June 2017
Volume 58, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2017
Hypoxic-Ischemic Insult Disrupts Normal Retinal Vascular Developmen
Author Affiliations & Notes
  • Nader Sheibani
    Ophthalmology and Visual Sciences, Univ of Wisconsin-Madison, Madison, Wisconsin, United States
  • Ismail Zaitoun
    Ophthalmology and Visual Sciences, Univ of Wisconsin-Madison, Madison, Wisconsin, United States
  • Pelin Cengiz
    Pediatrics, University of Wisconsin-Madison, Madison, Wisconsin, United States
  • Ulas Cikla
    Pediatrics, University of Wisconsin-Madison, Madison, Wisconsin, United States
  • Eshwar Udho
    Pediatrics, University of Wisconsin-Madison, Madison, Wisconsin, United States
  • Dila Zafer
    Pediatrics, University of Wisconsin-Madison, Madison, Wisconsin, United States
  • Christine M Sorenson
    Pediatrics, University of Wisconsin-Madison, Madison, Wisconsin, United States
  • Footnotes
    Commercial Relationships   Nader Sheibani, None; Ismail Zaitoun, None; Pelin Cengiz, None; Ulas Cikla, None; Eshwar Udho, None; Dila Zafer, None; Christine Sorenson, None
  • Footnotes
    Support  This work was supported by National Institutes of Health Grants EY022883 and P30 EY016665, Environmental Protection Agency 83573701, and an unrestricted departmental award from Research to Prevent Blindness. NS is a recipient of Alice R. McPherson-Retina Research Foundation Chair.
Investigative Ophthalmology & Visual Science June 2017, Vol.58, 4070. doi:
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      Nader Sheibani, Ismail Zaitoun, Pelin Cengiz, Ulas Cikla, Eshwar Udho, Dila Zafer, Christine M Sorenson; Hypoxic-Ischemic Insult Disrupts Normal Retinal Vascular Developmen. Invest. Ophthalmol. Vis. Sci. 2017;58(8):4070.

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

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Abstract

Purpose : A majority of surviving children with hypoxic-ischemic (HI) encephalopathy develop various visual impairments. These visual defects are generally attributed to injuries to cerebral cortex and perhaps visual processing systems. Recent evidence also suggests neuronal damage in the retina. Whether retinal vascular damage occurs after hypoxic-ischemic insult remains unknown.

Methods : The day of birth was considered postnatal day zero (PND0). HI injury was induced in PND9 C57BL/6J mice according to Vannucci’s HI procedure. Briefly, the left common carotid artery was electrosurgically cauterized and the whole animal was exposed to 10% O2 and 90% N2 at 37°C for 50 min. Sham operated mice underwent similar procedures without actual cauterization or hypoxia exposure. At PND12, different days after the HI insult, animals were sacrificed and eyes were enucleated and fixed. The retinal vasculature integrity was assessed by both wholemount and cryosection immunostaining and confocal microscopy.

Results : Our results showed that the blood vessels on the surface of the retina were pathologically enlarged with signs of degeneration. Attenuation of deep retinal vessel expansion was resulted in an avascular retinal periphery. Retinal vascular damage was apparent as early as one-day post HI insult. Moreover, we found vascular abnormalities persisted, with little signs of recovery from the acquired vascular lesions, even after 100 days post HI insult.

Conclusions : The HI insult resulted in abnormal retinal vascularization. These vascular malformations and deficiency could exacerbate neuronal damage in the retina. Thus, our findings urge the need for developing therapeutic strategies to protect neurovascular dysfunction not only in brain but also retina.

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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