Abstract
Reduced prostacyclin (PGI2) production by the vascular wall can cause platelet hyperaggregation, which is considered to be one pathogenesis of diabetic angiopathy. In the present study, we confirmed a stimulatory activity on PGI production (PGI2 stimulatory activity; PSA) in rat and human plasma derived serum (PDS) by cultured bovine aortic endothelial cells (EC) and rat lung fibroblasts (FB). Furthermore, the abnormality of PSA was studied in streptozotocin-induced (STZ) diabetic rats and human noninsulin-dependent diabetic patients (NIDDM) using these in vitro systems.Cultured EC and FB were incubated with DME medium containing rat and human PDS. After incubation, the concentration of 6-keto-PGF1α (a stable metabolite of PGI2) in the medium was assayed by RIA. 6-keto-PGF1α production by cultured EC and FB was stimulated by the addition of rat and human PDS in a time and dose dependent manner. The addition of 10% PDS from STZ diabetic rats or NIDDM showed a significant decrease in 6-keto-PGF1α production by cultured EC and FB as compared with that from controls. These findings suggested that PSA in PDS decreased in both STZ diabetic rats and human NIDDM. In addition, the reduced PSA was also present in NIDDM without diabetic vascular complications as well as NIDDM with vascular complications. Furthermore, the difference in PSA between NIDDM and controls still remained in PDS treated with dialysis. It is concluded that the decreased PSA in PDS can cause the reduction of PGI2 production by the vascular wall and play an important role in the pathogenesis of diabetic vascular complications.
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