饮食诱导的高胆固醇血症会抑制受伤兔主动脉中前列环素生成的恢复。
Diet-induced hypercholesterolemia inhibits the recovery of prostacyclin production by injured rabbit aorta.
作者信息
Eldor A, Falcone D J, Hajjar D P, Minick C R, Weksler B B
出版信息
Am J Pathol. 1982 May;107(2):186-90.
The effect of diet-induced hypercholesterolemia on the recovery of prostacyclin (PGI2) synthetic capacity was assessed at the luminal surface of previously injured rabbit aorta. Prostacyclin synthesis and release were measured by radioimmunoassay following arachidonic acid stimulation of deendothelialized and reendothelialized aortas of hypercholesterolemic rabbits. Assay of PGI2 production by aorta was performed at 15, 35, and 70 days following removal of endothelium with a balloon catheter. Prostacyclin production by both deendothelialized and reendothelialized areas of aorta from normocholesterolemic rabbits was initially low following injury and increased with time, reaching levels at 70 days equal to uninjured aortas. Prostacyclin production by both deendothelialized and reendothelialized areas of aorta from rabbits with moderately elevated serum cholesterol concentrations (203 to 350 mg/dl) was also initially low, but in contrast to normocholesterolemic rabbits, it did not increase with time. Results indicate that hypercholesterolemia like that seen in humans inhibits the recovery of PGI2 production in deendothelialized and reendothelialized areas of previously injured rabbit aorta.
在先前受伤的兔主动脉腔表面评估饮食诱导的高胆固醇血症对前列环素（PGI2）合成能力恢复的影响。在用花生四烯酸刺激高胆固醇血症兔的去内皮化和再内皮化主动脉后，通过放射免疫测定法测量前列环素的合成和释放。在用球囊导管去除内皮后15、35和70天对主动脉的PGI2产生进行测定。正常胆固醇血症兔的主动脉去内皮化和再内皮化区域的前列环素产生在损伤后最初较低，并随时间增加，在70天时达到与未受伤主动脉相等的水平。血清胆固醇浓度中度升高（203至350mg/dl）的兔的主动脉去内皮化和再内皮化区域的前列环素产生最初也较低，但与正常胆固醇血症兔相反，它不随时间增加。结果表明，人类中所见的高胆固醇血症会抑制先前受伤的兔主动脉去内皮化和再内皮化区域中PGI2产生的恢复。
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