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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 lipopolysaecharide(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 to18.0,22.2,26.2,34.8.39.6,38.8 mL·min~(-1)4 hours afterinjection of LPS(P<0.01).PVP of the 4 groups of ratsaccepting more than 0.1mg/kg·b.w of LPS was increasedfrom 1.04 tol.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 nodose-dependent manner was observed.PVF of PVL,IPOand sham-operated rats increased from 22.6 to 32.8,22.0 to28.0,14.0 to 34.8 mL·min~(-1)(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 to 61,67 to 61,52 to 44 kPa·min·L~(-1)after 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 was 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·kg~(-1)of LPS.CONCLUSION:Endotoxin could prompt portal hypertensionof the normal and noncirrhotic portal hypertensive rats byincreasing portal blood flow mainly.
AIM: To study the effects of endotoxin on portalhemodynamic of normal and noncirrhotic portal hypertensive mice. METHHODS: Normal rats were intraperitonealy injected with 0.1, 0.25, 0.5, 1.0, 2.0, 4.0 mg · kg -1 of lipopolysaecharide (LPS) , portal vein ligation (PVL) and intrahepatic portal occlusion (IPO) rats as well as sham-operated rats were treated with an intraperitoneal injection of 1.0 mg · kg -1 of LPS, the portal vein pressure (PVP), portalvenous 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 intravenous injection of LPS were increased from 14.0 to 18.0, 22.2, 26.2, 34.8 .39.6, 38.8 mL · min -1 for hours after injection of LPS (P <0.01) .PVP of the 4 groups of ratsaccepting more than 0.1 mg / kg · bw of LPS was increasedfrom 1.04 tol.25, 1.50, 1.80 , 1.95, 2.05 kPa (P <0.01). The contributions of PVF and PVP were in a dose-dependent manner of LPS. PVR of the 5 groups of rats was decreased from 51 to 42,4 4,48,45,44,47 kPa · min · L -1 (P <0.05) and nodose-dependent manner was observed. PVF of PVL, IPO and sham-operated rats increased from 22.6 to 32.8,22.0 to28. PVP decreased from 71 to 61, 67 to 61 (P <0.01), and PVP decreased from 1.86 to 2.24, from 1.74 to 1.95, from 1.04 to 1.80 kPa (P <0.01) , 52 to 44 kPa · min · L -1 after intraperitoneal injection of 1 mg · kg -1 of LPS. These fractions 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 two groups of PVR decreased in the two groups of PHT model rats andsham-operated rats (P> 0.05) after intraperitoneal injection 1 mg · kg -1 of LPS.CONCLUSION: Endotoxin could prompt portal hypertensionof the normal and noncirrhotic portal hypertensive rats byincreasing portal blood flow mainly.