Hemodynamic mechanisms of emerging portal hypertension caused by schistosomiasis in the hamster
✍ Scribed by James S. Morgan; Roberto J. Groszmann; Marcos Rojkind; Rosa Enriquez
- Publisher
- John Wiley and Sons
- Year
- 1990
- Tongue
- English
- Weight
- 739 KB
- Volume
- 11
- Category
- Article
- ISSN
- 0270-9139
No coin nor oath required. For personal study only.
✦ Synopsis
A hamster model of schistosomiasis has provided the first opportunity to sequentially examine the early phases of the development of portal hypertension in a natural model of chronic liver disease. Groups of hamsters were infected with 50 cercariae of Schistosoma mansoni and underwent hemodynamic evaluation at intervals of 5,8,12 and 20 wk after infection. A progressive rise in intrahepatic resistance (from 4.0 f 0.4 to 8.4 -c 1.0 mm Hg min * ml-' gm liver weight Ip < 0.011) appeared to play a major role in the initial stages of evolving portal hypertension. A gradual decline in portal blood flow (from 2.1 f 0.3 to 1.3 f 0.1 ml . min-' . gm-' liver weight [p < 0.011) was only partially compensated for by an increase in hepatic arterial flow. Accordingly, by week 20, total hepatic blood flow decreaeed 23%. Liver weight that increased markedly between 5 and 12 wk after infection, as a result of the acute accumulation of obstructing granulomas, stabilized between wk 12 and 20, while a gradual but progressive rise in hepatic collagen content was seen. Portal pressure increased 75% during the study period. Chronic examination of this natural model should help define the pathogenesis of the complications of portal hypertension and contribute to the basis for effective intervention in this disease process. (HEPATOLOGY 1990; 11:9& 104.)
The hemodynamic mechanisms that contribute to the evolution and maintenance of portal hypertension caused by schistosomiasis are not well understood. Prospective observations in humans are limited in many cases by the coexistence of other illnesses such as viral hepatitis or alcoholism (1-4). Human studies are also complicated by the heterogeneity of the clinical stage of presentation (2,4-6). However, several animal mod-