“剪切诱导的血小板活化”——一项批判性重新评估

"Shear induced platelet activation"--a critical reappraisal.

作者信息

Wurzinger L J, Opitz R, Wolf M, Schmid-Schönbein H

出版信息

Biorheology. 1985;22(5):399-413. doi: 10.3233/bir-1985-22504.

DOI:10.3233/bir-1985-22504

Abstract

Platelets were found to be stimulated by high shear exposure for 5 minutes. Using a new technique, shear stresses up to 255 N/m2, acting for pathophysiological relevant intervals of milliseconds did not elicit active release of beta-TG, beyond the amount explained by LDH-monitored passive lysis. Neither the plasma level of ionized calcium (citrate vs heparin anticoagulation), nor a potent platelet inhibiting agent like PgI2 (20 nM) did significantly alter platelet responses to short acting high shear stress. Ultrastructural signs of activation could largely be suppressed by adding ADP-scavengers. Direct "shear induced platelet activation" appears rather unlikely and mostly reducible to secondary biochemical activation by mediators, probably adenine nucleotides, from a small percentage of passively shear-destroyed platelets. The extent of this secondary activation is largely a matter of experimental conditions.

摘要

研究发现，血小板在高剪切力作用5分钟后会受到刺激。采用一项新技术，高达255 N/m²的剪切应力作用于生理病理相关的毫秒时间间隔时，除了由乳酸脱氢酶（LDH）监测的被动裂解所解释的量之外，并不会引发β-血小板球蛋白（β-TG）的主动释放。无论是离子钙的血浆水平（柠檬酸盐与肝素抗凝），还是像前列环素（PgI2，20 nM）这样的强效血小板抑制剂，都不会显著改变血小板对短效高剪切应力的反应。通过添加ADP清除剂，激活的超微结构迹象在很大程度上可以被抑制。直接的“剪切诱导血小板激活”似乎不太可能，并且大多可归因于一小部分被动剪切破坏的血小板所释放的介质（可能是腺嘌呤核苷酸）引发的继发性生化激活。这种继发性激活的程度在很大程度上取决于实验条件。