The DOI matches its Crossref record; 20 of the 20 references it cites were found in a registry or an index.
Characterization of A Reproducible Rat Model of Hepatic Veno–Occlusive Disease
Abstract
Lack of a reproducible animal model has hampered progress in understanding hepatic veno–occlusive disease (HVOD). This article characterizes a reproducible model of HVOD. Rats gavaged with monocrotaline, 160 mg/kg, were killed between days 1 and 10. Sections were evaluated by light microscopy with a standardized scoring system, by immunoperoxidase staining with ED–1 (monocytes, macrophages) and ED–2 (Kupffer cells) antibodies, and by transmission (TEM) and scanning electron microscopy (SEM). On days 1 and 2, the earliest manifestations were progressive injury to the sinusoidal wall with loss of sinusoidal lining cells, sinusoidal hemorrhage, and mild damage to central vein (CV) endothelium. On days 3 through 5 (“early HVOD”), there was centrilobular coagulative necrosis, severe injury to sinusoids, severe sinusoidal hemorrhage, and severe CV endothelial damage; inflammation with ED–1-positive cells was most marked on these days. Days 6 and 7 (“late HVOD”) were characterized by subendothelial and advential fibrosis of CVs, damage of the CV endothelium with subendothelial hemorrhage, and some restoration of the sinusoidal wall. Between days 8 and 10, sections showed interindividual variation ranging from mild, residual fibrosis to severe, late HVOD. From days 1 through 10, ED–2-positive cells were decreased in number, and the number of ED–1-positive cells was increased. Sinusoidal damage is the earliest change in HVOD. Coagulative necrosis follows sinusoidal injury and resolves with improvement in sinusoidal endothelial cell (SEC) morphology. Moderate–to–severe CV fibrosis occurs after reappearance of sinusoidal lining cells and resolution of hepatocyte necrosis. The inflammatory response within the lobule and CVs is a result of recruitment of monocytes, whereas Kupffer cells are decreased in number.
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VENOOCCLUSIVE DISEASE OF THE LIVER FOLLOWING BONE MARROW TRANSPLANTATION
JONES, R. J., LEE, K. S. K., BESCHORNER, W. E., VOGEL, V. G., GROCHOW, L. B., BRAINE, H. G., VOGELSANG, G. B., SENSENBRENNER, L. L., SANTOS, G. W., & SARAL, R. (1987) · Transplantation · doi:10.1097/00007890-198712000-00011 · Cited by 912
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Hepatic toxicity resulting from cancer treatment
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Self-citationPortmann, B. (1998) · Journal of Hepatology · doi:10.1016/s0168-8278(98)80245-6 · Cited by 549
The human liver after radiation injury. A form of veno-occlusive disease.
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Cited by
Sinusoidal Obstruction Syndrome (Hepatic Veno-Occlusive Disease)
Fan, C. Q., & Crawford, J. M. (2014) · Journal of Clinical and Experimental Hepatology · doi:10.1016/j.jceh.2014.10.002 · Cited by 274
Radiation-induced liver disease: current understanding and future perspectives
Kim, J., & Jung, Y. (2017) · Experimental & Molecular Medicine · doi:10.1038/emm.2017.85 · Cited by 260
Liver Sinusoidal Endothelial Cells
Sørensen, K. K., Simon‐Santamaria, J., McCuskey, R. S., & Smedsrød, B. (2015) · Comprehensive Physiology · doi:10.1002/cphy.c140078 · Cited by 257
Self-citationEarly Hepatic Microvascular Injury in Response to Acetaminophen Toxicity
ITO, Y., BETHEA, N. W., ABRIL, E. R., & MCCUSKEY, R. S. (2003) · Microcirculation · doi:10.1038/sj.mn.7800204 · Cited by 158
Self-citationZhuge, Y., Liu, Y., Xie, W., Zou, X., Xu, J., Wang, J., & Chinese Society of Gastroenterology Committee of Hepatobiliary Disease (2019) · Journal of Gastroenterology and Hepatology · doi:10.1111/jgh.14612 · Cited by 107
Metadata
- Authors
- DeLeve, L. D., McCuskey, R. S., Wang, X., Hu, L., McCuskey, M. K., Epstein, R. B., & Kanel, G. C.
- Venue
- Hepatology
- Published
- 1999-06
- Volume
- 29
- Issue
- 6
- Pages
- 1779-1791
- ISSN
- 0270-9139 (ISSN-L)
- OpenAlex
- W2006201383
- Cited by
- 324
- References
- 20
- FWCI
- 3.43
- Type
- journal article
- Language
- en
- Open access
- closed
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