Hepatic Steatosis Following Severe Burn Injury And Relationship To Immediately Fluid Resuscitation In Rats

Objective:To investigate the characteristics of hepatic steatosisfollowing severe burn injury, and the effects of immediately fluidresuscitation on the hepatic steatosis.Methods:1 Experimental proceduresOne hundred and forty four Sprague-Dawley rats ,weighing 230g-270g,were randomly divided into four groups: normal control(A,NC),singleburn(B,SB), immediately fluid resuscitation(C,IFR)and delayed fluidresuscitation(D,DFR),with 36 in each group. Each rat was anesthetizedwith ketamine. NCG S-D rats were subjected to 30% sham scald burns,other three groups were subjected to 30% full-thickness scald burns.IFRG received 4ml/%TBSA?kg of Ringer'solution immediately after burninjury. DFRG received Ringer'solution 6 h postburn as IFRG. SBG didn'treceive resuscitation.2 The histological and ultrastructural changesThe histological and ultrastructural changes in the liver weredynamically observed at 12,24,48,72 hours and 7, 21 days after burninjury.3 Serum total cholesterin(TC), triglyceride(TG),high densitylipoprotein(HDL), alkaline phosphatase(ALP) examinedSerum TC, TG, HDL, ALP were dynamically examined at 12, 24, 48, 72hours and 7, 21 days after burn injury. 4 Liver weight/body weight ratio recorded Body weight of each rat was measured before sampling blood, and sodid total liver weight after sampling blood. Liver weight/body weightratio was recorded. 5 Statistical analysis Statistical analysis was performed with q test, chi square test,Kruskal-Wallis test, and Spearman's rank correlation analysis.Significance was accepted at p < 0.05.Date was presented as mean ±SD. Results: 1 The histological and ultrastructural changes of liver 1.1 Histopathology By and large, the histology of liver tissue in NCG was normal. Therewas spotty parenchymal cell degeneration in SBG, such as severeballooning, acidophilic bodies, steatosis, with necrosis ofhepatocytes. Hepatic steatosis which was a diffuse lobular reaction,especially localized in zone 1 or zone 2, in the main, was a figureof microvacuolar deposition. This steatosis was present in the ratsas soon as hour 12 after burn following a pattern of small to largedroplet. The incidence and degree of steatosis was significant at 24,48, 72 hours, 7, 21 days postburn. Mild congestion was observed in IFRG.Hepatic steatosis that was mild, sporadic and focal presented in therats as soon as hour 12 after burn injury. The incidence was high at24, 48, 72 hours, but began to decrease on 7 days. Microvesicularlipidic droplets almost accumulated in zone 1 or 2 of liver acinus andwere seldom impair the entire lobule and develop around the centralveins. DFRG comprised a group of phenomenas including varying degreeof ballooning, steatosis, and acidophilic bodies, hepatocellularnecrosis. Hepatic steatosis, which disseminated entire lobule,particularly in zone 1 or zone 2, was mostly characteristic ofmicrovacuolar deposition. The incidence and occurrence of hepaticsteatosis resembled IFRG, but the severity of DFRG was between IFRGand DFRG. 1.2 Ultrastructural changes Organelles of hepatocytes were clear and normal in NCG. Hepatocyteswere evidently swollen after burn injury 12 hours in SBG. Many rounded,thin electronic dense lipidic vacuoles, some of them attaching thickelectronic intensity, and swollen mitochondrias and proliferatingendoplasmic reticulum, were observed. A portion of mitochondrialpyknosises emerged after burn 24 hours, rough endoplasmic reticulumsreduced 72 hours pustburn, but large numbers of smooth endoplasmicreticulums enlarged and went on to 21 days postburn. Collagen fibers,apoptotic hepatocytes and fat-storing cells in abundance werediscovered 21 days postburn. Swelling of rough endoplasmic reticulums,hepatocytes and mitochondrias were seen after burn injury 12 hours inIFRG. Mitochondrias swollen significantly and lipidic vacuoles weresmall after burn injury 24 hours. The cell degenerations went back 7days postburn in IFRG. From an ultrastructural standpoint, severe burnresulted in damage was more serious in DFRG than in IFRG at 12, 24,48, 72 hours and 7, 21 days. Mitochondrias swelled obviously after burninjury 12 hours. The cytoplasma dissolved out 72 hours postburn. Itwas observed that karyopyknosis, double nucleus, reduced euchromatin,and a group of rounded, thin electronic dense lipidic vacuoles, someof them attaching thick electronic intensity. Apoptotic hepatocyteswere seen 21 days postburn. 2 Serum total cholesterin(TC), triglyceride(TG),high densitylipoprotein(HDL), alkaline phosphatase(ALP) examinedPeripheral blood was collected from the inferior vena cava, andserum TC, TG, HDL, ALP levels were measured. Severe burn resulted inelevation of TC, TG, ALP, but reduction of HDL. The levels of TC, TG,and ALP in NCG, IFRG, DFRG, and SBG increased one by one, at the sametime, the level of HDL reversed. 3 Liver weight/body weight ratio recorded Severe burn resulted in elevation of liver weight/body weight ratio,and the elevation in NCG, IFRG, DFRG, and SBG increased one by one. Conclusion: 1 Hepatic steatosis was present in the rats as soon as hour 12 aftersevere burn injury, and went on 21 days postburn. Its incidence tendedto peak at 12, 24, 72 hours. This transformation following burn injurywas initially centrilobular, particularly in zone 1 or zone 2, but insevere cases it might involve the entire lobule. In the main,morphological alteration to hepatocytes was characteristic of fattymicrovacuolar deposition. 2 The immediately fluid resuscitation after burn injury mightrelief the severe degree of hepatic steatosis, decrease it's incidenceand reverse liver damage to a certain extent as soon as possible.