Petersen Line, Bek Toke
Department of Ophthalmology, Aarhus University Hospital, DK-8000, Aarhus C, Denmark.
Graefes Arch Clin Exp Ophthalmol. 2017 Oct;255(10):1965-1971. doi: 10.1007/s00417-017-3746-2. Epub 2017 Jul 27.
Occlusion of retinal vessels leads to retinal ischaemia and hypoxia, which induces vasodilatation in adjacent retinal areas in order to normalize retinal oxygenation. Previous studies have shown that NO and COX products are involved in hypoxia-induced dilatation of retinal arterioles in vitro and in vivo, and that this response is disturbed in patients with diabetes mellitus. However, it is unknown to what extent post-hypoxic recovery of the diameter of retinal arterioles depends on NO and COX products in normal persons and in diabetic patients. The Dynamic Vessel Analyzer (DVA) was used to study the post-hypoxic diameter changes of larger retinal vessels in 20 normal persons, 20 diabetic patients without diabetic retinopathy, and in 18 patients with diabetic maculopathy before and after inhibition of the synthesis of nitric oxide and COX products. In normal persons, the arterioles had re-constricted (p > 0.99) 2 minutes after termination of hypoxia in the absence of antagonists, but not after treatment with L-NMMA and diclofenac (p < 0.01 for all comparisons). In diabetic patients without retinopathy, the arterioles showed no diameter changes after termination of hypoxia during any of the interventions. In patients with diabetic maculopathy hypoxia had not dilated retinal arterioles (p > 0.1 for all comparisons) to allow the study of re-constriction. In all groups, the dilatation of venules remained significantly increased during the post-hypoxic observation period, both in the absence and in the presence of L-NMMA and diclofenac.Post-hypoxic constriction of retinal arterioles depends on NO and COX products, and is impaired in diabetic patients before the development of retinopathy. This disturbance may contribute to the development of diabetic retinopathy, and should be the target of future interventional studies aimed at preventing and treating the disease.ClinicalTrials.gov identifier: NCT01689090.
视网膜血管阻塞会导致视网膜缺血和缺氧,进而引起相邻视网膜区域的血管扩张,以实现视网膜氧合的正常化。先前的研究表明,一氧化氮(NO)和环氧化酶(COX)产物参与了体内外缺氧诱导的视网膜小动脉扩张,并且糖尿病患者的这种反应受到干扰。然而,在正常人和糖尿病患者中,视网膜小动脉直径的缺氧后恢复在多大程度上依赖于NO和COX产物尚不清楚。使用动态血管分析仪(DVA)研究了20名正常人、20名无糖尿病视网膜病变的糖尿病患者以及18名糖尿病黄斑病变患者在抑制一氧化氮和COX产物合成前后较大视网膜血管的缺氧后直径变化。在正常人中,在没有拮抗剂的情况下,缺氧终止后2分钟小动脉已重新收缩(p>0.99),但在用L-硝基精氨酸甲酯(L-NMMA)和双氯芬酸治疗后则没有(所有比较p<0.01)。在无视网膜病变的糖尿病患者中,在任何干预期间缺氧终止后小动脉直径均无变化。在糖尿病黄斑病变患者中,缺氧并未使视网膜小动脉扩张(所有比较p>0.1),因此无法研究重新收缩情况。在所有组中,无论是否存在L-NMMA和双氯芬酸,在缺氧后观察期内小静脉的扩张均保持显著增加。视网膜小动脉的缺氧后收缩依赖于NO和COX产物,并且在糖尿病患者视网膜病变发生之前就已受损。这种干扰可能有助于糖尿病视网膜病变的发展,并且应该成为未来旨在预防和治疗该疾病的干预性研究的目标。ClinicalTrials.gov标识符:NCT01689090。