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Acute alcohol administration to mice induces hepatic sinusoidal endothelial cell dysfunction

https://doi.org/10.1016/0928-4346(94)90016-7Get rights and content

Abstract

Ethanol administration to mice (4.4 g kg−1 body wt., i.p.) induced a marked increase (125%) in plasma hyaluronan (HA) concentration associated with a significant decrease (46%) in HA uptake by the isolated, perfused liver. Similar changes were obtained after i.v. administration ofEscherichia coli lipopolysaccaharide (1 mg kg−1 body wt.), a strong activator of Kupffer cells. Since: (a) hepatic HA uptake is predominantly a function of the sinusoidal endothelial cells, reflecting their functional state, and (b) liver is a major site of HA clearance from the blood, we conclude that alcohol alters sinusoidal endothelial cell functions, including HA endocytosis. Changes in Kupffer cell functional state may be a primary event underlying the effects of both ethanol and LPS on sinusoidal endothelial cells.

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