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Морфофункциональное состояние микроциркуляторного русла печени в условиях острой портальной гипертензии (анатомо-экспериментальное исследование)

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апа венасын тарылтаннан 7 туліктен кейін бауыр блшектеріні бір-біріне жаындап тыыздалып, синусоидтарды анмен толып, оларды арасындаы трабекулаларды жалананы байалады. Днекер тіндер блшектер арасында тыыздала бастаан. Тжіребені 15-ші тулігінде бауыр блшектер рылысы бзылып, келетін ан тамырлар бір-біріне жиі орналасып, орталы венаны шеткері ыысанын круге болады. Бауыр капсуласыны талшыты днекер тінні кбеюінен алыдааны аныталды. аапа венасын тарылтаннан 30 туліктен со бауырды фиброзды пайда болуы байалып, днекер тіндерді кбеюі байалды. Терминалды апа венуласыны ішкі диаметрі тарылуы жне терминалды бауыр артериясыны кееюі, бауыра келетін венозды анны азайатынын, ал артериалды анны кбейетінін болжауа болады. Баылау тобындаы егеуйрытардан алан нтижені, яни ртрлі апа гипертензиясыны даму барысын ылыми практикалы жмыстара негіз етіп алуа болады. Сонымен атар, бауырды тжірибелік гипертензиясында болатын гемомикроциркуляторлы згерістер осы патологияны патогенезін ашуа кмектеседі.

Serikpayev Zhandos Zhumabayevich


Morphofunctional state of hepatic microcirculatory bed under the conditions of acute portal hypertension

14.00.02 Human anatomy

Abstract of the thesis presented for academic degree

of Candidate of medical sciences

For interpretation of the character of disorders hemodynamics in different pathological conditions of liver it’s necessary to know its normal angioarchitectotonics. Microcirculatory bed has a special significance for regeneration of liver in post-resection period. That’s why its studying may give a valuable in knowledge for clearing up occurring shifts while the loss of liver’s part.

Portal hypertension is often accompanied by a number of chronic liver diseases and also by a complete or partial occlusion of portal vein trunk.

But hemomicrocirculatory liver bed in incomplete occlusion of portal vein hasn’t been sufficiently studied yet.

That’s why the purpose of the present work was studying morphofunctional state of hemomicrocirculatory hepatic bed under conditions of experimental hepatic and extrahepatic acute portal hypertension, caused by resecting 50% of liver and constricting 50% of portal vein lumen.

The experimental research was carried out on 205 white rats of both sex by mass from 200 to 240gr. We performed 3 series of experiments: the 1st – control; the 2nd – resection of 50% of liver; the 3d – stenosis of 50% of portal vein.

For studying hemomicrocirculatory hepatic bed on the 1st, 3d, 7th, 15th, 30th days in post-resection period a vascular network of an organ was filled by 0.5% nitro-acidic silver solution by Yu. E. Vyrenkov’s method.

In 2 days there were made sections from 50 to 200 mkm. Lightened sections were examined under light microscope. Some hepatic preparations were stained by hematoxilin – eosin.

The liver of white rat was composed of separate, well differentiated, various in size and volume, connected between each other by pons of hepatic tissue lobes: right lateral, right internal, left lateral, left internal, additional and caudal. Terminal portal venules represented by themselves microvessels by diameter of 64+3,2 mkm. The diameter of terminal arteriola made 49,1+2,2 mkm, which were destructed into precappilaries by diameter of 18+1,9 mkm, which formed peribillary capillary plexus by diameter of 7,5+0,4 mkm. The peculiarity of peribillary capillary plexus was in probability of its return but in terminal portal venule and various sinusoidal zones. Out of terminal carrying microvessels there was created a wide network of anastomotising between each other sinusoids by diameter of 250+12 mkm. Over the system of sinusoids the blood falls into terminal hepatic venula by 105+3,8 mkm diameter.

On resecting liver the first 7 days there was observed a process of regenerative hyperthrophy of functional-morphological unit of liver-acinus. The diameter of terminal portal venule lumen widened up to 87,5% and terminal hepatic artery - for 38,49% concerning initial data. Enlarged sizes of afferent vessels of hemomicrocirculatory hepatic bed also pointed to the process of regenerative hypertrophy of terminal hepatic venule (164+5,2 mcm). Later on (the 30th day after resection) the process of regenerative hypertrophy was replaced by regenerative – adaptative period, where the diameter of terminal portal venule lumen decreased (115+6,5 mcm). At the same time the increase of terminal portal venule length by 20% larger, than the size of terminal hepatic venule may be due to depositing function of the liver.

The degree of lobular regenerative hypertrophy correlated with changes of microcirculatory bed. The greater increase of lobular surface corresponded to stage of sprout within lobes of terminal vessels and revealing extrasinusoidal blood outflow. In these areas due to extending the ways of blood outflow through sinusoids there occurred sprouting septal vessels and neoplasms of lobes, that was likely a mechanism of adaptative character, providing a rapid output of passing to the liver blood.

In 7 days after stenosis of portal vein the hepatic lobules were drawn closer with each other, sinusoids were overfulled by the blood, trabecules between them became thin in some areas. Layers of intralobular connective tissue were wide. In 15 days after stenosis of portal vein in hepatic lobes ther was observed a disorder of architectonics due to becoming close trias and excentric position of central veins. Hepatic capsule was thickened due to the growth of fibrous connective tissue.

In 30 days after stenosis of portal vein in liver parenchyma, between the lobules there were formed wide layers of connective tissue by development of fibrosis. Stenosis of terminal portal venule lumen and enlargement of terminal hepatic arteriola was due to decreasing a volume of blood inflow over venous part and increasing blood inflow over arterial part of hemomicrocirculatory hepatic bed.

The revealed quantative characteristics of hemomicrocirculatory hepatic bed in intact rats and in different forms of portal hypertension may be a ground for carrying out scientific researches.

Dynamic changes occurring in hemomicrocirculatory hepatic bed in different forms of experimental acuteportal hypertension, will enlarge considerations about pathogenesis of the present pathology.

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