Prostanoids in the Vitreous of Diabetic and Nondiabetic Human Eyes with Retinal Detachment

Abstract

We measured prostaglandin E₂ (PGE₂) and prostacyclin levels in the vitreous bodies of 5 eyes of patients with diabetic retinopathy complicated by rhegmatogenous retinal detachment (RRD) and compared them with the corresponding levels in 9 nondiabetic eyes with the same condition as well as with 10 control eyes of deceased patients with no known ocular pathology. We also studied the effect of surgical retinal reattachment on vitreal PGE₂and prostacyclin levels in 4 eyes. Vitreal samples from both nondiabetic and diabetic eyes with RRD were obtained during vitrectomy, while samples from deceased subjects (controls) were obtained 2–6 h after death. Vitreal PGE₂ and prostacyclin levels in the control eyes approximated plasma levels (79.9 ± 20.5 and 124.5 ± 38.5 pg/ml, means ± SD, respectively), while RRD in the nondiabetic eyes was associated with increased levels of both PGE₂ and prostacyclin (3,170 ± 3,024 and 467 ± 283 pg/ml, respectively). In the diabetic eyes with diabetic retinopathy complicated by RRD, all of which underwent retinal photocoagulation, PGE₂ and prostacyclin levels were 2–4 times lower than those of the nondiabetic eyes with detached retina. Following surgical retinal reattachment, vitreal levels of both components in diabetics and nondiabetics showed a reduction suggesting that the surgical procedure for obtaining vitreal samples was not the cause for elevated prostaglandin levels in the eyes with detached retina. We showed that RRD is associated with an excessive accumulation of PGE₂ and prostacyclin in the vitreous, which is higher in nondiabetic than in diabetic eyes, indicating that diabetic retinopathy in laser-treated eyes might lead to reduced vitreal levels of these metabolites.

Preserved Pressure Autoregulation but Disturbed Cyclo-Oxygenase and Nitric Oxide Effects on Retinal Arterioles during Acute Hypoxia in Diabetic Patients without Retinopathy

“…Therefore, it is possible that these mechanisms may be involved in the pathophysiology of retinal vascular impairment in diabetic retinopathy. This notion is supported by the fact that the concentration of COX products in the vitreous is abnormal in diabetic animals [5] and in diabetic patients with proliferative retinopathy [6,7], and by the finding that diabetic patientshave abnormal endogenous NO synthesis, probably related to endothelial dysfunction [8,9]. It has previously been shown that interventions on the synthesis of NO and COX products interfere with diameter regulation of retinal arterioles during hypoxia in normal persons [10,11], but it remains unknown how these interventions may affect hypoxia-induced vasodilatation in diabetic patients, and especially whether the changes occur before the development of diabetic retinopathy to suggest a role in the early stages of the pathophysiology of the disease.…”

Ocular Delivery of Acetylsalicylic Acid by Repetitive Coulomb-Controlled Iontophoresis

“…The special role of prostaglandin E 2 (PGE 2 ) in the induction of vascular inflamma-tion in neovascular retinal disorders [22][23][24] and its association with pathologic conditions such as damage due to laser irradiation [25,26], optic nerve injury [19] and retinal detachment [27] are well known. The major importance of prostaglandins in ocular diseases and injuries has been established [28][29][30][31][32][33][34].…”

Prostacyclins in Diabetes: An Electrophysiological Study

“…Occlusive alteration of the vascular bed occurs, being mediated through platelet malfunction as a result of defects and aggregation of platelets [ 12,13]. Disturbances of hemostasis might be rebalanced by adding synthetic prostacyclin inhibiting the aggrega tion of platelets [2,3,14,15], Several studies correlated the plasma activity of prostaglan din and prostacyclin levels [16,17] with the development of diabetic retinopathies. Plas ma factors indicating prostacyclin-like activi ty in patients with diabetes mellitus were low er than in controls [ 18],…”