Ageing Has No Effect on the Volume Density of Hepatocytes, Reticuloendothelial Cells or the Extracellular Space in Livers of Female Sprague‐dawley Rats

Martin, Glenn E; Sewell, R. B.; Yeomans, Neville D; Smallwood, Richard A.

doi:10.1111/j.1440-1681.1992.tb00501.x

Cited by 13 publications

(9 citation statements)

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“…In both rats and, mice old age was associated with approximately a doubling in the numbers of desmin-positive HSC per 0.5 mm 2 . As such, the result is numerically consistent with that of Martin et al, [18] although our results were statistically significant. It is of interest that we have previously found an increase in the number of Kupffer cells in old age.…”

Section: Discussionsupporting

confidence: 93%

“…Previously, Enzan et al [7] commented that there was no change in the frequency of HSC, but this study was performed using electron microscopy and no data were provided [7]. Similarly Martin et al [18] concluded that there were no changes in HSC numbers in old age in rats. However, in their study, the volume of liver consisting of HSC increased from 0.43 ± 0.13% in young rats to 1.0 ± 0.24% in old rats but this did not reach statistical significance ( P = .075 with only 4 rats in each age group) [18].…”

Section: Discussionmentioning

confidence: 98%

“…Similarly Martin et al [18] concluded that there were no changes in HSC numbers in old age in rats. However, in their study, the volume of liver consisting of HSC increased from 0.43 ± 0.13% in young rats to 1.0 ± 0.24% in old rats but this did not reach statistical significance ( P = .075 with only 4 rats in each age group) [18]. In our study, desmin immunohistochemistry was used to determine the number of HSC present in liver.…”

Section: Discussionmentioning

confidence: 98%

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The Effects of Old Age on Hepatic Stellate Cells

Warren

Cogger

Fraser

et al. 2011

Current Gerontology and Geriatrics Research

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Aging is associated with marked changes in the hepatic sinusoid, yet the effect of old age on hepatic stellate cells (HSC) has not been well described. Transmission electron microscopy and immunohistochemistry were used to study the effects of aging on HSC in livers from rats (3-4 mths versus 24–27 mths) and mice (2-3 mths versus 20–22 mths). Desmin-positive HSC doubled in old age in both mice and rats. Alpha-smooth muscle actin- (αSMA-) positive cells did not increase significantly and remained only a small percentage of desmin-positive cells. Electron microscopy revealed that old age is associated with HSC that have a substantial increase in the number of lipid droplets which are larger in diameter. There was also a marked increase of HSC that protruded into the sinusoidal lumen in old mice. In conclusion, old age is associated with hyperplasia of HSC that are not activated and are engorged with lipid droplets.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 98%

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The Effects of Old Age on Hepatic Stellate Cells

Warren

Cogger

Fraser

et al. 2011

Current Gerontology and Geriatrics Research

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“…1,2,23 These results are consistent with past studies, all of which conclude that there are few gross structural changes in the liver with age. 1,2,23 Previous electron-microscopic studies have not reported specific investigations of sinusoidal structures in the intact aged liver 14,[24][25][26][27] ; however, our assessment by electron microscopy and immunohistochemistry revealed significant age-related changes within the sinusoidal endothelium and space of Disse. Scanning electron microscopy revealed a significant reduction in the porosity of the aged sinusoidal endothelium.…”

Section: Discussioncontrasting

confidence: 45%

Pseudocapillarization and associated energy limitation in the aged rat liver

2001

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Age-related impairment of drug metabolism by the liver is consistent with hepatocyte hypoxia, suggestive of the development of a diffusional barrier to oxygen supply. Because the effects of aging on the diffusional pathway (sinusoidal endothelium and space of Disse) have not been described, we performed comparative studies on the livers of Fischer F344 rats aged 4 to 7, 12 to 15, and 24 to 27 months. Lightmicroscopic examination revealed no evidence of fibrosis, cirrhosis, or other specific pathology. In contrast, scanning and transmission electron-microscopic examination revealed that aging is associated with pseudocapillarization of the sinusoidal endothelium, indicated by defenestration with reduced porosity, thickening of the endothelium, infrequent development of basal lamina, and only minor collagen deposits in the space of Disse. Furthermore, immunohistochemistry studies showed strong expression of collagen IV, moderate expression of factor VIII-related antigen, and weak expression of collagen I along the sinusoids of livers from old rats (P < .0001). In vitro 31 P magnetic resonance spectroscopy analysis showed that aging is associated with changes in high-energy phosphate and other metabolites, consistent with hepatocyte hypoxia. Aging in the liver is associated with changes in the sinusoidal endothelium and space of Disse that may restrict the availability of oxygen and other substrates. (HEPATOLOGY 2001;33:537-543.)The effect of aging in the liver is often considered to be of a lesser degree than in other organs. [1][2][3][4] The major recognized changes in the aging liver include reduction in liver mass and hepatic blood flow 1,4,5 ; however, it has been concluded that there are few other significant structural or biochemical changes in the liver. 1,2 On the other hand, even subtle agerelated changes may have profound consequences for the rest of the body. For example, any age-related impairment in hepatic drug and xenobiotic detoxification could partly explain the susceptibility of elderly persons to adverse drug reactions or illnesses with toxic etiology. 5 In vivo, the hepatic clearance of many drugs is reduced in elderly persons. Traditional theories have attempted to attribute this to age-related reduction of liver mass and blood flow. 6 However, in a recent review, 5 we noted that there appears to be selective reduction of the clearance of drugs that undergo phase I metabolism, associated with preservation of the clearance of drugs that undergo phase II metabolism. Even more puzzling, the in vitro activities of phase I enzymes are maintained into old age. 7 Because these paradoxes cannot be attributed to changes in blood flow and liver mass alone, we suggested an explanation based on oxygen supply, as the activities of phase I enzymes are highly oxygen-dependent because they require oxygen as a substrate. 8 We hypothesized the development of a barrier to oxygen diffusion, leading to functional intracellular hypoxia in the hepatocytes of the aging liver. This provides a plausible mechanism for i...

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“…Previous studies showed that Kupffer cells have been observed in increased numbers in older subjects, 34,35 whereas another study reported a reduction in the volume density with age. 36 The function of Kupffer cells in normal aging is not well understood. In this study, the number of CD68-positive cells in the elderly donors was lower than that in younger donors.…”

Section: Discussionmentioning

confidence: 99%

The Kupffer Cell Number Affects the Outcome of Living Donor Liver Transplantation from Elderly Donors

Hidaka

Eguchi

Takatsuki

et al. 2016

Transplantation Direct

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BackgroundThere have been no previous reports how Kupffer cells affect the outcome of living donor liver transplantation (LDLT) with an elderly donor. The aim of this study was to elucidate the influence of Kupffer cells on LDLT.MethodsA total of 161 adult recipients underwent LDLT. The graft survival, prognostic factors for survival, and graft failure after LDLT were examined between cases with a young donor (<50, n = 112) and an elderly donor (≥50, N = 49). The Kupffer cells, represented by CD68-positive cell in the graft, were examined in the young and elderly donors.ResultsIn a multivariable analysis, a donor older than 50 years, sepsis, and diabetes mellitus were significant predictors of graft failure after LDLT. The CD68 in younger donors was significantly more expressed than that in elderly donors. The group with a less number of CD68-positive cells in the graft had a significantly poor survival in the elderly donor group and prognostic factor for graft failure.ConclusionsThe worse outcome of LDLT with elderly donors might be related to the lower number of Kupffer cells in the graft, which can lead to impaired recovery of the liver function and may predispose patients to infectious diseases after LDLT.

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Ageing Has No Effect on the Volume Density of Hepatocytes, Reticuloendothelial Cells or the Extracellular Space in Livers of Female Sprague‐dawley Rats

Cited by 13 publications

References 9 publications

The Effects of Old Age on Hepatic Stellate Cells

The Effects of Old Age on Hepatic Stellate Cells

Pseudocapillarization and associated energy limitation in the aged rat liver

The Kupffer Cell Number Affects the Outcome of Living Donor Liver Transplantation from Elderly Donors

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