I.V. Zapuskalov
O.B. Kochmala
O.I. Krivosheina
O.B. Zapuskalova
J.I. Khoroshikh |
MECHANISM OF DEVELOPMENT OF PROLIFERATIVE VITREORETINOPATHY
IN DIABETES |
| Siberian State Medical University, Tomsk, Russia |
The investigation of the mechanics of blood circulation in the eye in health
and disease has allowed us to put forward the quite different theory on the
pathogenesis of diabetic changes in the fundus of eye and to propose the principally
other method of laser treatment. The interstitial fluid, flowing
from choriocapillaries, passes through the pigment epithelium and the outer
retinal layers, and is absorbed by the retinal vessels. At the acute increase
of the sugar concentration in the blood following meals, the osmotic blood pressure,
naturally, increases sharply. Thus, for example, the increase of the sugar level
in the blood by 100 mg% (5.55 mmol/l) increases the serum osmolarity roughly
by 5.5 mosm/l, which corresponds to 86 mm Hg. Therefore, if the sugar concentration
in the blood increases quite quickly, then the transmural osmotic pressure in
the retinal capillaries increases drastically. The fluid is drawn out
from the retinal tissue to the blood in retinal vessels, and this leads to the
sharp increase of the transmural hydraulic pressure in the retinal vessels.
Due to myogenic autoregulation, arterioles narrow up to the complete blockage
of the blood flow (with development of retinal microinfarctions), capillaries
stretch with formation of microaneurisms, and venules dilate with the pronounced
caliber irregularity. At hypoglycemia, the reverse process occurs with the development
of retinal edema, more pronounced in the macular area. The inflow of high-molecular
plasma component into the retinal tissue is naturally accompanied by the change
in the transcapillary difference of the colloidosmotic pressure. The consequence
of this is the change in the total pressure gradient, reflecting the relation
between the colloid-osmotic and hydrostatic pressures inside and outside a vessel.
The equilibrium distribution of the fluid between the intra- and extravessel
space is disturbed, and the fluid accumulates in the intercellular space,
aggravating the pathological changes of the retinal tissue in the macular area.
Once microaneurisms rupture and the internal or external border membrane breaks,
the blood issues into accessible spaces, just where the proliferative processes
occur. There is no doubt that the proliferative process can start developing
in the posterior pole of the eye after intravitreal and preretinal hemorrhages.
Among the blood corpuscles, coming into the eyeball cavity in this case, of
interest, in our opinion, are mononuclears. When mononuclears of the human blood
were cultivated in vitro under the conditions of the directed motion of the
nutrient medium, modeling the motion of the intraocular fluid, 48 hours
after the beginning of the experiment the cytochemical marking has revealed
young forms of the fibroblast population, being, most probably, fibroblast
precursor cell, in the cell culture. As a result, having passed through some
differentiation stages, young mesenchymal cells, present among mononuclear,
specialize under the modulating effect of microenvironmental factors and become
mature fibroblasts, synthesizing collagen.
