Научный журнал

European Journal of Natural History

ISSN 2073-4972

ИФ РИНЦ = 0,301

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Grigoryeva Y.V. 1 Kulakova O.V. 1 Chemidronov S.N. 1 Tulaeva O.N. 1

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1 Samara State Medical University of the RF Health Ministry

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The regenerative ultrastructural changes in lower uterine segment myocytes have been investigated with phase contrast and electron microscopic examinations after experimental dilatation. The myometrial myocytes damage provocation takes place unevenly after lower uterine segment dilatation. The fibrous connective tissue synthesis starts during the reparative regeneration, it leads to hystoarchitectonics disruption and local myometrium disfunction. The fibrillar structures synthesis in intercellular substance is carried out by phenotypic smooth muscle type transformation from contractile to “Synthesizing”. Smooth muscle cells are not involved in cell proliferation. The myocytes intracellular regeneration takes place in lower uterine segment.

Introduction. A visceral muscle tissues study that form the hollow organs walls and various sphincters, is the most actually and poorly known [3]. There is no common understanding between pathologists and obstetricians about morphological and functional features of the lower uterine segment [4]. There is opinion that the lower uterine segment sphincter performs the obturator function of pregnancy cervix, also it has an indicator function in progress of abnormal occurrences in parturition [2, 5]. In addition, the lower uterine segment postpartum restoration forms a full barrier for ascending infection progress. The lower uterine segment traumatic injuries in obstetric practice which occurred after violent expansion of the cervical canal in induced abortions and diagnostic curettage, promote lower uterine segment functional insufficiency in pregnancy and have the adversely affect birth outcomes. It is necessary to develop the methods for correction the caudal uterus functional insufficiency after injury in the absence of morphological evidence, so we determined the purpose of our research [1, 6].

The purpose of present study was to research reparative regeneration in rat functionally important lower uterine segment myometrium after tension in experiment.

First we have to simulate the rat lower uterine segment stretching, also we have to characterize the myometrium myocytes lesions in lower uterine segment after experimental tensile, at last we have to find the leading mechanisms of myometrium reparative regeneration for achievement.

Materials and methods. Thirty nulliparous mature white rats were used. The remaining intact rats were used as controls. “Rules to the Use of Animals in Research” were used in present experiment. The lower uterine segment was extended with the rat under Aether anesthesia. All the rats of the experiment group were killed under anesthesia using Aether. The materials were examined on third, seventh, tenth, fifteenth, twenty first days, that’s why the materials were fixed in glutaraldehyde, filled with Araldite-Epon mixture, then the materials were contrasted with uranyl acetate and lead citrate. Semithin and ultrathin sections were prepared. We used phase contrast and transmission electron microscopy.

Results and discussion. The uterus lower segment stretching leads to uneven smooth muscle tissue damages in myometrium. Some myocytes in functional syncytium retained their structure, other myocytes have dystrophic and necrotizing changes on the third day after injury (Fig. 1).The cytoplasmic matrix compaction took a place in myocytes. Nuclei were found at different stages of cell death. The cisterns of sarcoplasmic reticulum are expanded, parietal located caveolae particullary affected. Myocyte mitochondria are swollen, it leads to partial or total crist destruction. The number of specific organelles is purposed. Myocyte membranes are violated – it leads to destruction of intercellular interactions. Well known, there are two main leyomyocyte types of cell-cell junctions: mechanical (desmosomes) and functional (nexuses). There are preserved myocytes, which are visualized in the damaged lower uterine segment on 7–10 days after injury. Myofibrils decrease and free ribosomes and polysomes increase due to the development of granular endoplasmic reticulum are observed in preserved myocytes cytoplasm. This means that myocyte phenotype has changed from contractile to synthesize.

Intercellular spaces are expanded on the third day after lower uterine segment stretching. First, it is caused by interstitial edema and collagen stimulation by reactive inflammation cells. Than extracellular matrix is produced around cells since seventh till twenty first day after stretching. Intercellular spaces are filled with protein masses with fibrillar structure, which assembled into the fibers. The cells are packed in fibrillar matrix, their contacts are violated. Probably, these structural changes lead to myometrium dysfunction.

The fibrous connective tissue density is increased on twenty first day after stretching. There are cell location and newly formed fibers orientation disruption visualized in myometrium. (Fig. 2, 3).

Fig. 1. Lower uterine segment on third day after injury. Preserved leyomyocyte. TEM. 1000Х

Fig. 2. Lower uterine segment on 21 day after injury. The fibril-forming interstitial collagen. UTEM. 1200X

Fig. 3. Lower uterine segment on 21 day after injury. The collagenous fibers in myometrium. Phase-contrast microscopy. 1200Х

There were no found myocytes mitosis during the whole period of observation.

So, we have found diffuse changes in myometrium after uterus lower segment stretching. The intracellular regeneration has taken a place in myometrium. We have found the myocyte phenotype transformation from contractile to synthesize. The myocytes synthesize extracellular fibrill-forming collagen matrix. The cells are packed in fibrillar matrix, their contacts are violated. These structural changes lead to myometrium dysfunction

The work is submitted to the International Scientific Conference “Fundamental research”, Jordan, June, 9–16, 2014, came to the editorial office оn 25.04.2014.

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