Effect of Kupffer cell blockade on the development of acute toxic hepatitis

Kutina, S. N.; Mayanskii, D. N.

doi:10.1007/bf00844526

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“…The animals were decapitated 24, 48, 72, and 96 h after CCI 4 poisoning. The severity of liver injury was estimated morphometrically on paraffin sections stained with hematoxylin and eosin by measuring the size of necrosis zones and zones of hydropic balloon degeneration [2] and biochemically by measuring serum alanine aminotransferase activity (ALT). The blood was drawn from the retroorbital sinus immediately before decapitation.…”

Section: Methodsmentioning

confidence: 99%

“…Our previous experiments demonstrated that shorttime blockade of Kupffer cells (KC) by colloidal carbon, observed 2 h after its injection, enhanced liver injury caused by tetrachloromethane (CC14) and delayed liver recovery [2]. It is known that gadolinium chloride (GdCI3) selectively blocks KC, while repopulation of the liver with young macrophages starts not earlier than 4 days after intravenous injection of GdCI 3 [6,8].…”

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confidence: 99%

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Liver resistance to toxic effects of CCl4 under conditions of gadolinium chloride depression of Kupffer cells

2000

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Acute toxic hepatitis was modeled in (CBAxC57B1)F1 mice by single injection of 40% CCl(4) in oil. Pretreatment with gadolinium chloride, a selective blocker of Kupffer cells, considerably potentiated damage to hepatocytes leading to generalization of this process, delayed inflammatory infiltration, and inhibited reparative processes. Zymosan administered against the background of gadolinium chloride blockade improved liver resistance to CCl(4)-induced damage, intensified mononuclear infiltration, and accelerated reparative processes.

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Section: Methodsmentioning

confidence: 99%

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confidence: 99%