July 2019
Volume 60, Issue 9
ARVO Annual Meeting Abstract  |   July 2019
Rat model of posterior ischemic optic neuropathy
Author Affiliations & Notes
  • Fred N. Ross-Cisneros
    Neuro-Ophthalmology, Doheny Eye Institute, Los Angeles, California, United States
  • William Charles Sultan
    Neuro-Ophthalmology, Doheny Eye Institute, Los Angeles, California, United States
  • Samuel Asanad
    Neuro-Ophthalmology, Doheny Eye Institute, Los Angeles, California, United States
  • Alfredo A Sadun
    Ophthalmology, University of California at Los Angeles, Los Angeles, California, United States
    Neuro-Ophthalmology, Doheny Eye Institute, Los Angeles, California, United States
  • Footnotes
    Commercial Relationships   Fred Ross-Cisneros, None; William Sultan, None; Samuel Asanad, None; Alfredo Sadun, GenSight (F)
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science July 2019, Vol.60, 2265. doi:
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    • Get Citation

      Fred N. Ross-Cisneros, William Charles Sultan, Samuel Asanad, Alfredo A Sadun; Rat model of posterior ischemic optic neuropathy. Invest. Ophthalmol. Vis. Sci. 2019;60(9):2265.

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

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Purpose : To investigate a new rat model of posterior ischemic optic neuropathy (PION).

Methods : Eight Sprague-Dawley rats at 8 weeks old were used for this study, four receiving pressure-controlled hemorrhagic shock, the others for controls. The shock group were anesthetized, ventilated, monitored for body temperature, and catheterized in the femoral artery to monitor blood pressure and heart rate, the carotid artery for blood withdrawal to induce pressure-controlled hemorrhagic shock, and the jugular vein for replacing shed blood. Blood was heparinization and withdrawn while maintaining blood pressure at 30 mmHg. Shed blood volume was expressed as a percentage of calculated total blood volume [estimated from 6.12 mL/100 gm body weight]. After 30 minutes of shock, the rats were resuscitated with the reinfusion of total shed blood over a 30 minute period. Catheters were removed, vessels were tied off to prevent bleeding, incisions closed, given analgesia, and monitored for survival. After 6 weeks, the rats were euthanized, eyes and optic nerves were removed and immersion fixed in 10% formalin, dissected into intraorbital, intracanalicular, and intracranial regions, processed and embedded into paraffin blocks, and cut at 5 μm. The sections were stained with hematoxylin and eosin for general morphology and immunostained for axons and astroglia.

Results : The optic nerves in the experimental group all demonstrated optic atrophy with gliosis typical for an ischemic injury. These changes and axonal degeneration were observed primarily in the intracanalicular portion of the optic nerve. The remaining regions of the optic nerve anteriorly showed no direct signs of injury. In the intracanalicular nerve, a peripheral ring of optic nerve was relatively unaffected. Centrally, the axons were not spared. Controls were normal. This atrophy extended anteriorly and posteriorly along the intracanalicular optic nerve to slightly include both the intraorbital and intracranial regions. This atrophy and gliosis did not follow a vascular tree distribution and was in a pattern most consistent with watershed ischemia.

Conclusions : This pressure-controlled hemorrhagic shock model of PION in rats produced an infarct that was most pronounced in the intracanalicular region of the optic nerve . This is most consistent with watershed ischemia and a compartment syndrome. This model supports the concept that perioperative human PION is caused by blood loss induced shock.

This abstract was presented at the 2019 ARVO Annual Meeting, held in Vancouver, Canada, April 28 - May 2, 2019.


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