Acute retinal ischemia caused by controlled low ocular perfusion pressure in a porcine model. Electrophysiological and histological characterisation

TY - JOUR

T1 - Acute retinal ischemia caused by controlled low ocular perfusion pressure in a porcine model. Electrophysiological and histological characterisation

AU - Kyhn, Maria Voss

AU - Warfvinge, Karin

AU - Scherfig, Erik

AU - Kiilgaard, Jens F

AU - Prause, Jan Ulrik

AU - Klassen, Henry

AU - Young, Michael

AU - la Cour, Morten

AU - Kyhn, Maria Voss

AU - Warfvinge, Karin

AU - Scherfig, Erik

AU - Kiilgaard, Jens F

AU - Prause, Jan Ulrik

AU - Klassen, Henry

AU - Young, Michael

AU - la Cour, Morten

N1 - Keywords: Acute Disease; Amacrine Cells; Animals; Blood Pressure; Disease Models, Animal; Electroretinography; Female; Intraocular Pressure; Ischemia; Retinal Diseases; Retinal Ganglion Cells; Retinal Horizontal Cells; Retinal Vessels; Sus scrofa

PY - 2009/6/1

Y1 - 2009/6/1

N2 - The purpose of this study was to establish, and characterize a porcine model of acute, controlled retinal ischemia. The controlled retinal ischemia was produced by clamping the ocular perfusion pressure (OPP) in the left eye to 5 mm Hg for 2 h. The OPP was defined as mean arterial blood pressure (MAP) minus the intraocular pressure (IOP). It was clamped to 0-30 mm Hg by continuous monitoring of MAP and adjustment of the IOP, which was controlled by cannulation of the anterior chamber. Inner retinal function was assessed by induced multifocal electroretinography (mfERG) with comparisons of the amplitudes obtained in the experimental, left eye, and the control, right eye. Quantitative histology was performed to measure the survival of ganglion cells, amacrine cells and horizontal cells 2-6 weeks after the ischemic insult. An OPP of 5 mm Hg for 2h induced significant reductions in the amplitudes of iN1 to 20% (CI: 13-30%), and iP2 to 14% (95% CI: 8-22%) of their baseline values. No signs of recovery were found within the 6-week observation period. Quantitative histology revealed a highly significant reduction in the number of ganglion cells, amacrine cells and horizontal cells after the ischemic insult. This model seems to be suitable for investigations of therapeutic initiatives in diseases involving acute retinal ischemia.

AB - The purpose of this study was to establish, and characterize a porcine model of acute, controlled retinal ischemia. The controlled retinal ischemia was produced by clamping the ocular perfusion pressure (OPP) in the left eye to 5 mm Hg for 2 h. The OPP was defined as mean arterial blood pressure (MAP) minus the intraocular pressure (IOP). It was clamped to 0-30 mm Hg by continuous monitoring of MAP and adjustment of the IOP, which was controlled by cannulation of the anterior chamber. Inner retinal function was assessed by induced multifocal electroretinography (mfERG) with comparisons of the amplitudes obtained in the experimental, left eye, and the control, right eye. Quantitative histology was performed to measure the survival of ganglion cells, amacrine cells and horizontal cells 2-6 weeks after the ischemic insult. An OPP of 5 mm Hg for 2h induced significant reductions in the amplitudes of iN1 to 20% (CI: 13-30%), and iP2 to 14% (95% CI: 8-22%) of their baseline values. No signs of recovery were found within the 6-week observation period. Quantitative histology revealed a highly significant reduction in the number of ganglion cells, amacrine cells and horizontal cells after the ischemic insult. This model seems to be suitable for investigations of therapeutic initiatives in diseases involving acute retinal ischemia.

U2 - 10.1016/j.exer.2009.01.016

DO - 10.1016/j.exer.2009.01.016

M3 - Journal article

C2 - 19450446

SN - 0014-4835

VL - 88

SP - 1100

EP - 1106

JO - Experimental Eye Research

JF - Experimental Eye Research

IS - 6

ER -