The Relationship of Oxidative Stress to Thrombotic Tendency in Type 1 Diabetic Patients with Retinopathy

Diabetic Medicine - Tập 8 Số 9 - Trang 860-865 - 1991
P.E. Jennings1, M. McLaren1, N. Scott1, A.R. Saniabadi1, J. J. F. Belch1
1Dept. of Medicine, Ninewells Hospital and Medical School, Dundee, Scotland

Tóm tắt

Increased free radical activity may contribute to thrombosis via effects on platelet aggregation and the prostanoid balance. To investigate this further we studied 15 Type 1 diabetic patients with retinopathy, matched with uncomplicated Type 1 patients for age, duration of diabetes and HbA1, together with matched healthy non‐diabetic control subjects. The oxidative effects of free radicals as total diene conjugates and lipid peroxides were measured, together with redox status extracellularly as plasma albumin‐thiols and intracellularly as erythrocyte superoxide dismutase activity. Platelet count, aggregation of platelets in whole blood to collagen, thromboxane B2, and prostacyclin stimulating factor (PGI2SF) were also assessed. Free radicals measured as lipid peroxides were significantly higher (9.6 (8.1–11.6) μmol 1‐1 (median and interquartile range) in diabetic patients with retinopathy than in control subjects (8.1 (7.4–9.2) μmol l‐1; p < 0.05). There were also significant reductions in redox status both extracellularly as plasma albumin thiols (408 (383–473) vs 490 (456–517) μmol l‐1, p < 0.001) and intracellularly as erythrocyte superoxide dismutase activity (34 (27–41) vs 44 (36–51) g l‐1, p < 0.05) between patients with retinopathy and control subjects. Platelet counts were increased in diabetic patients with retinopathy (p < 0.05), as was collagen‐induced platelet aggregation (p < 0.01). Prostacyclin stimulating factor was reduced in patients with retinopathy (p < 0.05) and correlated within the plasma with lipid peroxides (r = – 0.53, p < 0.04) and albumin thiols (r = 0.64, p < 0.01). The results suggest that diabetic patients, particularly with retinopathy, are under oxidative stress and have an increased thrombotic tendency with increased platelet reactivity and a reduction in prostacyclin stimulating factor.

Từ khóa


Tài liệu tham khảo

10.1136/bmj.282.6273.1339

10.1111/j.1464-5491.1988.tb00955.x

Wolff SP, 1987, Diabetic Complications: Scientific and Clinical Aspects, 167

Nath N, 1984, Superoxide dismutase in diabetic polymorphònuclear leukocytes, Diabetes, 33, 586, 10.2337/diab.33.6.586

10.1097/00000441-198405000-00004

Jennings PE, 1987, Vitamin C metabolites and microangiopathy in diabetes mellitus, Diabetes Res, 6, 151

10.1016/S0140-6736(83)90989-3

10.1177/000456327601300125

10.1016/0003-9861(59)90090-6

Aust S, 1987, Handbook of Methods for Oxygen Free Radical Research, 203

10.1093/rheumatology/8.7.233

10.1177/000456327601300125

Saniabadi AR, 1987, Comparison of inhibitory actions of prostacyclin and a new prostacyclin analogue of the aggregation of human platelets in whole blood, Haemostasis, 17, 147

McLaren M, 1986, Umbilical artery perfusion: A method to measure prostacyclin production in vitro. Prog Lipid Res, 311

Granstron E, 1987, Advances in Prostaglandins, Thromboxane and Leukotriene Research, 587

10.1016/S0020-1693(00)85762-X

Maestro RF, 1980, An approach to free radicals in medicine and biology, Acta Physiol Scand, 492, 153

10.1016/0006-2944(81)90096-X

10.1007/BF01733829

10.1111/j.1464-5491.1988.tb00955.x

10.1111/j.1464-5491.1990.tb01302.x

Jones AF, 1988, Serum antioxidant activity in diabetes mellitus, Diabetes Res, 7, 89

10.1016/0891-5849(89)90082-8

10.1136/bmj.298.6669.281

10.1016/0003-9861(79)90038-9

Warso MA, 1983, Lipid peroxidation in relation to prostacyclin and thromboxane physiology and pathophysiology, Br Med Bull, 39, 277, 10.1093/oxfordjournals.bmb.a071833

10.1111/j.1464-5491.1987.tb00827.x

10.1111/j.1365-2362.1979.tb00927.x

10.1016/S0140-6736(79)92844-7

10.1038/271549a0