Effect of peroxisome proliferator-activated receptor γagonist rosiglita-zone on intestinal injury in rats undergoing orthotopic autologous liver transplantation by inhibiting inflammatory response / 中国病理生理杂志

AIM: To investigate the effect of rosiglitazone , a peroxisome proliferators-activated receptor γ(PPARγ) agonist, on the expression of PPARγ, the activation of NF-κB and intestine injury in the rats undergoing ortho-topic autologous liver transplantation ( OALT ) .METHODS: Sprague-Dawley male rats were randomly divided into 4 groups:control group, sham group, OALT group and rosiglitazone (0.3 mg/kg, iv) pretreatment (ROS+OALT) group. The OALT model was established , and the intestinal tissues were collected 8 h after the liver reperfusion .The intestinal tis-sue sections were stained to visualize the damage .The expression of PPARγand NF-κB in the tissues, the concentrations of diamine oxidase (DAO) and fatty acid-binding protein 2 (FABP2) in the serum and the concentration of TNF-αand IL-6 in the tissues were measured .RESULTS:Compared with sham group , the intestinal mucosa of the rats showed obvious pathological injury after liver reperfusion in OALT group and ROS group , the Chiu’s scores of intestinal mucosa was signifi-cantly higher , and the serum concentrations of DAO and FABP 2 increased ( P<0.05 ) .After rosiglitazone pretreatment , the injury of intestinal mucosa of the rats was alleviated , the Chiu’s scores was lower and the serum concentrations of DAO and FABP2 decreased (P<0.05), the PPARγexpression was obviously up-regulated in the intestinal tissues, the nuclear translocation of NF-κB was reduced and the concentrations of IL-6 and TNF-αwere decreased .CONCLUSION: During perioperative period of OALT in rats , the inflammatory responses are obvious .Furthermore, obvious intestinal injury oc-curs .PPARγagonist rosiglitazone obviously up-regulates PPARγexpression and inhibits the inflammation in the intestines , thus protecting against intestinal injury in rats undergoing OALT .

The interaction between oxidative stress and mast cell activation plays a role in acute lung injuries induced by intestinal ischemia-reperfusion.

BACKGROUND: Both oxidative stress and mast cells are involved in acute lung injuries (ALIs) that are induced by intestinal ischemia-reperfusion (IIR). The aim of this study was to further investigate the interaction between oxidative stress and mast cells during the process of IIR-induced ALI. MATERIALS AND METHODS: Thirty adult Sprague-Dawley rats were randomly divided into five groups: sham, IIR, IIR + compound 48/80 (CP), N-acetylcysteine (NAC) + IIR, and NAC + IIR + CP. All rats except those in the sham group were subjected to 75 min of superior mesenteric artery occlusion, followed by 2 h of reperfusion. The rats in the NAC + IIR and NAC + IIR + CP groups were injected intraperitoneally with NAC (0.5 g/kg) for three successive days before undergoing IIR. The rats in the IIR + CP and NAC + IIR + CP groups were treated with CP (0.75 mg/kg), which was administered intravenously 5 min before the reperfusion. At the end of the experiment, lung tissue was obtained for pathologic and biochemical assays. RESULTS: IIR resulted in ALI, which was detected by elevated pathology scores, a higher lung wet-to-dry ratio, and decreased expression of prosurfactant protein C (P < 0.05). Concomitant elevations were observed in the expression levels of the nicotinamide adenine dinucleotide phosphate oxidase subunits p47(phox) and gp91(phox) and the levels of hydrogen peroxide and malondialdehyde. However, superoxide dismutase activity in the lung was reduced (P < 0.05). The level of interleukin 6, the activity of myeloperoxidase, and the expression of intercellular adhesion molecule 1 were also increased in the lung. IIR led to pulmonary mast cell degranulation and increases in the plasma and pulmonary ß-hexosaminidase levels, mast cell counts, and tryptase expression in lung tissue. CP aggravated these conditions, altering the measurements further, whereas NAC attenuated the IIR-induced ALI and all biochemical changes (P < 0.05). However, CP abolished some of the protective effects of NAC. CONCLUSIONS: Oxidative stress and mast cells interact with each other and promote IIR-induced ALI.

Effects of dexamethasone administration at different times on intestinal ischemia-reperfusion injury and inducible nitric oxide syntlase activity in mice / 中华麻醉学杂志

ObjectiveTo evaluate the efffects dexamethasone (DEX) administration at different times on intestinal ischemia-reperfusion(I/R) injury and inducible nitric oxide synthase(iNOS) activity in mice.Methods Tirty-five healthy male Kunming mice weighing 20-24 g were randomly divided into 5 groups( n =7 each): Sham operation group (group Ⅰ ); intestinal I/R group (group Ⅱ ); DEX administration before ischemia group (group Ⅲ ); DEX administration during ischemia group ( group Ⅳ) and DEX administration at the begining of reperfusion group (group Ⅴ ).Intestinal I/R injury was induced by clamping the superior mesenteric artery for 30 min.Normal saline10 mg/kg,DEX 10 mg/kg was injected iv at 30 min before ischemia in groups Ⅱ and Ⅲ respectively.DEX 10 mg/kg was injected iv at 5 min of ischemia in groupⅣ and immediately at the begining of reperfusion in group Ⅴ.The mice were sacrificed at 3 h of reperfusion,and then the small intestinal tissues were taken for determination of intestinal pathological score( Chiu score),iNOS activity and nitric oxide (NO) content.ResultsChiu score was significantly higher in groups Ⅱ - Ⅴ,and iNOS activity and NO content were sinificantly higher in groups Ⅱ,Ⅳ and Ⅴ than in group Ⅰ ( P ＜ 0.05).Chiu score,iNOS activity and NO content were sinificantly lower in group Ⅲ,and were higher in group Ⅴ than in group Ⅱ ( P ＜ 0.05).There was no significant difference in the indexes mentioned above between groups Ⅱ and Ⅳ ( P ＞ 0.05).ConclusionDEX administration before ischemia can reduce intestinal I/R injury by inhibiting iNOS activity; DEX administration during ischemia has no effcet on intestinal I/R injury and iNOS activity; DEX administration at the begining of reperfusion aggravates intestinal I/R injury by enhancing iNOS activity.

Effects of non-ventilated lung with nitrous oxide on intrapulmonary oxygenation and lactic acid level in arterial blood during one lung anesthesia / 中国病理生理杂志

AIM: To investigate the effects of non-ventilated lung with N_2O on systemic oxygenation and lactic acid level in arterial blood during one lung anesthesia. METHODS: Twenty-two patients, ASA Ⅰ-Ⅲ, scheduled for selective pulmonary surgery, were randomly divided into two groups: control group (group A, n=11) and observation group (group B, n=11). Group A: the non-ventilated lung was kept open to the air; group B: N_2O 2 cmH_2O through CPAP system was insufflated into the non-ventilated lung during one lung ventilation. The anesthesia was induced with intravenous midazolam (0.05 mg?kg~(-1)), propofol (0.5-1.0 mg?kg~(-1)), fentanyl (4 ?g?kg~(-1)), and vecuronium (0.1 mg?kg~(-1)) and was maintained with inhaling isoflurane. Blood gas analysis and lactic acid was recorded 20 min after two-lung ventilation (TLV) in the supine position, 20 min after one-lung ventilation (OLV) in the supine position, 20 min and 40 min after OLV in the lateral position and at the end of operation and the shunt fraction was calculated. RESULTS: PaO_2 in group B was significantly higher than that in group A (P