摘要
AIM: To study the effects of endotoxin on portal hemodynamic of normal and noncirrhotic portal hypertensive rats. METHODS: Normal rats were intraperitoneally injected with 0.1, 0.25, 0.5, 1.0, 2.0, 4.0mg.kg(-1) of lipopolysaccharide(LPS) respectively, portal vein ligation(PVL) and intrahepatic portal occlusion (IPO) rats as well as sham-operated rats were treated with an intraperitoneal injection of 1.0mg.kg(-1) of LPS, the portal vein pressure(PVP), portal venous flow(PVF), inferior vena cava pressure(IVCP) and portal vein resistance(PVR) were detected 4 hours after injection. RESULTS: PVF of the 5 groups of rats accepting intraperitoneal injection of LPS were increased from 14.0 to 18.0, 22.2, 26.2, 34.8, 39.6, 38.8 mL.min(-1) 4 hours after injection of LPS(P【0.01). PVP of the 4 groups of rats accepting more than 0.1mg/kg.b.w of LPS was increased from 1.04 to 1.25, 1.50, 1.80, 1.95, 2.05 kPa(P【0.01). The increments of PVF and PVP were in a dose-dependent manner of LPS. PVR of the 5 groups of rats was decreased from 51 to 42,44,48,45,44,47 kPa.min.L(-1) (P【0.05) and no dose-dependent manner was observed. PVF of PVL, IPO and sham-operated rats increased from 22.6 to 32.8, 22.0 to 28.0, 14.0 to 34.8 mL.min(-1) (P【0.01), and PVP increased from 1.86 to 2.24, 1.74 to 1.95, 1.04 to 1.80 kPa(P【0.01), PVR decreased from 71 to 61, 67 to 61, 52 to 44 kPa.min.L(-1) after intraperitoneal injection of 1mg.kg(-1) of LPS. The increments of PVF and PVP of PVL and IPO rats were significantly less than the sham-operated rats(P【0.01), There was no significant difference between the amounts of PVR decreased in the two groups of PHT model rats and sham-operated rats(P】0.05) after intraperitoneal injection 1mg.kg(-1) of LPS. CONCLUSION: Endotoxin could prompt portal hypertension of the normal and noncirrhotic portal hypertensive rats by increasing portal blood flow mainly.
AIM: To study the effects of endotoxin on portalhemodynamic of normal and noncirrhotic portal hypertensiverats.METHODS: Normal rats were intraperitonealy injected with 0.1,0.25, 0.5, 1.0, 2.0, 4.0 mg@kg-1 of lipopolysaccharide( LPS ) respectively, portal vein ligation ( PVL ) andintrahepatic portal occlusion (IPO) rats as well as sham-operated rats were treated with an intraperitoneal injection of1.0 mg@kg-1 of LPS, the portal vein pressure(PVP), portalvenous flow(PVF), inferior vena cava pressure(IVCP) andportal vein resistance (PVR) were detected 4 hours afterinjection.RESULTS: PVF of the 5 groups of rats acceptingintraperitoneal injection of LPS were increased from 14.0 to18.0, 22.2, 266.2, 34.8, 39.66, 38.8 mL@min-1 4 hours afterinjection of LPS ( P ＜ 0. 01 ). PVP of the 4 groups of ratsaccepting more than 0.1 mg/kg@ b. w of LPS was increasedfrom 1.04 to1.25, 1.50, 1.80, 1.95, 2.05 kPa(P＜0.01). Theincrements of PVF and PVP were in a dose-dependentmanner of LPS. PVR of the 5 groups of rats was decreasedfrom 51 to 42,44,48,45,44,47 kPa@min@ L-1 ( P＜ 0.05) and nodosedependent manner wes observed. PVF of PVL, IPOand sham-operated rats increased from 22.66 to 32.8, 22.0 to28.0, 14.0 to 34.8 mL@min1 ( P＜ 0.01), and PVP increasedfrom 1.86 to 2.24, 1.74 to 1.95, 1.04 to 1.80 kPa(P＜0.01),PVR decreased from 71 to61, 67 to61, 52 to 44 kPa@min@ L-1after intraperitoneal injection of 1 mg@ kg-1 of LPS. Theincrements of PVF and PVP of PVL and IPO rats weresignificantly less than the sham-operated rats ( P ＜ 0. 01 ),There wes no significant difference between the amounts ofPVR decreased in the two groups of PHT model rats andsham-operated rats( P＞ 0.05) after intraperitoneal injection 1mg@kg1 of LPS.CONCLUSION: Endotoxin could prompt portal hypertensionof the normal and noncirrhotic portal hypertensive rats byincreasing portal blood flow mainly.
