Медицинская литература. Новинки

 

 

 

 

 

 

Патогенетические аспекты гнойного холангита,, почему нет системной воспалительной реакции при механической желтухе?

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Цель работы. Установить патофизиологические механизмы развития системной воспалительной реакции при холангите. Используя медицинские поисковые системы PUBMED, MD Consult и National Library of Medicine, проанализированы данные литературы с 1980 по 2008 гг. Также использованы результаты собственных экспериментальных и клинических исследований. При сравнении экспрессии рецепторов лимфоцитов у 28 больных установлено, что часть их блокирована неизвестным фактором. Во время экспериментальных исследований клеток Купфера показано, что исчерпание их фагоцитарной функции введением в кровь туши приводит к нарушению микроциркуляции в печени. Экспериментальный холангит приводит к более глубокому и быстрому нарушению микроциркуляции печени, чем механическая желтуха. При сравнении морфологических препаратов печени крыс выявлено выраженное воспаление с большим возбуждением клеток Купфера и расширением синусоид печени при экспериментальном холангите, чем при механической желтухе. Дополняя собственные результаты данными литературы, автор предположил, что транслокация бактерий и эндотоксина при ахолии не может быть главным источником системной воспалительной реакции при холангите. Однако системная воспалительная реакция, вызванная инфицированием желчи, может привести к вторичному повреждению клеток печени.

Ключевые слова:
механическая желтуха, контаминация желчи, холангит, клетки Купфера, сепсис, печень.

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Pathophysyologic Aspects of Purulent Cholangitis,, or Why Does not Appear Systemic Inflammatory Response Syndrome in Obstructive Jaundice?

The aim of the study was to find out pathophysilogic mechanisms of systemic inflammatory response origin in cholangitis. Applying internet medical search systems: PABMED, MD Consult и National Library of Medicine an analysis of English''language literature from 1980 to 2008 was carried out. In edition results of former own experimental and clinical researches are presented. Comparison of lymphocyte receptor expression of 28 cholangitis patients in autoplazma and bovin serum albumin revealed, that in patient plasma some lymphocyte receptors are blocked by unknown factor. Kuppfer cell experimental investigation displayed, that exhaustion of these cells phagocyte capacity by means of charcoal insertion into the mesenteric vein lead to the liver microcirculatory disturbances. Experimental cholangitis caused more profound microcirculatory disturbances, then obstructive jaundice. Morphological comparison of liver samples of rats with experimental obstructive jaundice and cholangitis revealed inflammation in both cases with more intensive excitation of kuppfer cells, accompanied with more extensive sinusoidal dilatation in cholangitis samples. Supporting results of own research with literary data author offers assumption, that endotoxin and bacterial translocation caused by acholia can not be the main source of systemic inflammatory response in cholangitis. Induced by bile infection latter can cause secondary injury of the liver cells.

Keywords:
obstructive jaundice, bile contamination, cholangitis, kuppfer cells, sepsis and liver.