最大收缩作用明显小于1微克/毫升胶原蛋白的作用。这表明从血小板释放的收缩剂浓度取决于聚集刺激物的浓度。与外源性5-羟色胺的浓度-效应曲线比较表明,如果血小板超声处理后出现的血小板上清液的收缩性完全是由于5-羟色胺引起的,那么其浓度约为3.3×10^(-6)摩尔/升(每10^9个血小板6.6纳摩尔)。这项研究表明,在某些以高血压为特征且已发现循环免疫复合物的临床情况下,免疫复合物在体内激活血小板可能会释放足够浓度的5-羟色胺,以收缩外周血管并导致高血压。