X. EFFECTS OF DEFICIENCY 



117 



the order of \'eins, divide into small terminals of the order of venules, and 

 it is from the latter that hlood enters the hepatic sinusoids (Figs. 13 and 

 14). These terminal venules ("distril)utors") of the portal vehi should be 

 regarded as the most significant landmarks for orientation of lesions in 

 relation to the functional lobular units of the liver. Unhai)pily, in micro- 



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Fi(i. 15. Cleared and injected (India ink) slice (100 m) of liver of a rat fed a choline- 

 deficient diet for approximately one year. The white arrow (right center) points to 

 a large branch of the portal vein. Fibrosis in non-portal regions has destro3'ed the 

 sinusoidal patterns e.xcept for small trees at the ends of the terminal venules of the 

 portal vein. Note the manner in which the trabeculae (clear areas in illustration) 

 embrace the cunduding portion of the portal vein as indicated by the position of the 

 arrow. Fibrosis at this site is periportal in an anatomical sense only. In functionally 

 periportal positions around the terminal portal venules, the sinusoidal jjattern is 

 relatively intact. XIOO. 



sections, these venules, with their accompanying bile radicles and hepatic 

 arterioles, are small and insignificant. Each veiuile supplies a parenchymal 

 unit which is many limes its diameter in section (about 10 |i and several 

 hiuidred microns, respectively), and therefore thin random sections of the 

 unit freciuently fail to include its small afferent vessels. In contrast, the 

 large, non-ierminnl veins ("conductors") of the portal system readily attract 

 the attention of the moiphologist by \'irtue of their large diameter and their 

 lengthy course as they pass through many parenchymal vuiits to which 

 they are not direclhj related in a functional sense. The relation of the latter 



