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прогрессирующее уменьшение массы тела подопытных животных с неопластических процессов. Установлено достоверное уменьшение как массы, так и пространственных характеристик селезенки в динамике эксперимента. Выяснение патогенетических механизмов органометричних изменений селезенки в условиях экспериментально смоделированного неопластического процесса требует дальнейшего гистологического исследования изменений структурных компонентов исследуемого органа.
Ключевые слова: масометрия, органометрии, селезенка, экспериментальный онкогенез, белая крыса.
Статтянадшшла 2.07.2017 р.
investigated. A progressive decrease in the body weight of experimental animals with a neoplastic process was found. A significant decrease in both the mass and spatial characteristics of the spleen in the dynamics of the experiment has been established. The determination of the pathogenic mechanisms of organometric changes in the spleen under conditions of an experimentally modeled neoplastic process requires further histological examination of changes in the structural components of the organ.
Key words: Mass and organometric parameters, spleen, experimental oncogenesis, white rats.
Рецензент Срошенко Г.А.
DOI 10.26724 / 2079-8334-2017-3-61-138-142
УДК 617.731-007.2+617.731-088.85+617.7-001.22+617.7-001.15+617.7-009+617.7-073.178+6016-092.2
THE ROLE OF NEUROHUMORAL DYSFUNCTION IN PATHOGENESIS OF THE
TRAUMATIC OPTIC NEUROPATHY
e-mail: natalymoyseenko@gmail.com
The neurohumoral properties's changes in the hypothalamus as a result of TON are unknown. The purpose of the study: to study neurohumoral dysfunction in the traumatic optical neuropathy's pathogenesis. Methods. The traumatic damage to the orbital part of the right optic nerve was reproduced in 60 sexually mature rabbits in the experiment. There were two groups of animals of 30 individuals: intact and experimental. Electronic microscopy of the hemithin and ultrathin sections and the morphometry of the cranial part of the right optic nerve and the suprachismic nucleus of the hypothalamus one month after the injury. It has been established that traumatic damage to the orbital part of the optic nerve causes reactive edema and destructive changes in the cranial part of the optic nerve and the suprachiasmic nucleus of the hypothalamus. The reducing the volumetric neurosecretory granules density and the pycnomorphic cells' number at the last stage of development increasing were detected. This reduces the corticosteroids production that cause inflammatory reactive damage to the optic nerve. Conclusion. Hence, neurohumoral dysfunction is an important mechanism for the pathogenesis of traumatic optical neuropathy, and its correction will have positive effects for treatment.
Key words: traumatic optical neuropathy, neurohumoral dysfunction, suprachiasmic nucleus of the hypothalamus, neurosecretory granules.
The traumatic optic neuropathy (TON) is poly etiological disease. The proponents of metabolic theory of TON's pathogenesis consider the ionic neurotransmitters selection homeostasis imbalance (including electro cytotoxicity of glutamate). The secondary mechanisms of optic nerve injury are nerve cells' apoptosis, the lipid degradation, inflammatory and immune responses imbalance [6]. The neurochemical factors induce toxic and activate inflammatory substances such as prostaglandins [5], oxidation reaction, chemokines and inflammatory cytokines. Destroy of the hematoencephalic barrier causes nerve tissue swelling [12, 13, 18].
The craniocerebral trauma is the most often reason of TON. The craniocerebral trauma leads functional suppression of anterior hypothalamus where suprachiasmic nuclei [8] and pituitary gland dysfunction [9, 14]. In 39% craniocerebral trauma cases there is corticotropic hormone blood content's decrease [17].
However, how does the neurohumoral properties of the hypothalamus changes as a result of the optic nerve's traumatic damage, and whether this effect on the TON are not known.
The purpose was to study the importance of neurohumoral dysfunction in the pathogenesis of traumatic optical neuropathy.
Material and methods. An experimental study was carried out in vivarium of the Ivano-Frankivsk National Medical University. The traumatic damage to the orbital part of the right optic nerve was reproduced in mature rabbits of the chinchilla [15]. The retention of experimental animals and their withdrawal from the experiment occurred according to the rules given in "Guide for the Care and Use of Laboratory Animals, NIH Publication 86-23".
Animals were randomly assigned to two groups of animals. The control (intact) group of 30 individuals did not have any intervention and anesthesia. The experimental group of 30 individuals has got right optic nerve crush. In operation room after a general (Sydazyn 1.5 V / m) and local anesthesia (2% Lidocaine 0.5 ml subcutaneously), antiseptic treatment of the surgical field, insection of the outer
third of arches was performed the cut skin of right eye, dull bundle soft tissue incision of the periosteum of the orbital process frontal bones. It made the blunt separation of optic nerve. The nerve taken by surgical clip at the apex of the orbit and behind the muscular funnel. The compression, stretching and rotation orbital part of right optic nerve with its crush to the teeth of surgical tweezers were done during 10 minutes. The wound sewn. The ipsilateral relative afferent pupillary defect indicated optic nerve injury. The morphological analysis (electron microscopy of the hemi thin and ultrathin sections and morphometry) of the cranial part of the right optic nerve and suprachiasmatic nucleus (SN) hypothalamus of the experimental animals of both group was carried out in a blinded fashion in the electron microscopy laboratory of the Human Anatomy Department of the Ivano-Frankivsk National Medical University after the withdrawal from the experiment (using guillotine). In experimental group section was done in one month after the injury. The concentration of peripheral blood cortisol and adreno-corticotropic hormone (ACTH) in serum were determined in intact group and in experimental group in 1 month after injury.
The study was randomized, indicating the principle of randomization. The average values are given in the form M ± m, where M is the arithmetic mean, m is the standard error of the mean.
Results and its discussion. As results of study it was found edema and destructive change of the sheath of myelin neural fibers (MNF) in light optic microscope level at the 30th day after right optic nerve orbital part damage. The axial cylinders of MNF are reduced and they can't be detected in some nerve fibers. The myelin sheath (MS) of such fibers occupies almost all the entire fiber's area (Fig. 1). There are single MNFs with signs of anisochromy, partial flaking and destruction of the myelin sheath. In addition, there were observed small part of the MNF with preserved structure. Around of microvessel and in the subpereneural space the endoneural connective tissue is swelling.
The area of the axial cylinders of the right optic nerve is not statistically significantly different from the control group and is 0,92±0,61 mkm2 (control - 0,96±0,72 mkm2, p=0,93457) according to the morphometric analysis. The area of MNF larges up to 3,09±1,98 mkm2 (control - 2,25±1,53 mkm2, p=0,026336). The index g lows down to 0,29±0,08 (control - 0,42±0,06). This may be sign of MS's edema. In the suprachiasmic nucleus of hypothalamus the number of neuro secretive cells (NSC) with peripheral chromatolysis and hypochromic nucleuses increases at the 30th day after orbital part optic nerve injury (Fig. 2). It is found small vacuoles in the periphery of perikarion of some NSC. There are kariopicnosis and somewhere kariolisis in the majority of NSC._
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ill»» Injury, |mhii«'iI vvilli u |»olychr»nm« »ly»« mnyn xlooo lltHiil lliln n»u iiiim ilyM Ity iiii'lliylMiu* IiIiii*. Mhjui i fill,
N<tfc*: I i'tionui of endoneural connective iumm. » kwilllni Mid dMnwilv* nhu«h i itormoohnimlu neuri mm with ceiiiriil olmniiuiulyM«, 2 NNC im i
chunye» In ill« MS and reduction of the m*I«I cylinder* of MNI'. 4 newly formed |*»il|ilu»ry til ilio |imi'IIiiu'Iiiii will» miiihII viiviiiiIvm, lmi'liipW>nitM* mill luirliillftlft, 1 collngin Ah«ri, 5 • DhmhliMii, jilym-yi*«*, A vlmml i>niHnlnwi> ft mIihiIhw wlln, fi viiiillliiry.
The area of NSC's perikarion increases in comparison with the intact group from 244,12±35,50 mkm2 to 276,59±38,02 mkm2 (p=0,0428). The area of nucleus does not change. For intact group the nucleus area is 78,58±14,30 mkm2, and for experimental - 71,93±15,67 mkm2 (p=0,1515). The nuclear-cytoplasmic index (NCI) for experimental group increases from 0,47±0,07 to 0,35±0,07 (p=0,0001). These dates don't sing increase of functional activities' NSC, but they can indicate nuclear and cellular edema and destruction. It also indicates secondary hypothalamic reactive damages that comes after traumatic injury of optic nerve.
The ultrastructural sings of destructive changes were indicated in intracranial part of optic nerve in experimental group. There were find edema and enlargement of MS (Fig. 3 a). In the inner myelin lamellas of experimental group were seen different forms and size invaginations (Fig 3 a, 6).
There were big diameter of MNF with weak MS (Fig. 3 a). The axoplasm of axial cylinder of such fibers was electron-transparent. There were indicated the lysis of neurofibrils and mitochondrias. These were sings local axial swelling and nutrients transport depression. Inner myelin lamellas of MNF formed multiple invaginations. There are many vacuoles of different diameter and edematous mitochondrias with an enlightened matrix and broken crystals in the axoplasm. These changes can be interpreted like axonal nutrition transport destroy [18, 19].
It was found else axonal uneven contours, varicose enlargement and local narrowing, some axons fragmented in the places without MS. The endoneurial edema begins to decrease, it reveals fine-grained products of myelin collapse.
Also the neurolemmocyte number and size increase were detected. There are structure less MS homogeneous mass's degradation. There was seen granular endoplasmic reticulum's (GER) hypertrophy in their cytoplasm (Fig. 3 a). Degenerative myelin fragments are present among of intensive dye myelin's masses. Some neurolemmocyte have moderate electron optical density cytoplasm with filled organelles. Other cells have expanded perinuclear space and cytoplasm with single vacuoles (Fig. 3 b). Such structural neurolemmocyte's reorganization indicates their high functional activity. This is caused by damaged MNF phagocytosis and regenerative proses.
In addition there are some new MNF among of destructive changed MNF. New MNF are round, by small caliber, with normal MS and mezaxon (Fig. 3 b). Their axoplasm is moderate electron-optical density and contains young mitochondria and microtubules.
There are endoneurial edema wish many fibroblasts and collagen fibers. MNF are demyelinated with MS derogation and fragmentation. Some authors explain such changes by axotomy due to energetic and protein imbalance [1, 7].
We have find in experimental group ultrastructural changes in NSC of hypothalamic SN that correlate with optic nerve damages. We have seen GERs tanks expansion, mitochondrial matrix illumination and crystal destruction with subsequent formation of vacuoles, increase of the number of primary and secondary lysosomes, destruction of structural elements of the Golgi complex in the majority of light NSC (Fig. 4). Nucleus of NSC are low electron-optical density with minor invasions of the nuclear shell. The dark NSC have small vacuoles and lysosomes. The number of GERs tanks increases. They become larger. There are multivascular corpuscles and individual neurosecretory granules (NG).
Jestructive changes found at the 30» day after traumatic injury. Magn.: a. b) 4800. 5) FiS- 4-Th<! hypothalamic NSC reactive (a)and hydropic dystrophy (6) al the 30»
•vj( „ j day after optic nerve orbital part crush. Electronograms. Magn.: a, 6) 8000.
Notes: 1 - the edema ofMNFs axolemma. 2 - the bundle of la,ncllas of myelin. Nores: 1 nucleus of NSC is a low-electron-optical density with minor 3 - the MS's edema. 4 - MNF with normal form. 5 - neurolemmocyte of moderate invasions of the nuclear shell. 2 - The destruction of the structural elements of the
ileetron-optical density is filled with cellular organelles. 6 - GER s hypertrophy. 7 - GolSi complex. 3 - Expansion of GER s tanks. 4 - Illumination of the mitochondrial
[he myelin fragments phagocytizcd in the neurolemmocyte-, cytoplasm. and destruction of crystal with the subsequent formation of vacuoles (5).
There were single NSC with hydropic dystrophy. The NG's volumetric density of light neurons in experimental group was significantly reduced compared to the intact group of animals from 6,95±0,36% to 2,24±0,19% (p=0,0002). The NG volumetric density of dark NSC in experimental group was also significantly reduced compared to the intact group of animals from 3,56±0,12% to 1,14±0,04% (p=0,0002). There are a lot of dark cells with great destructive change. They have not NG. They contain only some lysosomes. Some authors indicate such cells like pycnomorphic. They are on the last stage of their life cycle [2]. The above morphological changes in the structure of the hypothalamus occurred on the background of changes in the concentration of hormones in the blood. It was found cortisol content's decrease that in the experimental group in the of compared with intact animals from 92,31±3,26 Mg / dl go 11,79±0,12 Mg / dl (p<0,05) and ACTH content's decrease from 11,64±0,43 Pg / ml to 6,91±0,09 Pg / ml (p<0,05). Thus, according to the study, it was found that traumatic damage to the orbital part of the optic nerve causes the suprachiasmic nucleus of the hypothalamus' secondary reactive destruction. The volumetric density of neurosecretory granules' reducing and the number of pycnomorphic cells at the last stage of development increasing lead corticosteroids production suppression, which in turn contributes to
inflammatory reactive damage to the optic nerve, which obviously require correction that may have a neuroprotective effect for the recovery of the optic nerve.
The correction of suprachiasmic nucleus of the hypothalamus' secondary neurohumoral dysfunction will have positive effects for traumatic optical neuropathy treatment.
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РОЛЬ НЕЙРОГУМОРАЛЬНО! ДИСФУНКЦП В ПАТОГЕНЕЗ1 ТРАВМАТИЧНО!' ОПТИЧНО1 НЕЙРОПАТП Мойсеенко Н. М.
Змши нейрогуморальних властивостей
ппоталамусу в наслщок ТОН не вщомо. Мета дослщження: вивчити нейрогуморально! дисфункцп в патогенезi травматично! оптично! невропатп. Методи. Вщтворено в експеримент травматичне пошкодження орбпально! частини правого зорового нерву у 60 статевозрших кролiв. Було двi групи тварин по 30 особин штактш та експериментальна. Електронну мкроскотю натвтонких та ультратонких зрiзiв та морфометрто крашально! частини правого зорового нерву та супрахiазмального ядра ппоталамусу через мюяць тсля травми. Встановлено, що травматичне пошкодження орб^ально! частини зорового нерву викликае реактивний набряк i деструктивш змши
РОЛЬ НЕЙРОЛОГИЧЕСКОЙ ДИСФУНКЦИИ В ПАТОГЕНЕЗЕ ТРАВМАТИЧЕСКОЙ ОПТИЧЕСКОЙ НЕЙРОПАТИИ Мойсеенко Н. Н.
Изменения нейрогуморальных свойств гипоталамуса вследствие ТОН не известно. Цель исследования: изучить нейрогуморальной дисфункции в патогенезе травматического оптической невропатии. Методы. Воспроизведен в эксперименте травматическое повреждение орбитальной части правого зрительного нерва в 60 половозрелых кроликов. Было две группы животных по 30 особей интактные и экспериментальная. Электронную микроскопию полутонких и ультратонких срезов и морфометрию краниальной части правого зрительного нерва и супрахиазмального ядра гипоталамуса через месяц после травмы. Установлено, что травматическое повреждение орбитальной части зрительного нерва вызывает реактивный отек и деструктивные изменения краниальной части зрительного нерва и супрахиазмального
крашально! частини зорового нерву i супрахiазмального ядра ппоталамусу. Зменшення об'емно! щiльностi нейросекреторних гранул i збiльшення кiлькостi ткноморфних клiтин, якi знаходяться на останнш стадii' розвитку, знижуе продукцiю кортикостеро!дав, що в свою чергу, сприяе запальним реактивним пошкодженням зорового нерву. Висновок. Отже нейрогуморальна дисфункцiя е важливим мехашзмом патогенезу травматичнiй оптичнш невропатп, а !! корекцiя матиме позитивш наслiдки для лiкування.
Ключовi слова: травматична оптична невропатiя, нейрогуморальна дисфункщя, супрахiазмальне ядро гiпоталамусу, нейросекреторш гранули.
Стаття надiйшла 7.08.2017 р.
ядра гипоталамуса. Уменьшение объемной плотности нейросекреторных гранул и увеличение количества пикноморфного клеток, которые находятся на последней стадии развития, снижает продукцию кортикостероидов, в свою очередь, способствует воспалительным реактивным повреждением зрительного нерва. Вывод. Итак нейрогуморальная дисфункция является важным механизмом патогенеза травматической оптической невропатии, а ее коррекция будет иметь положительные последствия для лечения.
Ключевые слова: травматическая оптическая невропатия, нейрогуморальная дисфункция, супрахиазмальне ядро гипоталамуса, нейросекреторные гранулы.
Рецензент Безкоровайна I.A.
DOI 10.26724 / 2079-8334-2017-3-61-142-145 УДК 611.842:615.212.7]-08
МОРФОЛОГ1ЧН1 ЗМ1НИ СУДИННО1 ОБОЛОНКИ ОЧНОГО ЯБЛУКА ЗА УМОВ ТРИВАЛОГО ВПЛИВУ НАРКОТИЧНИХ АНАЛЬГЕТИК1В
e-mail: uljaska.p@gmail.com
Динамiчне зростання юлькосп oci6, змушених впродовж тривалого часу вживати наркотичнi анальгетики призвело до поширеносп захворювань нарколопчиого профiлю в Укра!ш, що становить близько одного мшьйона oci6. Аналiз фахово! лiтератури пiдтверджуe важливiсть вивчення ще! проблематики. Враховуючи поодинокiсть праць, що стосуються впливу наркотичних анальгетиюв на структуру очного яблука нашою метою е встановити особливостi структури суднино! оболонки очного яблука за умов 6-тижневого впливу ото!ду в експеримен'п. Дослiдження виконанi на 24 статевозрших бiлих щурах-самцях. Матерiал дослщження представлений гiстопрепаратами судинно! оболонки очного яблука бших щурiв. Через 6 тижшв введення щурам налбуфiну уражаеться як гемомкроциркуляторне русло, так i сполучнотканинна основа власне судинно! оболонки. Вщсутня диференцiацiя шарiв райдужки та фрагментащя вiйкових вiдросткiв. Виявленi змши райдужки, вiйкового тiла та власне судинно! оболонки очного яблука носять деструктивний характер.
IGii040Bi слова: судинна оболонка, опю!д, налбуфш, експеримент.
Робота е фрагментом НДР «Структура оргатв та гх кровоносного русла в онтогенезi, nid дieю лазерного оnромiнення та фармацевтичних засобiв, при порушеннях кровопостачання, реконструктивных операщях та цукровому дiабетi» (номер державногреестрацг 0110U001854).
Впродовж останшх десятил1ть динамiчно зростае кшьюсть ос1б, змушених впродовж тривалого часу вживати наркотичш анальгетики [5]. Часто це пов'язано з необхщшстю зменшення больового синдрому, особливо у вшськово-польовш хiрургi!, онкологи, травматологи, стоматологи [10]. Проте, дана законом1ршсть спостерйаеться i серед ос1б молодого та працездатного в1ку, що не обумовлена л1кувальними щлями. Тому не викликае подиву дат поширеност1 захворювань нарколопчного профшю в Укра!ш, що становить близько одного мшьйона ос1б. Св1това практика дуже схожа, адже у 2012 рощ, за р1зними ощнками, вщ 165 мшьйошв до 315 мшьйошв людей у вщ1 15-64 роюв у всьому свт вживали наркотичш середники (UNODC 2013) [7].
Анатз фахово! л1тератури шдтверджуе важливють вивчення ще! проблематики значною кшьюстю проведених дослщжень щодо змш структури оргашв i систем за умов дй наркотичних середниюв [1, 2, 3]. Проте проблема морфолопчно! перебудови судинно! оболонки очного яблука при використанш налбуфшу залишаеться вщкритою, адже представлена лише поодинокими працями [6, 8, 9], що носять характер окремих спостережень та вимагають подальшого грунтовного вивчення. Особливо гостро вщчуваеться суперечливють даних щодо особливостей м1кроструктури судинно! оболонки очного яблука щура шд впливом ошо!ду.
Метою роботи було встановити особливосп структури ус1х вщдшв судинно! оболонки очного яблука за умов 6-тижневого впливу ото!ду в експеримент!.
Матерiал та методи дослщження. Дослщження виконаш на 24 статевозрших бших щурах-самцях, в1ком 4,5-7,5 мюящв i масою тша 130-150 г. Введення налбуф1ну проводили внутршньом'язево щоденно в доз1 15,2 мг/кг маси тша тварини, зпдно з формулою [4]: D1 =
