Abstract

The aim of the study. To examine the changes in structure and morphometry in sensorimotor cortical edema with cell swelling in mature white rats after common carotid artery occlusion of various durations.Material and methods. Acute ischemia was modeled on white adult Wistar rats by 20-, 30- and 40-min occlusion of the common carotid arteries (CCA). Histological (hematoxylin-eosin and Nissl staining), immunohistochemical (NSE, MAP-2, GFAP) and morphometric methods were used. Morphometry was assessed on hematoxylin and eosin-stained specimens using ImageJ 1.53 plug-ins (Find Maxima, Find Foci). Statistical hypothesis testing (nonparametric criteria) was performed using Statistica 8.0 software.Results. In the sensorimotor cortex (SMC) of white rats after 20, 30 and 40 minutes of CCA occlusion the signs of cytotoxic brain edema appeared, focal destructive and adaptive changes of neurons and astroglia evolved. The edema persisted throughout the observation period (7 days). The increase in the relative area, the number of cell swelling zones and their hydration (pixel brightness) was significant. On days 1 and 3 after CCA occlusion, some of the SMC astrocyte processes underwent destruction. Subpial and perivascular zones suffered to a greater extent. Mild and moderate (after unilateral 30-min CCA occlusion) to moderate and severe (after bilateral 40-min CCA occlusion) scattered structural and functional changes of the SMC with large areas of clearing in the «porous» neuropil, severe perivascular and perineuronal edema of the astrocyte processes developed. The latter was associated with a moderate reduction of the total neuronal density.Conclusion. After occlusion of CCA, signs of edema with cellular swelling appeared in the SMC amid dystrophic and necrotic pyramidal neurons and activated neuroglial cells. To a greater extent, the signs of brain swelling were evident three days after bilateral 40-min occlusion of CCA.

Highlights

  • Цитотоксический отек-набухание головного мозга возникает при отравлении или гипоксии в результате нарушения клеточного метаболизма, удержания в клетках натрия и воды [1,2,3,4]

  • Acute ischemia was modeled on white adult Wistar rats by 20, 30- and 40-min occlusion of the common carotid arteries (CCA)

  • Morphometry was assessed on hematoxylin and eosin-stained specimens using ImageJ 1.53 plug-ins (Find Maxima, Find Foci)

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Summary

Introduction

Цитотоксический отек-набухание головного мозга возникает при отравлении или гипоксии в результате нарушения клеточного метаболизма, удержания в клетках натрия и воды [1,2,3,4]. Связанный с гипоксией цитотоксический отек мозга наблюдается, например, при локальной и тотальной острой ишемии, черепно-мозговой травме [4]. Патогенетические механизмы и структурные проявления отека-набухания при ишемии хорошо изучены. Существует тенденция рассматривать отек и набухание как взаимосвязанные проявления дисфункции водно-электролитного обмена, заканчивающиеся либо необратимой гидропической дистрофией, либо восстановлением водно-ионного баланса и гидратации клеточных белков. Отек — это, прежде всего, скопление жидкости в межклеточных пространствах мозга (свободная жидкость). Имеющим в основе прочное связывание интраструктуральной воды с внутриклеточными биоколлоидами [4,5,6,7,8]

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