Joist J H, Dolezel G, Cucuianu M P, Nishizawa E E, Mustard J F
Blood. 1977 Jan;49(1):101-12.
The effects of lysolecithin (LPC) on aggregation, serotonin release, shape, and lysis of rabbit, pig, or human platelets in platelet-rich plasma (PRP) or Tyrode albumin solution were examined during prolonged incubation. LPC added to citrated or heparinized PRP from humans or rabbits at a final concentration above 100 muM caused instantaneous inhibition of platelet aggregation induced by adenosine diphosphate (ADP), epinephrine (human PRP only), collagen, or thrombin. The inhibitory effect of LPC was found to be partially reversible over a period of 60-90 min. LPC at final concentrations above 30 muM also caused inhibition of ADP-, collagen-, and thrombin-induced aggregation and collagen- and thrombin-induced release of serotonin in suspensions of rabbit, pig, or human platelets. With washed platelets, the inhibitory effect not only rapidly disappeared but was followed by transient potentiation of aggregation and serotonin release. This potentiating effect of LPC was most pronounced when thrombin was used as stimulus. Both inhibition and potentiation were observed at concentrations of LPC that did not cause a significant change in platelet shape or loss from platelets of lactic dehydrogenase. Inhibition and potentiation were also observed when platelets were added to suspending medium containing LPC, although considerably higher concentrations of LPC were required under these conditions. Potentiation was not observed when LPC was added to citrated or heparinized rabbit or human PRP or to washed rabbit platelets suspended in a medium containing 4% bovine serum albumin. It seemed likely that some or all of the observed effects of LPC on platelet function were due to structural modification of the platelet membrane insufficient to result in gross membrane damage or platelet lysis. In addition, the results of experiments using 14C-LPC seemed to indicate that the observed potentiating effect of LPC on platelet function may be related to its rapid uptake and metabolism by the platelets.
在长时间孵育过程中，研究了溶血卵磷脂（LPC）对富血小板血浆（PRP）或台氏白蛋白溶液中兔、猪或人血小板的聚集、5-羟色胺释放、形态及溶解的影响。以终浓度高于100μM将LPC添加到来自人或兔的枸橼酸化或肝素化PRP中，可瞬间抑制由二磷酸腺苷（ADP）、肾上腺素（仅人PRP）、胶原或凝血酶诱导的血小板聚集。发现LPC的抑制作用在60 - 90分钟内部分可逆。终浓度高于30μM的LPC还可抑制兔、猪或人血小板悬液中由ADP、胶原和凝血酶诱导的聚集以及由胶原和凝血酶诱导的5-羟色胺释放。对于洗涤后的血小板，抑制作用不仅迅速消失，随后还会出现聚集和5-羟色胺释放的短暂增强。当以凝血酶作为刺激物时，LPC的这种增强作用最为明显。在LPC浓度未引起血小板形态显著变化或乳酸脱氢酶从血小板中丢失的情况下，观察到了抑制和增强作用。当将血小板添加到含有LPC的悬浮介质中时，也观察到了抑制和增强作用，尽管在这些条件下需要相当高浓度的LPC。当将LPC添加到枸橼酸化或肝素化的兔或人PRP中或添加到悬浮于含有4%牛血清白蛋白的介质中的洗涤兔血小板中时，未观察到增强作用。LPC对血小板功能的部分或全部观察到的效应似乎可能是由于血小板膜的结构改变，这种改变不足以导致明显的膜损伤或血小板溶解。此外，使用14C-LPC的实验结果似乎表明，观察到的LPC对血小板功能增强作用可能与其被血小板快速摄取和代谢有关。
