June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
Arterial hypertension induces retinal degeneration in mice with pressure-overload cardiac hypertrophy
Author Affiliations & Notes
  • Shu-Huai Tsai
    Department of Medical Physiology, Baylor Scott & White Health, Texas A&M Health Science Center, Temple, TX
  • Wankun Xie
    Department of Ophthalmology, Baylor Scott & White Health, Texas A&M Health Science Center, Temple, TX
  • Robert H Rosa
    Department of Ophthalmology, Baylor Scott & White Health, Texas A&M Health Science Center, Temple, TX
  • Travis W Hein
    Department of Ophthalmology, Baylor Scott & White Health, Texas A&M Health Science Center, Temple, TX
  • Lih Kuo
    Department of Medical Physiology, Baylor Scott & White Health, Texas A&M Health Science Center, Temple, TX
    Department of Ophthalmology, Baylor Scott & White Health, Texas A&M Health Science Center, Temple, TX
  • Footnotes
    Commercial Relationships Shu-Huai Tsai, None; Wankun Xie, None; Robert Rosa, None; Travis Hein, None; Lih Kuo, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 4862. doi:https://doi.org/
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      Shu-Huai Tsai, Wankun Xie, Robert H Rosa, Travis W Hein, Lih Kuo; Arterial hypertension induces retinal degeneration in mice with pressure-overload cardiac hypertrophy. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):4862. doi: https://doi.org/.

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

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Abstract

Purpose: The etiology and mechanism of hypertensive retinopathy are not fully understood. Transverse aortic coarctation (TAC) between the two common carotid arteries elicits cardiac hypertrophy and 40-50% increase in blood pressure to the right carotid artery, but its impact on the ocular circulation is unknown. The present study was aimed at using the TAC mouse model to investigate whether elevated blood pressure causes retinal injury.

Methods: Mice were subjected to TAC for 1 or 3 months by banding the aortic arch between the left common carotid artery and the right brachiocephalic artery, which gives rise to the right common carotid artery. Sham-operated mice served as controls. Central retinal artery (CRA) blood velocity was measured by Doppler ultrasound. Retinal fundus imaging, spectral domain optical coherence tomography (SD-OCT), and histological examination were used to assess retinal abnormalities.

Results: Induction of TAC in mice for 1 month had no effect on the body weight but caused cardiac hypertrophy with increased heart-to-body weight ratio by 45% and decreased left ventricular fractional shortening by 51%. As compared to the sham-operated mice, blood flow velocity in the right CRA of TAC mice was increased by 45% at 1 month and 3 months after surgery. For the left eye, CRA blood velocity had no change at 1 month but was decreased by 23% at 3 months after aortic banding. Fundus imaging showed no apparent retinal abnormality between sham and TAC mice. Attenuation of the retinal nerve fiber layer and the inner retina was found in the right eye of TAC mice by SD-OCT. Histological examination of the retina indicated a decrease in the thickness of the inner nuclear layer in both right and left eyes in TAC mice at 3 months after surgery. Cell loss and morphological changes were found in the ganglion cell layer (GCL), indicating GCL degeneration in the TAC mice.

Conclusions: Elevated right carotid arterial blood pressure by TAC leads to increased CRA blood flow and retinal degeneration in mice. In the later phase, the compensatory reduction of left carotid arterial perfusion, which leads to left CRA blood flow deficiency, also causes retinal injury. This experimental model may be useful for studying the mechanisms and potential treatments of retinopathy in association with chronic changes in systemic blood pressure and ocular perfusion.

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