X. EFFECTS OF DEFICIENCY 



119 



plexus. Howe^■er, cells bordering jiiiK^tions between sinusoids and terminal 

 portal venules ob^'iously have prior access to any essential food factors 

 (including choline) . Actually it is cells more remote from these favored sites 

 that would first develop evidence of deficiency when the amount of an 

 essential substance reaching the liver is insufficient to supply all parts of 

 the organ. Cells adjacent to large conducting (but not distributing) portal 



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Fig. 17. Tins is a, paraffin section of the liver of a rat comparable to the prepara- 

 tion illustrated in Figs. 15 and 16. The lower left portion of the field is occupied by a 

 large bile duct, branches of the hepatic artery, and a small portion of a large branch 

 of the portal vein. These structures are encircled by trabeculae, and to this extent 

 the fibrosis is periportal. But the small terminal branches of the portal vessels are 

 free of fibrosis, and in this functional sense the distribution of the trabeculae is non- 

 portal. The white arrow indicates a small terminal portal area which is enlarged in 

 Fig. 18. Hemato.xylin and cosin stain. X200. 



vessels are in a position which is no more favorable for obtaining metabo- 

 lites that may be in short supply than cells in other non-portal regions 

 equally remote from the site at which blood enters the parenchymal imit. 

 Both fatty and fibrotic lesions in choline-deficient rats make their initial 

 appearance and reach their most advanced stages in those portions of the 

 hepatic lobule which are farthest from the sites at which blood leaves 

 terminal portal venules to enter the sinusoids of each parenchymal unit. 

 The most non-portal areas of the liver are those which surround the radicles 

 of the hepatic vein, and these pericentral regions are the first sites of both 



