摘要
Abstract Objective To evaluate the role of increased portal pressure and portosystemic shunting in elevated level of prostacyclin (PGI 2) in portal hypertension. Methods Thirty six male Sprague Dawley rats were divided into four groups: prehepatic portal hypertension (PHPH, 8 rats), intrahepatic portal hypertension (IHPH, 9), end to side portacaval shunt (PCS, 8), and sham operated controls (SO, 11). Two weeks after surgery, free portal pressure (FPP) was measured; systemic and splanchnic hemodynamics was studied by radioactive microsphere technique and blood sample from the femoral artery was obtained to measure the level of plasma 6 keto PGF 1 α with radio immunoassay. Results The FPP (mmHg) in IHPH, PHPH, PCS and SO rats was 13.10±1.02, 12.10±1.52, 3.0±0.82 and 6.86±0.69, respectively. The value of FPP was significantly increased in IHPH, PHPH rats and significantly decreased in PCS rats when compared to SO rats. Cardiac index (CI) and portal venous inflow (PVI) were in the order of PCS>PHPH>IHPH>SO rats. Portosystemic shunting (PSS) in PCS, PHPH, IHPH was 99.7±0.29%, 76.02±20.62% and 30.34±10.18%, respectively. The concentrations of plasma 6 keto PGF 1α (ng/ml) in PHPH, IHPH, PCS and SO rats were 6.93±2.43, 5.09±2.27, 2.36±1.01 and 1.56±0.61, respectively. The concentrations of plasma PGI 2 in PHPH, IHPH and PCS rats were significantly higher than those in SO rats. Furthermore, the concentrations of plasma PGI 2 in PHPH and IHPH rats were also significantly higher than those in PCS rats. Moreover, a closed positive correlation existed between plasma PGI 2 and FPP (r=0.67, P<0.001). Conclusions The results of the present study suggest that the elevated PGI 2 in portal hypertension is mainly due to the overproduction of PGI 2 in vascular epithelium cells induced by increased portal pressure, whereas portosystemic shunting and liver dysfunction play a secondary role. In addition, the results of this study do not support that PGI 2 mediated the hyperhemodynamics in portal hypertension.
Abstract Objective To evaluate the role of increased portal pressure and portosystemic shunting in elevated level of prostacyclin (PGI 2) in portal hypertension. Methods Thirty six male Sprague Dawley rats were divided into four groups: prehepatic portal hypertension (PHPH, 8 rats), intrahepatic portal hypertension (IHPH, 9), end to side portacaval shunt (PCS, 8), and sham operated controls (SO, 11). Two weeks after surgery, free portal pressure (FPP) was measured; systemic and splanchnic hemodynamics was studied by radioactive microsphere technique and blood sample from the femoral artery was obtained to measure the level of plasma 6 keto PGF 1 α with radio immunoassay. Results The FPP (mmHg) in IHPH, PHPH, PCS and SO rats was 13.10±1.02, 12.10±1.52, 3.0±0.82 and 6.86±0.69, respectively. The value of FPP was significantly increased in IHPH, PHPH rats and significantly decreased in PCS rats when compared to SO rats. Cardiac index (CI) and portal venous inflow (PVI) were in the order of PCS>PHPH>IHPH>SO rats. Portosystemic shunting (PSS) in PCS, PHPH, IHPH was 99.7±0.29%, 76.02±20.62% and 30.34±10.18%, respectively. The concentrations of plasma 6 keto PGF 1α (ng/ml) in PHPH, IHPH, PCS and SO rats were 6.93±2.43, 5.09±2.27, 2.36±1.01 and 1.56±0.61, respectively. The concentrations of plasma PGI 2 in PHPH, IHPH and PCS rats were significantly higher than those in SO rats. Furthermore, the concentrations of plasma PGI 2 in PHPH and IHPH rats were also significantly higher than those in PCS rats. Moreover, a closed positive correlation existed between plasma PGI 2 and FPP (r=0.67, P<0.001). Conclusions The results of the present study suggest that the elevated PGI 2 in portal hypertension is mainly due to the overproduction of PGI 2 in vascular epithelium cells induced by increased portal pressure, whereas portosystemic shunting and liver dysfunction play a secondary role. In addition, the results of this study do not support that PGI 2 mediated the hyperhemodynamics in portal hypertension.
