Restrain Kupffer Cell Can Imporve Liver Of Rats Caused By I/R With Hepalobectom

Objective: To investigate the influence of Kupfer cells(KCs)inhibition on livermicrocireulation in the rats with hepalobectomy.Methods: The HP model of Spra-Dawley(SD)rat by cutting left lobe wasused．The KCs were inactivated by gadolinium chloride(GdCI3) at1and2d beforeoperation via tail vein．Seventity-eight healthy male SD rats were randomly divided into4groups：control group，sham operation group(Sham group)，HP group(left loberesection+NSgroup)and GdCl3group(left lobe resection+GdCl3group)．Eachgroup were sacrificed at24h after operation．The blood was collected to detect thelevels of alanine aminotransferase(ALT)，aspartate aminotransferase(AST)，endothelin-1(ET-1)and nitrogen monoxide(NO)．The liver was harvested to analyze themessenger RNA(mRNA)expressions of ET-1，eNOS，iNOS and HO-1by reversetranscriptase polymerase chain reaction(RT-PCR)Results:1,Pathology detetion: hepatocytes had mild edema, no significantdegeneration and necrosis in group A; in group B,part of the hepatic sinusoidemergered stenosisand that were full of red blood cells,we also found spotty necrosisand a amound of focal necrosis,moreever,portal area appears inflammatory cellinfiltration;in the group C liver sinusoidal postoperative narrow heavier, sinuserythrocyte stasis,even cell debris visible; severe edema of liver cells showed a class ofelliptical or circular,focal necrosis and large tractsnecrosis;there wereheavier degree of inflammatory cell infiltration of the portal area;in group Dpostoperative remnant liver tissue liver sinusoids appeared expansion, varying degreesof congestion were innbliver sinusoids and central vein of the portal area; hepatocyte showed edem and large nuclei,which aassociated with vacuolar, fattydegeneration,and mainly focal necrosis;portal area appears inflammatory cellinfiltration,serological detection,but less heavier than group C:2,SerologicalTesting:levels of ALT, AST.ET-1in the serum were significantly higher in group A (P<0.05),the level of NO was significantly lower in group A (P <0.05) in group B; therewere significantly higher levels of ALT AST.ET-1in the serum in group C than that ingroup A and group B(P <0.05), however,NO level was significantly lower in group A and group B (P <0.05);levels of ALTAST.ET-1of serum were significantly higher in group D than that in group A and groupB (P <0.05) but lower than group C, furthermore the level of NO was significantlylower in group A and group B (P <0.05), but higher than the C group (P <0.05).3,Polymerase chain reaction Detection(PCR): ET-1, eNOS, iNOS and of HO-1mRNA expression level in group B were significantly higher (P <0.05) compared withgroup A;ET-1, eNOS, iNOS and HO-1mRNA also expressed higher levels than thegroup A and group B (**P<0.05); expression levels of iNOS and HO-1mRNA weresignificantly lower than group C (Δ*P <0.05), ET-1and eNOSmRNA slightly reduced,but not statistically significant compared with the group C.Conclusion:1, hepatic ischemia-reperfusion model successfully were able to inducemicrocirculatory disorders2, Hepatolobectomy could significantly increase the liver cell damage andmicrocirculation disorders with Pringle.3, inhibition of KC cells could significantly improve microcirculationdisorders and alleviate liver damage with injection of gadolinium chlorideprior to operation.4, KC may participate in regulating iNOSmRNA and HO-1mRNA,removing KC may improve microcirculation and alleviate liver injury.