Computer-morphometric analysis of nerve tissue edematous changes in progressive and stable cerebral infarction

Shavrin, V. A.; Shulyatnikova, T. V.

doi:10.14739/2310-1237.2015.2.50994

Cited by 1 publication

(1 citation statement)

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“…During ischemia, condensed and dark ultrastructure of ischemic neurons reflects declining anabolic cellular processes and the predominance of catabolic reactions to ascertain the maximal economy of energy resources. This develops in parallel with the diminution of specialized cellular functions, which is aimed towards long-term self-preservation in adverse conditions and provides a mechanism for cell survival [61]. The ischemic component is highly inherent in SAE due to the violation of systemic and cerebral blood circulation; therefore, ischemic shrunken neurons are characteristic of this condition [62][63][64].…”

Section: Microglial Reactivity In Saementioning

confidence: 99%

Reactive Microgliosis in Sepsis-Associated and Acute Hepatic Encephalopathies: An Ultrastructural Study

Shulyatnikova

Tumanskyi

Hayden

2022

IJMS

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Sepsis and acute liver failure are associated with severe endogenous intoxication. Microglia, which are the resident immune brain cells, play diverse roles in central nervous system development, surveillance, and defense, as well as contributing to neuroinflammatory reactions. In particular, microglia are fundamental to the pathophysiology of reactive toxic encephalopathies. We analyzed microglial ultrastructure, morphotypes, and phagocytosis in the sensorimotor cortex of cecal ligation and puncture (CLP) and acetaminophen-induced liver failure (AILF) Wistar rats. A CLP model induced a gradual shift of ~50% of surveillant microglia to amoeboid hypertrophic-like and gitter cell-like reactive phenotypes with active phagocytosis and frequent contacts with damaged neurons. In contrast, AILF microglia exhibited amoeboid, rod-like, and hypertrophic-like reactive morphotypes with minimal indications for efficient phagocytosis, and were mostly in contact with edematous astrocytes. Close interactions of reactive microglia with neurons, astrocytes, and blood–brain barrier components reflect an active contribution of these cells to the tissue adaptation and cellular remodeling to toxic brain damage. Partial disability of reactive microglia may affect the integrity and metabolism in all tissue compartments, leading to failure of the compensatory mechanisms in acute endogenous toxic encephalopathies.

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