Intestinal microflora in rats with ischemia／reperfusion liver injury

Objectives:To investigate the intestinal microflora status related to ischemia/reperfusion(I/R)liver injury and explorethe possible mechanism.Methods:Specific pathogen free grade Sprague-Dawley rats were randomized into three groups:Controlgroup(n=8),sham group(n=6)and I/R group(n=10).Rats in the control group did not receive any treatment,rats in the I/R groupwere subjected to 20 min of liver ischemia,and rats in the sham group were only subjected to sham operation.Twenty-two hourslater,the rats were sacrificed and liver enzymes and malondialdehyde(MDA),superoxide dismutase(SOD),serum endotoxin,intestinal bacterial counts,intestinal mucosal histology,bacterial translocation to mesenteric lymph nodes,liver,spleen,andkidney were studied.Results:Ischemia/reperfusion increased liver enzymes,MDA,decreased SOD,and was associated withplasma endotoxin elevation in the I/R group campared to those in the sham group.Intestinal Bifidobacteria and Lactobacillidecreased and intestinal Enterobacterium and Enterococcus     

Activation of Akt and cardioprotection against reperfusion injury are maximal with only five minutes of sevoflurane postconditioning in isolated rat hearts

It had been proved that administration of sevoflurane for the first two minutes of reperfusion effectively protects the heart against reperfusion injury in rats in vivo.Our aim was to investigate the duration of effective sevoflurane administration and its underlying mechanism in isolated rat hearts exposed to global ischemia/reperfusion(I/R) injury.Adult male Sprague-Dawley rats were randomly divided into six groups(n=12):a sham-operation group,an I/R group,and four sevoflurane postconditioning groups(S2,S5,S10,and S15).In the S2,S5,S10,and S15 groups,the duration times of sevoflurane administration were 2,5,10,and 15 min after the onset of reperfusion,respectively.The isolated rat hearts were mounted on the Langendorff system,and after a period of equilibrium were subjected to 40 min global ischemia and 120 min reperfusion.Left ventricular(LV) hemodynamic parameters were monitored throughout each experiment and the data at 30 min of equilibrium and 30,60,90,and 120 min of reperfusion were analyzed.Myocardial infarct size at the end of reperfusion(n=7 in each group) and the expression of myocardial phosphorylated Akt(p-Akt) after 15-min reperfusion were determined in a duplicate set of six groups of rat hearts(n=5 in each group).Compared with the I/R group,the S5,S10,and S15 groups had significantly improved left ventricular end-diastolic pressure(LVEDP),left ventricular developed pressure(LVDP),and the maximal rate of rise or fall of the LV pressure(±dP/dtmax),and decreased myocardial infarct size(P<0.05),but not the S2 group.After 15 min of reperfusion,the expression of p-Akt was markedly up-regulated in the S5,S10,and S15 groups compared with that in the I/R group(P<0.05),but not in the S2 group.Sevoflurane postconditioning for 5 min was sufficient to activate Akt and exert maximal cardioprotection against I/R injury in isolated rat hearts.