Sinzinger H, Feigl W, Silberbauer K, Oppolzer R, Winter M, Auerswald W
Exp Pathol (Jena). 1980;18(3):175-80. doi: 10.1016/s0014-4908(80)80018-4.
Unaltered human arterial tissue as well as different types of macroscopically and microscopically characterized atherosclerotic lesions were microdissected under a preparation microscope. The prostacyclin formation was examined using its potent platelet aggregation inhibition in vitro according to Moncada's bioassay. In contrast to different PGI2-formation in various experimental animal models the generation in the different lesion types in terms of wet weight was statistically significantly (p less than 0.001) diminished in comparison to normal control tissue. However, the PGI2- formation in different lesion types is comparable. Accepting the hypothesis delivered earlier by us, that the arterial wall is able to react upon exogenous noxes with a temporarily enhanced PGI2-formation, followed (after ceasing) by a decrease of PGI2-synthesis (exhaustion phenomenon) it can be concluded, that the critical stage is prior to the fatty streak formation, which is a preatherosclerotic lesion. Therefore, PGI2-generation-exhaustion might be mainly responsible for initiation and progression of atherosclerosis, probably before any detectable morphological alterations.
在解剖显微镜下对未改变的人体动脉组织以及不同类型的经宏观和微观特征鉴定的动脉粥样硬化病变进行显微切割。根据蒙卡达生物测定法，利用前列环素在体外对血小板聚集的强效抑制作用来检测前列环素的生成。与各种实验动物模型中不同的前列环素生成情况相反，不同病变类型中按湿重计算的前列环素生成量与正常对照组织相比在统计学上有显著降低（p<0.001）。然而，不同病变类型中的前列环素生成情况具有可比性。接受我们之前提出的假说，即动脉壁能够对外源性有害物质做出反应，暂时增强前列环素的生成，随后（停止刺激后）前列环素合成减少（耗竭现象），可以得出结论，关键阶段是在脂肪条纹形成之前，脂肪条纹是一种动脉粥样硬化前期病变。因此，前列环素生成耗竭可能主要是动脉粥样硬化起始和进展的原因，可能在任何可检测到的形态学改变之前。
