Retinal Electrophysiologic Response to IOP Elevation in Brain-Dead Organ Donors

13 Pages Posted: 27 Oct 2022

See all articles by Christopher A. Girkin

Christopher A. Girkin

University of Alabama at Birmingham - Department of Ophthalmology and Visual Sciences

Mary Anne Garner

University of Alabama at Birmingham - School of Medicine

Massimo A. Fazio

University of Alabama at Birmingham - Department of Ophthalmology and Visual Sciences

Mark Clark

University of Alabama at Birmingham - Department of Ophthalmology and Visual Sciences

Udayakumar Karuppanan

University of Alabama at Birmingham - Department of Ophthalmology and Visual Sciences

Meredith Hubbard

University of Alabama at Birmingham - Department of Ophthalmology and Visual Sciences

Gianfranco Bianco

University of Alabama at Birmingham - Department of Ophthalmology and Visual Sciences

Seth T. Hubbard

University of Alabama at Birmingham - School of Medicine

Brad Fortune

Legacy Research Institute

Gross K. Alecia

University of Alabama at Birmingham - School of Medicine

Abstract

Purpose: The relationships between intraocular pressure (IOP), ocular perfusion pressure (OPP), retinal perfusion, and retinal electrophysiologic responses have been explored experimentally across several animal models. These studies have demonstrated that elevated IOP reduces OPP, and when this reduction in OPP exceeds the autoregulatory capacity of the retina vasculature, retinal perfusion and electrophysiologic responses are reduced. This study aimed to evaluate these interactions for the first time in the living human eye.

Methods: Five eyes from three research-consented brain-dead organ donors underwent optical coherence tomography with angiographic (OCT/A; Spectralis, Heidelberg Engineering) and electroretinographic (ERG, Diagnosys LLC) measurements while IOP was manometrically-elevated stepwise to pressures of 10, 30 and 50 mmHg. Systemic blood pressure (BP) was monitored continuously during testing. Correlation analysis was applied to assess association between ERG and OPP changes. In a single eye, prolonged IOP elevation was induced with viscoelastic injection and serial ERG measurements were obtained.

Results: Reductions in inner retinal function defined by photopic ERG were observed with elevation in IOP and concomitant reduction in OPP. Reductions, especially in b -wave, and photopic negative response (PhNR) amplitudes and implicit times were significantly correlated with elevation in IOP and reduction in OPP. There were more appreciable changes in perfusion and functional responses in eyes tested while systemic blood pressure was lower. With prolonged IOP elevation, selective loss of the PhNR response was observed.

Conclusions: In the living human eye, retinal perfusion and inner retinal function are acutely impacted by elevation of IOP, and this impact is related to systemic BP and OPP. This novel approach provides a viable model to study the autoregulatory responses to IOP elevation in the living human eye.

Note:

Funding Information: Heidelberg Engineering, Topcon Healthcare, Research to Prevent Blindness, EyeSight Foundation of Alabama, National Eye Institute (R01 EY028284).

Declaration of Interests: Christopher Girkin: Commercial Relationship(s); Code F (Financial Support): Heidelberg Engineering, Topcon Healthcare; Mary Anne Garner: Commercial Relationship: Code N (No Commercial Relationship) | Massimo Fazio: Commercial Relationship(s); Code F (Financial Support): Heidelberg Engineering, Topcon Healthcare | Mark Clark: Commercial Relationship: Code N (No Commercial Relationship) | Udayakumar Karuppanan: Commercial Relationship: Code N (No Commercial Relationship) | Gianfranco Bianco: Commercial Relationship: Code N (No Commercial Relationship) | Meredith Hubbard: Commercial Relationship: Code N (No Commercial Relationship) | Seth Hubbard: Code N (No Commercial Relationship) | Brad Fortune: Heidelberg Engineering, GmbH (F, equipment support), Perfuse Therapeutics, Inc. (F, C), Perceive Biotherapeutics, Inc. (C) | Alecia K. Gross: Code N (No Commercial Relationship).

Ethics Approval Statement: All components of this study adhered to the Declaration of Helsinki and were approved by the UAB Institutional Review Board and LoH Research Review Board. Research within LoH only occurs if not at the expense of organ donation, with IRB approval, and with specific consent. All research consents are obtained from the donor’s family by dedicated staff who are trained to speak with families in a culturally sensitive and compassionate manner.

Keywords: Retinal ganglion cell, optic nerve head, intraocular pressure, ocular perfusion pressure, retina, optical coherence tomography, human, electroretinography

Suggested Citation

Girkin, Christopher A. and Garner, Mary Anne and Fazio, Massimo A. and Clark, Mark and Karuppanan, Udayakumar and Hubbard, Meredith and Bianco, Gianfranco and Hubbard, Seth and Fortune, Brad and Alecia, Gross K., Retinal Electrophysiologic Response to IOP Elevation in Brain-Dead Organ Donors. Available at SSRN: https://ssrn.com/abstract=4234251 or http://dx.doi.org/10.2139/ssrn.4234251

Christopher A. Girkin (Contact Author)

University of Alabama at Birmingham - Department of Ophthalmology and Visual Sciences ( email )

Birmingham, AL
United States

Mary Anne Garner

University of Alabama at Birmingham - School of Medicine ( email )

Massimo A. Fazio

University of Alabama at Birmingham - Department of Ophthalmology and Visual Sciences ( email )

Mark Clark

University of Alabama at Birmingham - Department of Ophthalmology and Visual Sciences ( email )

Udayakumar Karuppanan

University of Alabama at Birmingham - Department of Ophthalmology and Visual Sciences ( email )

Meredith Hubbard

University of Alabama at Birmingham - Department of Ophthalmology and Visual Sciences ( email )

Gianfranco Bianco

University of Alabama at Birmingham - Department of Ophthalmology and Visual Sciences ( email )

Seth Hubbard

University of Alabama at Birmingham - School of Medicine ( email )

Brad Fortune

Legacy Research Institute ( email )

Gross K. Alecia

University of Alabama at Birmingham - School of Medicine ( email )

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