Prostacyclin production reduced in diabetics with vascular complications.

Abstract

Concentrations of plasma 6-keto-prostaglandinFltt (6-kcto-PGFl0!), a stable metabolite of prostacyclin, were measured by radioimmunoassay before and after 3 min of induced ischemia in 45 diabetics and 23 controls matched for age. In the 45 diabetics, 15 had no vascular complications (group I), 10 had a macroangiopathy (group II), 10 had a microangiopathy (group III) and 10 had both macroangiopathy and microangiopathy (group IV). Plasma levels of 6-keto-PGFlQ; before forearm ischemia were significantly lower in group IV diabetics than in non-diabetic controls (188 ± 17 pg/ml and 245 ± 14 pg/ml, respectively). After 3 min of ischemia, plasma 6-keto-PGFia concentrations were increased in control subjects by 34% and by 21% in group I diabetics. In group III diabetics as well as diabetics with atherosclerotic vascular lesions (groups II and IV), no significant change was observed after 3 min of ischemia. These results suggest that impaired vessel wall prostacyclin production may to some extent be responsible for the developmentof diabetic retinopathy and nephropathy as well as atherosclerotic vascular complications.

Diabetic macular edema, retinopathy and age-related macular degeneration as inflammatory conditions

“…This evidence [ 45 , 46 ] is in support of the role of pro-inflammatory eicosanoids in DME, DR and AMD [ 47 – 51 ]. In this context, it should be noted that in patients with DR, reduced plasma and vitreal concentrations of PGE 1 and PGI 2 were reported [ 52 – 55 ], while those of TXs and LTs were increased [ 50 , 54 – 56 ]. These results suggest that in DME, DR and AMD there is an imbalance between vasodilator and platelet anti-aggregator PGE 1 and PGI 2 and platelet aggregator and vasoconstrictor TXA 2 and LTs, leading to ischemic vasoconstriction of retinal vessels and enhanced platelet aggregation.…”