Morphology of the arterial edema. Gelatinous elevations of intima of the aorta and coronary vessels
At a microscopic examination Aortic wall in the zone of the OOI was observed focalintimal edema, which is an insudate, spreading the elements of the connective tissue of the intima. In all cases, the insudate spread to the entire thickness of the intima, reaching the inner elastic membrane.
In most cases, in the zone of the intima edema, desquamation endothelium. In the subendothelial layer of the intima,loosening and spreading of collagen and elastic fibers, MMC. Focal metachromasia of the main substance, irregular distribution of glycosaminoglycans was detected. In the zone of the OOI, swelling, splitting, chaotic arrangement of collagen and elastic fibers, clumps and filaments of fibrinogen are traced.
Internal elastic membrane sharp thinned, fragmented, split. In this zone, focal proliferation of the MMC, their focal aggregations under the BEM, neoplasm of the elastic and collagen fibers, penetration of the GM K from the media into the intima through defects of the VEM are noted. In all cases of the aortic OOI, a lesion of the main substance was detected in the form of focal metachromasia, pericellular edema, accumulation of acidic and neutral glycosaminoglycans.
Thus, greyish gelatinous intimal aorta elevations are a consequence of its focal edema. Such local accumulation of fluid can theoretically result from both a delay in the absorption of blood plasma, normally perfused from the lumen of the vessel in the vasa vasorum and feeding the vessel wall, and an increase in the penetration of blood proteins into the intima. The etiologic factors that activate these mechanisms seem to be very diverse, and, as was proved for the mechanism of atherogenesis, some of them can cause a purely mechanical trauma to the endothelium or the underlying intimal tissue, altering its metabolism and leading to a disruption permeability of the endothelium.
Normally, through vascular wall there is a moderate amount of albumin, a smallthe number of a- and beta-lipoproteins, a very small number of globulins; fibrinogen is normal in the intima is not included or is present in small amounts. Since edematous fluid in the foci of intimal edema mostly consists of albumins and globulins and mechanically separates connective tissue fibers and MMC, without changing their structural integrity, it can be completely adsorbed by vasa vasorum and the normal structure of the intima can be completely restored. Consequently, this stage of serous focal edema of the intima is a reversible process.
In case of further increase permeability endothelium in intima penetrate large moleculesfibrinogen and cause serous-fibrinous edema. Fibrinogen precipitates in tissues, fibrin in the form of fibrous and granular formations accumulates in the OOI. In the late stages of development in the zone of the OOI, the phenomena of the organization of serous fibrinous insulin begin to develop with the development of fibrous connective tissue, proliferation of the MMC with their fat metamorphosis, degeneration and extracellular release of lipids, which can lead to the formation of lipid fibrous atherosclerotic plaques.
In view of the small number of observations focal edema of intima of the aorta in children. in this work was not possibleanalyze the material in the age-sexual and ethnic aspects. We made an attempt to conduct a histomorphological characterization of focal edema of intima of the aorta as an early preterosclerotic lesion.