Jennings P E, McLaren M, Scott N A, Saniabadi A R, Belch J J
Department of Medicine, Ninewells Hospital and Medical School, Dundee, Scotland.
Diabet Med. 1991 Nov;8(9):860-5. doi: 10.1111/j.1464-5491.1991.tb02125.x.
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) mumol l-1 (median and interquartile range) in diabetic patients with retinopathy than in control subjects (8.1 (7.4-9.2) mumol l-1; p less than 0.05). There were also significant reductions in redox status both extracellularly as plasma albumin thiols (408 (383-473) vs 490 (456-517) mumol l-1, p less than 0.001) and intracellularly as erythrocyte superoxide dismutase activity (34 (27-41) vs 44 (36-51) g l-1, p less than 0.05) between patients with retinopathy and control subjects. Platelet counts were increased in diabetic patients with retinopathy (p less than 0.05), as was collagen-induced platelet aggregation (p less than 0.01). Prostacyclin stimulating factor was reduced in patients with retinopathy (p less than 0.05) and correlated within the plasma with lipid peroxides (r = -0.53, p less than 0.04) and albumin thiols (r = 0.64, p less than 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.
自由基活性增加可能通过影响血小板聚集和前列腺素平衡而导致血栓形成。为进一步研究这一问题，我们对15名患有视网膜病变的1型糖尿病患者进行了研究，这些患者在年龄、糖尿病病程和糖化血红蛋白方面与无并发症的1型患者相匹配，同时还选取了相匹配的健康非糖尿病对照者。测量了自由基作为总二烯共轭物和脂质过氧化物的氧化作用，以及细胞外作为血浆白蛋白硫醇和细胞内作为红细胞超氧化物歧化酶活性的氧化还原状态。还评估了血小板计数、全血中血小板对胶原的聚集、血栓素B2和前列环素刺激因子（PGI2SF）。以脂质过氧化物测量的自由基在患有视网膜病变的糖尿病患者中显著高于对照者（9.6（8.1 - 11.6）μmol l-1（中位数和四分位间距），对照者为8.1（7.4 - 9.2）μmol l-1；p < 0.05）。视网膜病变患者与对照者相比，细胞外作为血浆白蛋白硫醇的氧化还原状态也显著降低（408（383 - 473）对490（456 - 517）μmol l-1，p < 0.001），细胞内作为红细胞超氧化物歧化酶活性也显著降低（34（27 - 41）对44（36 - 51）g l-1，p < 0.05）。患有视网膜病变的糖尿病患者血小板计数增加（p < 0.05），胶原诱导的血小板聚集也增加（p < 0.01）。视网膜病变患者的前列环素刺激因子降低（p < 0.05），且在血浆中与脂质过氧化物相关（r = -0.53，p < 0.04），与白蛋白硫醇相关（r = 0.64，p < 0.01）。结果表明，糖尿病患者，尤其是患有视网膜病变的患者，处于氧化应激状态，血栓形成倾向增加，血小板反应性增强，前列环素刺激因子减少。
