Inoguchi T, Umeda F, Watanabe J, Ibayashi H
Haemostasis. 1986;16(6):447-52. doi: 10.1159/000215323.
Reduced prostacyclin (PGI2) production by the vascular wall has been proposed as a possible cause of macro- or microangiopathy in diabetes mellitus. In the present study, we confirmed the stimulatory activity on PGI2 (PSA) production in plasma-derived serum (PDS) by cultured aortic endothelial cells. Furthermore, the abnormality of PSA was examined in diabetic PDS. PSA in PDS from non-insulin-dependent diabetics significantly decreased as compared with that in PDS from age-matched control subjects. There was no difference in PSA in PDS between diabetic patients with and without vascular complications such as retinopathy and nephropathy. In addition, after treatment with dialysis, PSA in diabetic PDS was still not restored to that in normal PDS. These findings suggest that relatively heat-stable (56 degrees C, 30 min) and nondialyzable PGI2 stimulatory substance(s) may decrease in diabetic PDS. It is concluded that a reduction in PDS-stimulated PGI2 production by the vascular wall can play an important role in the pathogenesis of vascular lesions in diabetes mellitus.
血管壁前列环素（PGI2）生成减少被认为是糖尿病大血管或微血管病变的一个可能原因。在本研究中，我们证实了培养的主动脉内皮细胞对血浆源性血清（PDS）中PGI2（PSA）生成具有刺激活性。此外，我们检测了糖尿病患者PDS中PSA的异常情况。与年龄匹配的对照受试者的PDS相比，非胰岛素依赖型糖尿病患者的PDS中PSA显著降低。有无视网膜病变和肾病等血管并发症的糖尿病患者的PDS中PSA没有差异。此外，透析治疗后，糖尿病患者PDS中的PSA仍未恢复到正常PDS中的水平。这些发现表明，相对耐热（56℃，30分钟）且不可透析的PGI2刺激物质可能在糖尿病患者的PDS中减少。得出的结论是，血管壁对PDS刺激的PGI2生成减少可能在糖尿病血管病变的发病机制中起重要作用。
