Literature DB >> 9143673

Morphological changes during hepatocellular maturity in neonatal rats.

B Alexander1, M A Guzail, C S Foster.   

Abstract

BACKGROUND: Hepatocellular maturation is characterised by the progressive transition from an architecture in which hepatocyte plates are at least two cells thick to the familiar adult pattern in which liver cell plates are predominantly single-cell in thickness. A similar process also has been noted during compensatory hyperplasia following damage, or destruction to the hepatic parenchyma. The pathological events that underlie these processes remain inadequately explained. A new morphological approach has been developed to study the maturity of rat neonatal livers in order to identify the factors which govern the structured morphogenesis of the liver in greater detail.
METHODS: Sections of hepatic tissue obtained from the left lateral and right posterior lobes from neonatal rats were studied at 8, 10, 11, 13, 14, 18, 23, and 28 days postpartum. These were mounted, fixed, and stained with haematoxylin and eosin and analysed using a modified point-counting technique. Following validation of the technique, the proportion of single-cell plates to double-cell plates was then calculated at each time point.
RESULTS: Liver sections from 8-day neonatal rats had the lowest percentage of single-cell thick plates of 16.9 +/- 4.6% and the lowest standard deviation (mean +/- SD). The hepatic architecture had fully matured by 28 days and was characterised by predominantly single-cell plates (84.6 +/- 4.6%) lining the hepatic sinusoids. During the intervening time, the standard deviations increased significantly, peaking between 18-23 days, and reflected the rapidly changing morphology of the liver during this maturation process of the conversion of double-cell plates to single-cell plates.
CONCLUSIONS: It is concluded that the process of hepatocellular maturity in the neonatal Sprague-Dawley rat is reproducibly complete by 28 days and that further studies may now be conducted to determine the anatomical and pathophysiological changes that govern this important transition.

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Year:  1997        PMID: 9143673     DOI: 10.1002/(SICI)1097-0185(199705)248:1<104::AID-AR12>3.0.CO;2-T

Source DB:  PubMed          Journal:  Anat Rec        ISSN: 0003-276X


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