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Влияние гипотиреоза на динамику формообразовательных процессов в очаге гнойного воспаления

Влияние гипотиреоза на динамику формообразовательных процессов в очаге гнойного воспаления

Abstract

Изучено влияние дефицита гормонов щитовидной железы на течение воспаления. На модели гнойного воспаления у крыс показано, что динамика формообразовательных процессов о очаге повреждения при гипо и эутиреозе в целом сходна. Последовательность событий соответствует классической схеме: повреждение — отек — лейкоцитарный вал — макрофагическаяинфильтрация — фиброзирование. Однако при гипотиреозе, вследствие снижения энергетического статуса клеток, реализующих воспаление, все стадии процесса протекают медленно, и воспаление переходит в хроіаіческую форму.

Effect deficiency of the thyreoid hormons on the inflammatory dynamic were studied. Morphological analysis indicates that respons to demage connective tissue are develop standard reaction: oedema — leukocyte phase — macrophage phase — fibroblast phase. Deficiency of the thyreoid hormons lead to slowing — down of all inflammatory phases and the process loses the adaptive character. Took place the incomplete inflammation.

Keywords

ГИПОТИРЕОЗ, ГНОЙНОЕ ВОСПАЛЕНИЕ, ФОРМООБРАЗОВАТЕЛЬНЫЕ ПРОЦЕССЫ

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selected citations
These citations are derived from selected sources.
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
0
Average
Average
Average