Harrison H E, Reece A H, Johnson M
Diabetologia. 1980 Jan;18(1):65-8. doi: 10.1007/BF01228305.
Diabetic patients have a high susceptibility to microvascular complications, atherosclerosis and thrombosis. Platelet hyperreactivity possibly related to an imbalance in arachidonic acid metabolism may be involved. Aortic rings or renal cortex produced a potent inhibitor of platelet aggregation, identified as prostacyclin (PGI2). Release of PGI2 by tissues from streptozotocin -- diabetic rats (aorta: 0.07 +/ 0.1 ng/mg wet weight; renal cortex 0.004 +/- 0.001 ng/mg wet weight) was significantly depressed when compared with controls (aorta: 0.26 +/- 0.07 ng/mg wet weight; renal cortex: 0.009 +/- 0.001 ng/mg wet weight). Treatment of diabetic animals with insulin for 8 days restored PGI2 production to normal. The finding that PGI2 is depressed in the aorta and in the kidney, tissues which develop angiopathy, and that this is normalised by insulin, suggests that impaired PGI2 production, perhaps associated with platelet hyperreactivity may play a role in the vascular complications of diabetes.
糖尿病患者对微血管并发症、动脉粥样硬化和血栓形成高度易感。血小板高反应性可能与花生四烯酸代谢失衡有关，可能参与其中。主动脉环或肾皮质产生了一种强效的血小板聚集抑制剂，被鉴定为前列环素（PGI2）。与对照组相比，链脲佐菌素诱导的糖尿病大鼠组织（主动脉：0.07±0.1纳克/毫克湿重；肾皮质：0.004±0.001纳克/毫克湿重）释放的PGI2显著降低（主动脉：0.26±0.07纳克/毫克湿重；肾皮质：0.009±0.001纳克/毫克湿重）。用胰岛素治疗糖尿病动物8天可使PGI2产生恢复正常。PGI2在发生血管病变的主动脉和肾脏组织中降低，且经胰岛素治疗后恢复正常，这一发现表明，PGI2产生受损，可能与血小板高反应性有关，可能在糖尿病血管并发症中起作用。
