Platelet interaction with bacteria. IV. Stimulation of the release reaction.
Platelet interaction with bacteria. IV. Stimulation of the release reaction.
复制标题
血小板与细菌的相互作用。
作者：
C. Clawson;G. Rao;J. White
在金黄色葡萄球菌诱导的血小板聚集过程中，测量了用 14C-5-羟色胺预标记的人血小板释放的 14C-血清素。血小板-细菌相互作用（PBI）与胶原蛋白、凝血酶或肾上腺素一样有效刺激血小板释放反应。阻止血小板聚集的抑制剂也阻止了 PBI 的释放反应。当与聚集浊度测量相关时，释放的连续测量显示释放的开始与血小板形状变化和早期聚集的开始之间密切相关。聚赖氨酸（一种能够聚合血小板颗粒内容物的试剂）的超微结构研究表明，颗粒成分被分泌到形成聚集体的血小板之间捕获的细菌区域。血小板过氧化物酶活性仍然局限于血小板的致密管状系统内。
Release of 14C-serotonin from human platelets prelabeled with 14C-5-hydroxytryptamine was measured during platelet aggregation induced by Staphylococcus aureus. Platelet-bacteria interaction (PBI) was as potent a stimulus of the platelet release reaction as collagen, thrombin, or epinephrine. Inhibitors which blocked platelet aggregation also prevented the release reaction of PBI. Sequential measurements of release, when correlated with nephelometry of aggregation, showed close correlation between the onset of release and the onset of platelet shape change and early aggregation. Ultrastructural studies with polylysine, an agent capable of polymerizing platelet granule contents, revealed that granule components are secreted to the region of the bacteria trapped between platelets in the forming aggregates. Platelet peroxidase activity remained localized within the dense tubular system of the platelets.