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Experimental ischemic liver injury and regeneration over 3 months: Histological observations in the rat
Author(s) -
Manenti Antonio,
Botticelli Laura,
Pradelli John M.,
Botticelli Annibale R.
Publication year - 1997
Publication title -
pathology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 74
eISSN - 1440-1827
pISSN - 1320-5463
DOI - 10.1111/j.1440-1827.1997.tb03716.x
Subject(s) - ischemia , medicine , pathology , glycogen , necrosis , liver injury , lobules of liver , hypoxia (environmental) , blood supply , surgery , chemistry , organic chemistry , oxygen
Liver histopethology of segmental portal Ischemia occuring over a long‐term period has not been previously described. For these reasons histological changes In the rat liver were studied from 1 h to up to 90 days after a left lateral and middle segmental portal obstruction. Within 3 h, the hepatocytes showed glycogen depletion In Rappaport zones 1 and 2 and pericentral and central lobular congestion of sinusolds and veins, whereas within 3 days, vein thrombosis appeared in the center of the lobule and liver necrosis was observed in Rappaport zones 2 or 3 or both, followed by restitutio ad intergrum of the liver lobule morphology after 20–40 days. These results can be explained in light of two conditions occurring in the rat liver: (i) the pecullar low sensitivity of the liver to O 2 debit and the protective or vasoactive effects used during hypoxia; and (11) the sinusoldal network as a collateral source of the hepatic vascular system. Therefore, morphologlcai assessment of this arteriolar and sinusoidal system, implicated in assuring efficient collateral blood supply in the rat liver with portal Ischemia, is essential for understanding the mechanisms behind a natural and timely repair of ischemic injuries in the human Iiver.