The effects of ethanol on the sinusoidal endothelial fenestration of rat liver.

Kanaoka, Hikoharu; Okanou, Takeshi; Sawa, Yoshihiko; Kachi, Kazutomo; Ohta, Yoshiharu; Morimoto, Michio; Kagawa, Keiichiro; Yuki, Takehiko; Takino, Tatsuro

doi:10.2957/kanzo.29.198

Cited by 1 publication

(5 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Ethanol feeding for 8 weeks decreased the number of fenestrations and increased the fenestration diameter, which was associated with a reduction in endothelial porosity in both the centrilobular and periportal sinusoids. The decreased porosities contrast the data reported by Kanaoka et al (1988) above but these changes are in accord with those found in human alcoholics and in alcohol‐fed baboons (Horn et al, 1987; Mak & Lieber, 1984). Interestingly, TEM showed there was marked endocytic activity associated with the sinusoidal endothelial cells after chronic ethanol consumption, which could be a factor leading to the reduced porosity.…”

Section: Chronic Ethanol Ingestion In Rats and Micesupporting

confidence: 87%

“…After 6 weeks of ethanol feeding, the endothelial porosity was higher in zone 3 in association with fewer fenestrations and an increased diameter of fenestrations. The findings are like those reported in rats by Kanaoka et al (1988), but the higher porosity data are dissimilar to the lower porosity data of Tanikawa et al (1991). The sinusoids in zone 3 appear to be tortuous and narrow, which is thought to be related to the ballooning of hepatocytes compressing the sinusoids.…”

Section: Chronic Ethanol Ingestion In Rats and Micesupporting

confidence: 81%

“…Fenestrations of the hepatic sinusoid lack both bridging diaphragms and underlying basal lamina and their sizes and numbers are heterogenous across the liver lobule. In rats, periportal fenestrations are larger in diameter and fewer in number whereas centrilobular fenestrations are smaller in diameter and greater in number, which was first observed and reported by Wisse et al (1983) and later in other studies (Kanaoka et al, 1988;Okanoue et al, 1999;Takashimizu et al, 1999). For fine structure F I G U R E 2 TEM micrographs of endothelial fenestrations.…”

Section: Terminologymentioning

confidence: 66%

“…6.2 | Ethanol in sucrose solution and ethanol withdrawal: 3 months feeding Rats were chronically fed ethanol (35%, wt/vol) containing 12% sucrose for 3 months (Kanaoka et al, 1988) and the fenestration morphology was assessed by SEM. The ethanol diet decreased the fenestration number while the fenestration diameter was increased in zone 3, opposing the values of the control rats.…”

Section: Ethanol In Water: 28 Days Ingestionmentioning

confidence: 99%

“…Incidentally, in alcohol‐induced type V hyperlipoproteinemia, abstinence from alcohol substantially reduces the plasma triglyceride levels suggesting refenestration of the sinusoids and regaining a normal porosity (Fraser et al, 1995). Indeed, in rats, the withdrawal of ethanol following a long‐term feeding regimen led to restoration of the fenestrations and the porosity to control values (Kanaoka et al, 1988; Wang et al, 2005). On the other hand, acute ethanol was found to dilate the fenestrations, at least transiently (Charels et al, 1986; Fraser et al, 1982; Mori et al, 1991).…”

Section: Ethanol Sieve Plate Hyperlipidemia and Atherosclerosismentioning

confidence: 99%

See 4 more Smart Citations

Alcohol‐associated capillarization of sinusoids: A critique since the discovery by Schaffner and Popper in 1963

Mak

Kee

Shin

2021

The Anatomical Record

View full text Add to dashboard Cite

This article reviews the literature on capillarization of hepatic sinusoids since its discovery in 1963. Liver sinusoidal endothelial cells are uniquely fenestrated and lack an underlying basement membrane. In chronic liver disease, the sinusoids capillarize and transform into systemic capillaries, a process termed capillarization of sinusoids. The histopathology is marked by defenestration, basement membrane formation, and space of Disse fibrogenesis. Capillarized sinusoids compromise the bidirectional exchange of materials between sinusoids and hepatocytes, leading to hepatocellular dysfunction. Sinusoidal capillarization was first described in active cirrhosis of alcoholics in 1963. Since then, it has been found in early and progressive stages of alcoholic hepatic fibrosis before the onset of cirrhosis. The sinusoidal structure is not altered in alcoholic steatosis without fibrosis. Defenestration impairs the ability of the endothelium to filter chylomicron remnants from sinusoids into the Disse's space, contributing to alcohol‐induced postprandial hyperlipidemia and possibly atherosclerosis. Ethanol also modulates the fenestration dynamics in animals. In baboons, chronic alcohol consumption diminishes endothelial porosity in concomitance with hepatic fibrogenesis and in rats defenestrates the endothelium in the absence of fibrosis, and sometimes capillarizes the sinusoids. Acute ethanol ingestion enlarges fenestrations in rats and contracts fenestrations in rabbits. In sinusoidal endothelial cell culture, ethanol elicits fenestration dilation, which is likely related to its interaction with fenestration‐associated cytoskeleton. Ethanol potentiates sinusoidal injury caused by cocaine, acetaminophen or lipopolysaccharide in mice and rats. Understanding ethanol's mechanisms on pathogenesis of sinusoidal capillarization and fenestration dynamics will lead to development of methods to prevent risks for atherosclerosis in alcoholism.

show abstract

Section: Chronic Ethanol Ingestion In Rats and Micesupporting

confidence: 87%

Section: Chronic Ethanol Ingestion In Rats and Micesupporting

confidence: 81%