Chronic murine schistosomiasis is a natural disease model of portal hypertension closely mimicking the clinical and histological features of human hepatic schistosomiasis. W e studied the splanchnic and systemic hemodynamics in the murine model of schistosomiasis by radioactive microsphere technique. Mice infected with 60 cercariae of Schistosoma mansoni (n = 8) were studied hemodynamically 11 wk after the infection and were compared with age-matched healthy controls (n = 11). Mean portal venous inflow in the infected mice (3.82 -t 0.32 ml/min) was 61% higher than in the healthy animals (2.37 2 0.25 ml/min; p < 0.01). A twofold increase in hepatic arterial flow was also seen in mice with schistosomiasis (0.47 f 0.14 ml/min) as compared with controls (0.16 0.03 ml/min; p < 0.05). whereas splanchnic arteriolar resistance (60.91 f 7.64 vs. 101.21 f 11.06 mm H g . min . ml-'. g m ; p i 0.05) and peripheral vascular resistance (112.05 f 14.05 vs 254.53 f 29.86 mm Hg.min.rnl-'. g m ; p < 0.01) were reduced. There was a significant increase in cardiac index (752 f 99 vs. 453 f 55 ml * min-' * kg body weight-'; p < 0.05) and reduction in mean arterial pressure (81.37 -t 3.09 vs. 101.45 f 5.85 mm Hg; p < 0.05) in the infected animals compared with controls. These observations clearly demonstrate the existence of a hyperdynamic circulatory state in this model of portal hypertension. (HEPATOLOGY 1991; 13581-584.)
Chronic murine schistosomiasis provides a natural disease model of gradually evolving portal hypertension. The hepatic histological changes seen in chronic murine schistosomiasis closely resemble the hepatic lesions seen in man (1). DeWitt and Warren (2) have shown development of portosystemic collaterals and esophageal