Alteration of ocular blood pressure and flow leads to ophthalmic vascular and neuroretinal dysfunction

Abstract

Purpose : Although systemic hypertension is a major risk factor for retinopathy, its impact on the ocular circulation and retinal function remains unclear. Transverse aortic coarctation (TAC) induces differential blood pressure/flow distribution to the left vs. right eye. Herein, utilizing the TAC model, we investigated the impact of ocular blood pressure/flow alteration on ophthalmic vasomotor regulation and retinal function.

Methods : TAC was performed in mice by banding the aorta between the brachiocephalic artery and the left common carotid artery (CCA). Sham-operated mice served as controls. Blood velocity in the central retinal artery (CRA) was measured by Doppler ultrasound. Ophthalmic arteries were isolated, cannulated, and pressurized for functional study. Retinal function and morphology were examined using electroretinography and optical coherence tomography, respectively.

Results : TAC for one month elicited left ventricular hypertrophy and dysfunction. Mean arterial pressure was increased by 50% and decreased by 30% in the right and left CCAs, respectively. Mean blood velocity was gradually increased by 40% and decreased by 20% in the right and left CRAs, respectively, at 4 weeks after aortic banding. Fundus imaging revealed no changes in the retinal vessel diameters in both eyes. The responses of right (hypertensive) ophthalmic arteries to the endothelium-dependent, nitric oxide-mediated vasodilators acetylcholine and adenosine were significantly reduced and the vasoconstriction to endothelin-1 was increased in TAC animals. In contrast, the responses of left ophthalmic (hypotensive) arteries to the above agonists were unchanged. Decreased retinal oscillatory potentials and increased implicit times in the scotopic electroretinogram were found in both right and left eyes. No significant changes in retinal morphology were observed in both eyes.

Conclusions : The elevation of blood pressure and flow to the ocular circulation for 4 weeks causes ophthalmic vascular dysfunction, which is associated with impaired retinal function without altering retinal morphology. The ophthalmic vasomotor function is insensitive to hypotensive insult; however, the insufficient blood flow might cause retinal injury possibly due to ischemia from exhausted vasodilator reserve. Our results provide further insight on the development of retinopathy in the early phase of ocular blood pressure and flow alterations.

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