Inoguchi T, Umeda F, Watanabe J, Ibayashi H
Third Department of Internal Medicine, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Diabetes Res Clin Pract. 1987 Sep-Oct;3(5):243-8. doi: 10.1016/s0168-8227(87)80047-5.
We recently reported that serum stimulatory activity on prostacyclin (PGI2) production by cultured bovine aortic endothelial cells decreased in noninsulin-dependent diabetic patients. In the present study, this activity was compared in streptozotocin-induced (STZ) diabetic rats and controls. Platelet-poor plasma-derived serum (PDS) from Wistar male rats stimulated 6-keto-PGF1 alpha production (a stable metabolite of PGI2) by cultured bovine aortic endothelial cells, rat lung fibroblasts, and rat aortic rings in a time- and dose-dependent manner. Namely, PDS from rats has a stimulatory activity on PGI2 production (PGI2 stimulatory activity; PSA). Furthermore, PSA in PDS from STZ diabetic rats (n = 12) significantly decreased as compared with that from control rats (n = 10) using three types of in vitro systems. The reduction in PDS-stimulated PGI2 production by the vascular wall may lead to platelet hyperaggregation and thrombus formation in diabetics, which is considered to be involved in the pathogenesis of diabetic macro- or microangiopathy.
我们最近报道，非胰岛素依赖型糖尿病患者血清对培养的牛主动脉内皮细胞产生前列环素（PGI2）的刺激活性降低。在本研究中，对链脲佐菌素诱导（STZ）的糖尿病大鼠和对照组的这种活性进行了比较。来自Wistar雄性大鼠的贫血小板血浆衍生血清（PDS）以时间和剂量依赖的方式刺激培养的牛主动脉内皮细胞、大鼠肺成纤维细胞和大鼠主动脉环产生6-酮-PGF1α（PGI2的稳定代谢产物）。也就是说，大鼠的PDS对PGI2产生具有刺激活性（PGI2刺激活性；PSA）。此外，使用三种体外系统，与对照大鼠（n = 10）相比，STZ糖尿病大鼠（n = 12）的PDS中的PSA显著降低。血管壁PDS刺激的PGI2产生减少可能导致糖尿病患者血小板过度聚集和血栓形成，这被认为与糖尿病大血管或微血管病变的发病机制有关。
