Hepatic microvascular development in relation to the morphogenesis of hepatocellular plates in neonatal rats
Version of Record online: 23 SEP 2003
Copyright © 2003 Wiley-Liss, Inc.
The Anatomical Record Part A: Discoveries in Molecular, Cellular, and Evolutionary Biology
Volume 275A, Issue 1, pages 1019–1030, November 2003
How to Cite
McCuskey, R. S., Ekataksin, W., LeBouton, A. V., Nishida, J., McCuskey, M. K., McDonnell, D., Williams, C., Bethea, N. W., Dvorak, B. and Koldovsky, O. (2003), Hepatic microvascular development in relation to the morphogenesis of hepatocellular plates in neonatal rats. Anat. Rec., 275A: 1019–1030. doi: 10.1002/ar.a.10117
- Issue online: 3 OCT 2003
- Version of Record online: 23 SEP 2003
- Manuscript Accepted: 7 JUN 2003
- Manuscript Received: 22 APR 2003
- NIH. Grant Number: 5-PO1-HD26013
The development of hepatic microvascular heterogeneity after birth, and its temporal relationship to the development of parenchymal cell plates have received little attention. As a result, the morphogenesis of some of the parameters contributing to this heterogeneity in suckling and weaned rats was studied as a function of time between postpartum days 4 and 30 using in vivo light microscopic, electron microscopic, and immunocytochemical methods. During the early suckling period, the sinusoid network is highly anastomotic, with little evidence of zonation, and the parenchymal cell plates contain multiple cells and are irregularly arranged throughout the lobule. Sinusoidal endothelial fenestration is sparse at 4 days, but phagocytic Kupffer cell (KC) function already exists and exhibits zonal heterogeneity, with more cells located in the periportal zone. With increasing age, endothelial fenestrae increase and organize as sieve plates. Widened centrilobular radial sinusoids form through a loss (“drop-out”) of intersinusoidal sinusoids (ISS). Concomitantly, the associated cell plates straighten and become one cell thick. Hepatocyte DNA synthesis and mitosis are higher in the periportal zone, which retains thickened cell plates and anastomotic sinusoids. The centrilobular sinusoids may widen to accommodate the increased volume of blood that results from the loss of ISS as well as the increased numbers of periportal sinusoids containing flow that feed these vessels. KC phagocytic activity increases during the suckling period concomitant with an increase of gut-derived endotoxin in the portal blood, which suggests that the KCs may be releasing mediators that affect sinusoid diameter, blood flow, endothelial fenestration, and perhaps parenchymal growth either directly or through the stimulation of growth factors. Anat Rec Part A 275A:1019–1030, 2003. © 2003 Wiley-Liss, Inc.