April 2009
Volume 50, Issue 13
ARVO Annual Meeting Abstract  |   April 2009
Hyperglycemia Induces Endothelial Dysfunction in Retinal Arterioles in Cats
Author Affiliations & Notes
  • K. Sogawa
    Asahikawa Medical College, Asahikawa, Japan
  • T. Nagaoka
    Asahikawa Medical College, Asahikawa, Japan
  • S. Nakabayashi
    Asahikawa Medical College, Asahikawa, Japan
  • T. Omae
    Asahikawa Medical College, Asahikawa, Japan
  • A. Takahashi
    Asahikawa Medical College, Asahikawa, Japan
  • I. Tanano
    Asahikawa Medical College, Asahikawa, Japan
  • T. Tani
    Asahikawa Medical College, Asahikawa, Japan
  • A. Yoshida
    Asahikawa Medical College, Asahikawa, Japan
  • Footnotes
    Commercial Relationships  K. Sogawa, None; T. Nagaoka, None; S. Nakabayashi, None; T. Omae, None; A. Takahashi, None; I. Tanano, None; T. Tani, None; A. Yoshida, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science April 2009, Vol.50, 398. doi:
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    • Get Citation

      K. Sogawa, T. Nagaoka, S. Nakabayashi, T. Omae, A. Takahashi, I. Tanano, T. Tani, A. Yoshida; Hyperglycemia Induces Endothelial Dysfunction in Retinal Arterioles in Cats. Invest. Ophthalmol. Vis. Sci. 2009;50(13):398.

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

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Purpose: : To investigate the effect of acute hyperglycemia on retinal microcirculation and endothelial function in cats and whether the removing of the superoxide can prevent the retinal endothelial dysfunction caused by hyperglycemia.

Methods: : Hyperglycemia was induced by intravenous administration of 25% glucose to keep plasma glucose concentration at 30 mM. We measured the vessel diameter (D) and blood velocity (V) simultaneously and calculated the retinal blood flow (RBF) in second-order retinal arterioles by laser Doppler velocimetry. We performed the topical administration of PBS, endothelium-dependent vasodilator bradykinin (BK), and endothelium-independent vasodilator sodium nitroprusside (SNP) into the vitreous cavity to evaluate the endothelial function in retinal arterioles. As an osmolality control, we administration of 25% mannitol. In addition, we also induced systemic hyperoxia to examine the endothelial function during hyperglycemia non-invasively. To determine the influence of the superoxide on hyperglycemia-induced change on retinal circulation, TEMOL was administrated in drinking water for 14 days.

Results: : Hyperglycemia induced the increases in D, V, and RBF compared with the baseline. BK-induced increases in D, V and RBF were significantly declined whereas SNP-induced increases were not attenuated during acute hyperglycemia. The recovery of the decreased RBF to baseline after systemic hyperoxia was also significantly inhibited by acute hyperglycemia. The pretreatment of TEMPOL significantly prevented the reduction of BK-induced increase in RBF during hyperglycemia (P<0.05).

Conclusions: : The present results suggest that acute hyperglycemia increases retinal blood flow probably via the increased osmolality and may cause the retinal endothelial dysfunction, partially via the increased oxidative stress. Systemic hyperoxia can be used for the non-invasive clinical examination to evaluate the retinal endothelial function during hyperglycemia in patients with diabetes mellitus.

Keywords: diabetic retinopathy • retina • oxidation/oxidative or free radical damage 

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