Abstract
Portal Hypertension is a frequent complication of cirrhosis and causes significant morbidity and mortality. Increased intrahepatic resistance is the primary factor but portal hypertension is also associated with changes in systemic and porto-sytemic collateral circulation. Cirrhosis is a state of vasoregulatory imbalance with excess vasoconstrictors and less vasodilators in hepatic circulation and the reverse is true for systemic circulation. Multiple pathophysiologic mechanisms including endothelial dysfunction, sinusoidal remodeling and angiogenesis are involved in increasing resistance in hepatic vascular bed. Current evidence suggests that these changes in vasoreactivity contribute to a significant proportion of intrahepatic vascular resistance and that they are reversible, providing an attractive target for therapeutic intervention.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1016-1019 |
| Number of pages | 4 |
| Journal | Hepatology Research |
| Volume | 39 |
| Issue number | 10 |
| DOIs | |
| State | Published - 2009 |
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Keywords
- Endothelial dysfunction
- Hepatic stellate cells
- Pathobiology
- Portal hypertension
- Sinusoidal remodeling
ASJC Scopus subject areas
- Hepatology
- Infectious Diseases
Cite this
New insights into the pathobiology of portal hypertension. / Guturu, Praveen; Shah, Vijay.
In: Hepatology Research, Vol. 39, No. 10, 2009, p. 1016-1019.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - New insights into the pathobiology of portal hypertension
AU - Guturu, Praveen
AU - Shah, Vijay
PY - 2009
Y1 - 2009
N2 - Portal Hypertension is a frequent complication of cirrhosis and causes significant morbidity and mortality. Increased intrahepatic resistance is the primary factor but portal hypertension is also associated with changes in systemic and porto-sytemic collateral circulation. Cirrhosis is a state of vasoregulatory imbalance with excess vasoconstrictors and less vasodilators in hepatic circulation and the reverse is true for systemic circulation. Multiple pathophysiologic mechanisms including endothelial dysfunction, sinusoidal remodeling and angiogenesis are involved in increasing resistance in hepatic vascular bed. Current evidence suggests that these changes in vasoreactivity contribute to a significant proportion of intrahepatic vascular resistance and that they are reversible, providing an attractive target for therapeutic intervention.
AB - Portal Hypertension is a frequent complication of cirrhosis and causes significant morbidity and mortality. Increased intrahepatic resistance is the primary factor but portal hypertension is also associated with changes in systemic and porto-sytemic collateral circulation. Cirrhosis is a state of vasoregulatory imbalance with excess vasoconstrictors and less vasodilators in hepatic circulation and the reverse is true for systemic circulation. Multiple pathophysiologic mechanisms including endothelial dysfunction, sinusoidal remodeling and angiogenesis are involved in increasing resistance in hepatic vascular bed. Current evidence suggests that these changes in vasoreactivity contribute to a significant proportion of intrahepatic vascular resistance and that they are reversible, providing an attractive target for therapeutic intervention.
KW - Endothelial dysfunction
KW - Hepatic stellate cells
KW - Pathobiology
KW - Portal hypertension
KW - Sinusoidal remodeling
UR - http://www.scopus.com/inward/record.url?scp=73849149973&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=73849149973&partnerID=8YFLogxK
U2 - 10.1111/j.1872-034X.2009.00553.x
DO - 10.1111/j.1872-034X.2009.00553.x
M3 - Article
VL - 39
SP - 1016
EP - 1019
JO - Hepatology Research
JF - Hepatology Research
SN - 1386-6346
IS - 10
ER -