P. Onori et al., Hepatic microvascular features in experimental cirrhosis: a structural andmorphometrical study in CCl4-treated rats, J HEPATOL, 33(4), 2000, pp. 555-563
Background/Aims: In this study a detailed morphometrical analysis of the he
patic microvasculature in the different zones of hepatic parenchyma was per
formed in normal and cirrhotic rat liver (CCl4-induced). The aims were to d
etect, in CCl4-induced cirrhosis, the real presence of the "capillarization
" of hepatic sinusoids and to assess alterations of the sinusoid/parenchyma
ratio within the nodule.
Methods: Cirrhosis was promoted by controlled intragastric CCl4 administrat
ion. Scanning electron microscopy of the vascular corrosion cast technique
associated,vith light microscopy and transmission electron microscopy were
used.
Results: Evidence of connective tissue in the space of Disse was found only
in sinusoids located near portal tracts or large fibrotic areas, and this
was also confirmed by laminin immunohistochemistry In contrast, all the int
ranodular sinusoids lacked real basal membrane and connective fibers in the
space of Disse and, displayed normal fenestrations. The parenchymal area,
sinusoidal area, mean sinusoidal area, sinusoidal perimeter, hepatocyte are
a and the reciprocal ratios were all considered in the morphometrical analy
sis. The sinusoids were of uniform size in the periportal, periseptal and p
ericentral areas of the cirrhotic liver without the typical zonal differenc
es of the normal liver. The areas occupied by sinusoids per unit of parench
yma and the sinusoid/hepatocyte interfaces disposable for metabolic exchang
es were markedly smaller (p<0.01) in cirrhotic than normal liver.
Conclusion: Our findings indicate that capillarization of hepatic sinusoids
occurs only in very limited regions of the cirrhotic parenchyma, and thus
this phenomenon does not have relevant functional consequences. Furthermore
, the cirrhotic parenchyma appears not to be supplied by sinusoids and lack
s features of zonation, which is a condition that could play a major role i
n the development and progression of liver failure.