June 2017
Volume 58, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2017
Post-hypoxic recovery of the diameter of retinal arterioles is impaired in diabetic patients without retinopathy.
Author Affiliations & Notes
  • Line Petersen
    Aarhus University Hospital, Aarhus, Denmark
  • Toke Bek
    Aarhus University Hospital, Aarhus, Denmark
  • Footnotes
    Commercial Relationships   Line Petersen, None; Toke Bek, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science June 2017, Vol.58, 230. doi:https://doi.org/
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      Line Petersen, Toke Bek; Post-hypoxic recovery of the diameter of retinal arterioles is impaired in diabetic patients without retinopathy.. Invest. Ophthalmol. Vis. Sci. 2017;58(8):230. doi: https://doi.org/.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose : 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.

Methods : 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.

Results : In normal persons the arterioles had re-contracted (p>0.99) two minutes after termination of hypoxia in the absence of antagonists, but not in patients treated 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-contraction. 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.

Conclusions : Post-hypoxic contraction 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.

This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.


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