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A Rat Model of Proliferative Vitreoretinopathy Induced by Dispase

Session Details

Session Title: Quick Fire Free Paper 2

Session Date/Time: Thursday 11/09/2014 | 11:00-12:30

Paper Time: 11:55

Venue: Boulevard D

First Author: : M.Tikhonovich RUSSIA

Co Author(s): :    S. Gavrilova              

Abstract Details

Purpose:

To design a rat model of proliferative vitreoretinopathy (PVR) by intravitreal injection of dispase in different concentrations. Screening models of PVR for rats are currently not developed. Most of the works were carried out on rabbits whose eyes are very different from human. Typically, the animals are injected with one type of cells involved in formation of PVR. Such models are inappropriate for investigation of PVR initiation process. Our work is based on EM Frenzel`s et al. research (1998) carried out on rabbits. Dispasewas injected intravitreally, causing inflammation and disruption of the blood- barrier, followed by the development of PVR.

Setting:

The research was made on the physiology and general pathology academic department of the faculty of base medicine in M.V. Lomonosov Moscow State University, Russia. This work was supported by RFBR grant № 14-04-01318-A

Methods:

The work was carried out with rats of Rattus norvegicus species (N=60; weight=347,9±61,5 g). Rats were separated in four groups (15 species in each): a control group which received the intravitreal injection of 2 µl of sterile Ringer saline solution, and three groups which received the intravitreal injection of 2 µl of dispase in concentrations of 0,03U – D1 group, 0,07U – D2 group and 0,15U – D3 group correspondingly. The enucleation of the eyes was made during the first, sixth, and eighth weeks of the experiment. Histopathology. Enucleated eyes were embedded in paraffin and sectioned for light microscopy. Histologic examination was performed after hematoxylin and eosin staining.

Results:

In the control group PVR was not observed. After the dispase injection into the eyes hemorrhage was observed for 21% of animals. Already during the first week of the experiment, we found a dose-related retinal changes and a membrane formation. Since the first week significant changes were observed in retina in the D3 group: a violation of its architectonics, a photoreceptor degeneration. By the eighth week changes were so crucial that it was often impossible to distinguish individual layers. Dispase induced the membranes formation starting from the first week. In the D1 group in the first week membranes were barely visible or absent, but dispase caused thickening, undulating changes of retinal layers. By the sixth week in the D1 the membranes were noted in 100% of rats. Besides that the retinal condition was significantly better than in D2 and D3 groups, a similar situation was observed during the eighth week. In the D2 group, during the first week PVR developed in 40% of cases, by the sixth – in 60%. The retinal condition in this group had intermediate severity of injury: the destruction was less pronounced than in the D3 group, but much stronger than in the D1.

Conclusions:

The optimal dose of dispase administered by intravitreal injection required to simulate the stable result of proliferative vitreoretinopathy development is the smallest one in our work - 0,03U. The optimal moment of time for observing the signs of proliferative vitreoretinopathy is six weeks after the beginning of the experiment.

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