Sinzinger H, Rogatti W
Wilhelm Auerswald Atherosclerosis Research Group, Vienna, Austria.
J Physiol Pharmacol. 1994 Mar;45(1):27-40.
It is the aim of this paper to review our findings in vitro, in experimental animals and in human on arterial wall lipid metabolism. Radiolabelling of LDL indicates that experimentally induced lesions in hypercholesterolemic rabbits do show less lipid accumulation if treated with prostaglandins (PGI2, PGE1, 13,14-dihydro-PGE1) or stimulators of prostaglandin synthesis (isradipine, a calcium channel blocker of the dihydropyridine family). Endogenous blockade of cyclooxygenase by ASA-pretreatment results in a complete abolishing of this apparently PG-mediated benefit. In-vivo studies using autologous 123I-labeled LDL without therapeutic intervention exhibit a quite good reproducibility of the imaging technique. While PGE1 (at 2 different therapeutic regimens) is inducing lipid lesion regression, the comparable benefit induced by isradipine again disappears with concomitant ASA-therapy. Quantitative estimation of arterial wall lipid metabolism in patients undergoing vascular surgery demonstrates that PGI1- (and cAMP-) increase are paralleled by a several-fold increase of acid and neutral cholesterol ester hydrolase and a decrease in net arterial cholesterol ester content. This benefit again disappears with concomitant ASA-therapy. These findings are allowing to conclude that (exogenously added or endogenously stimulated) prostaglandins do significantly improve arterial wall lipid metabolism.
本文旨在综述我们在体外、实验动物和人体中关于动脉壁脂质代谢的研究结果。低密度脂蛋白（LDL）的放射性标记表明，在高胆固醇血症兔中，经实验诱导的病变若用前列腺素（前列环素I2、前列腺素E1、13,14-二氢前列腺素E1）或前列腺素合成刺激剂（异搏定，一种二氢吡啶类钙通道阻滞剂）治疗，脂质蓄积会减少。用阿司匹林预处理对内源性环氧化酶进行阻断，会导致这种明显由前列腺素介导的益处完全消失。使用自体123I标记的LDL且无治疗干预的体内研究显示，成像技术具有相当好的可重复性。虽然前列腺素E1（在2种不同治疗方案下）可诱导脂质病变消退，但异搏定诱导的类似益处会在同时进行阿司匹林治疗时再次消失。对接受血管手术患者的动脉壁脂质代谢进行定量评估表明，前列环素I1（和环磷酸腺苷）增加的同时，酸性和中性胆固醇酯水解酶增加数倍，动脉胆固醇酯净含量降低。这种益处也会在同时进行阿司匹林治疗时消失。这些发现使我们可以得出结论，（外源性添加或内源性刺激的）前列腺素确实能显著改善动脉壁脂质代谢。
