Objective To investigate the pathological characteristics of hepatic energy metabolism changes following hepatic inflow occlusion and the tolerant limit to ischemia in cholestatic rats.Methods On the day 7 after rats biliary obstruction, the survival rate, hepatic mitochondrial respiratory function, content of ATP, and the ketone body ratio in arterial blood were investigated following the different duration of hepatic ischemia and reperfusion with portal blood bypass.Results The survival rate on postoperative day 10 was 100%, 100% and 40% subjected to 30, 60 and 90min of hepatic vascular occlusion. The hepatic energy metabolic function was decreased markedly following ischemia, and was increased markedly on 24 hours following reperfusion subjected to 30, 60min of hepatic vascular occlusion, but it had less increase with 90min of hepatic vascular occlusion.Conclusion The hepatic energy metabolic function injury is reversible in cholestatic rats, and the rats can tolerate hepatic inflow occlusion within 60min, but the hepatic energy metabolic function injury is irreversible after 90min of hepatic occlusion.
SD mice were selected for Collin’s solution (4℃) infusion into the portal vein with different pressure to preserve the liver transplants. The following parameters were determined ①liver tissue aderine ribonucleotide including adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), ②cytoplasmic free Ca２＋ in single liver cell (［Ca２＋］i) and ③tissue pathologic ultrastructure change by highperformance liquid chromatography into quantimeter and pathologic examination respectively. The result suggested that with the infusion pressure becoming higher, the liver free Ca２＋(［Ca２＋］i), tissue aderine ribonucleotide, EC and tissue pathologic ultrastructure changed obviously. This result shows ［Ca２＋］i, EC and tissue aderine ribonucleotide might indicate the viability of liver transplant, and using low pressure infusion has benefit effect on liver preservation.Key wordsCold infusion pressureViability of liver transplantEnergy metabolismLiver cell free Ca２＋
Aippuric acid test(HAT) and hepatic energy metabolism and mitochondrial oxidative phosphorylation activity in rabbit with acute obstractive jaunidce was studied.The result showed that the HAT values were decreased from 98.4±32.0mg/h to 32.7±17.6mg/h(Plt;0.001),energy charge(EC) decreased from 0.81±0.01 to 0.72±0.02(Plt;0.001),and phosphorylation rate(PR)decreased from 62.1V5.1 to 38.3V2.4(Plt;0.001).Correlation coefficients between HAT and EC was 0.786,(Plt;0.001).This result suggests that HAT can be used as an indicator of hepatic energy metabolism status in acute obstructive jaundice.
Objective\ To study the mechanism of myocardial protection of exogenous creatine phosphate (CP) against ischemia reperfused injury in modified isolated perfused working rat heart model.\ Methods\ Seventy two rats were divided into five groups.The rat hearts of five groups undergone Langendorff perfused were arrested and made totally ischemic for 40 minutes at 37℃ and reperfused for 20 minutes. St.Thomas cardioplegic solution wasn’t used in group A;It was used immediately after ischemia in group B and grou...
Objective To investigate the effect of S-adenosylmethionine (SAM) on mitochondrial injury that was induced by ischemia-reperfusion in rat liver. Methods Fifty-four rats were randomly divided equally into 3 groups: control group, ischemia-reperfusion group (I/R group), and SAM-treated group (SAM group). Hepatic ischemia had been only lasted for 30 min by obstructing the blood stream of hepatic portal vena (the portal vena was only separated but not obstructed in control group). The rats of SAM group received SAM intraperitoneally 2 h prior to ischemia. Blood samples of each group were collected from the inferior cava vena at 0, 1 and 6 h after reperfusion and the serum levels of AST and ALT were detected. Mitochondrial super oxidedismutase (SOD), malondialdehyde (MDA), adenosine triphosphate (ATP) and energy charge (EC) in samples of liver tissue were detected, and the mitochondrial ultrastructure was observed with electronmicroscope. Results The serum levels of AST, ALT and mitochondrial MDA at 0, 1 and 6 h after reperfusion in the I/R group were significantly higher than those in the control group, whereas the levels of mitochondrial SOD, ATP and EC were significantly lower than those in the control group (P＜0.01). Except the value of 0 h, when it comes to SAM group, the levels of AST, ALT and mitochondrial MDA were significantly lower (P＜0.05) and the levels of mitochondrial SOD, ATP and EC were significantly higher (P＜0.05, P＜0.01) than those in the I/R group, respectively. The mitochondrial ultrastructure was injured obviously in I/R group when compared with that in control group. The number of mitochondria decreased and the mitochondria swelled, making the crista became obscure and the density of matrix became lower. The above changes in SAM group were less obvious when compared with those in I/R group. Conclusion SAM may protect mitochondrion against hepatic ischemia injury, since it may prevent mitochondrial lipid peroxidation, increase ATP, and eventually improve energy metabolism after ischemia-reperfusion.
ObjectiveTo summarize the latest research progress of autophagy on regulation of tumor energy metabolism. MethodThe latest research progresses of the regulation mechanism of autophagy on the energy metabolism of tumor cells and the influence on the biologic behavior of tumor in recent years were reviewed. ResultThe autophagy could affect the biological behavior of the tumor by influence of the tumor cell glucose uptake, glycolysis, oxidative phosphorylation, lipid metabolism, and amino acid metabolism. ConclusionsThe regulation of autophagy on tumor energy metabolism provides a theoretical basis for the survival mechanism of tumor under the stress condition. What's more, to research the mechanism of autophagy on regulation of energy metabolism and the effect on tumor biologic behavior will contribute to the development of new and more effective personalized anticancer therapy. As far as the research progress about tumor cells energy metabolism regulated by autophagy, what we must be revealed is whether other factors including oncogene, anti-oncogene, and signaling pathways take part in this regulation and what influence would be on the biological behavior of different tumors.