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Updated: Aug 1, 2026
A Mouse Model of Retinal Ischemia-Reperfusion Injury Through Elevation of Intraocular Pressure
Published on: July 14, 2016
[Effect of ischemia-reperfusion on membrane structure and function in rat retina]
1Department of Ophthalmology, Jinan Command General Hospital of PLA, Jinan 250031.
Objective:
To study the effect of ischemia-reperfusion on membrane structure and function in rat retina.
Methods:
Thirty-two SD rats were randomly grouped into 4 groups. Group 1 served as the control group, group 2, 3 and 4 served as reperfusion 3 hours, 30 hours and 5 days respectively. The intraocular pressure (IOP) was raised to occlude retinal and choroidal blood vessels to form retinal ischemia; afterwards the IOP was lowered to normal to allow reperfusion. The animal was sacrificed after reperfusion. The colorimetric determination of phosphorus was used to investigate Na(+)-K(+)-ATPase activity of rat retina; the cellular membrane was labelled by fluorescence probe DPH to detect its fluidity which was measured by means of fluorescence spectrophotometer.
Results:
Na(+)-K(+)-ATPase and membrane influidity were damaged at early stage. The longer the ischemia, the more serious was the reperfusion injury.
Conclusions:
The mechanism of the decrease of Na(+)-K(+)-ATPase activity is due to the production of substances involved in peroxidation and excitatory amino acid (EAA) which are produced during reperfusion. They can damage the Na(+)-K(+)-ATPase directly. Lipid peroxidation disrupts membrane integrity and causes decrease of membrane influidity. For these reasons, membrane stability is reduced and Na(+)-K(+)-ATPase protein function is changed.
