Abstract
BackgroundIt has been postulated that ethanol affects hepatic sinusoidal and perisinusoidal cells. In the current experimental study, we investigated the early effect of a single intravenous dose of ethanol on the diameter of liver sinusoidal endothelial fenestrae in New Zealand White rabbits. The diameter of fenestrae in these rabbits is similar to the diameter found in humans with healthy livers. The effect of ethanol on the size of fenestrae was studied using transmission electron microscopy, because plastic embedding provides true measures for the diameter of fenestrae.ResultsAfter intravenous administration of a single dose of 0.75 g/kg, ethanol concentration peaked at 1.1 ± 0.10 g/l at ten minutes after injection. Compared to control rabbits (103 ± 1.1 nm; n = 8), the average diameter of fenestrae in ethanol-injected rabbits determined at 10 minutes after injection was significantly (p < 0.01) smaller (96 ± 2.2 nm; n = 5). Detailed analysis of distribution histograms of the diameters of fenestrae showed that the effect of ethanol was highly homogeneous.ConclusionA decrease of the diameter of fenestrae 10 minutes after ethanol administration is likely the earliest morphological alteration induced by ethanol in the liver and underscores the potential role of liver sinusoidal endothelial cells in alcoholic liver injury.
Highlights
It has been postulated that ethanol affects hepatic sinusoidal and perisinusoidal cells
Chronic ethanol exposure leads to defenestration in liver sinusoidal endothelial cells which is paralleled by the deposition of a basal lamina [5]
We have recently shown that the diameter of fenestrae in human healthy livers, fixed by injecting glutaraldehyde into fresh wedge biopsies, is similar compared to fenestrae in the livers of New Zealand White rabbits [9] and is significantly smaller than in mice [10] or rats [11]
Summary
It has been postulated that ethanol affects hepatic sinusoidal and perisinusoidal cells. Capillarization of hepatic sinusoids further impairs microcirculatory exchange of nutrients and the clearance of waste products, enhances tissue fibrosis, and will affect the hepatic parenchyma and its metabolism. Whereas this sequence of events has been corroborated by several studies, it is not well established to which extent a single administration of ethanol affects liver sinusoidal endothelial cells. Scanning electron microscopy studies in vivo showed significant decreases of the diameter of sinusoidal endothelial fenestrae [8], suggesting that the transport of plasma substances from sinusoids to parenchymal liver cells may already be impaired by acute ethanol intake
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