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Background@#Neurolytic celiac plexus block (NCPB) is a typical treatment for severe epigastric cancer pain, but the therapeutic effect is often affected by the variation of local anatomical structures induced by the tumor. Greater and lesser splanchnic nerve neurolysis (SNN) had similar effects to the NCPB, and was recently performed with a paravertebral approach under the image guidance, or with the transdiscal approach under the guidance of computed tomography. This study observed the feasibility and safety of SNN via a transdiscal approach under fluoroscopic guidance. @*Methods@#The follow-up records of 34 patients with epigastric cancer pain who underwent the splanchnic nerve block via the T11-12 transdiscal approach under fluoroscopic guidance were investigated retrospectively. The numerical rating scale (NRS), the patient satisfaction scale (PSS) and quality of life (QOL) of the patient, the dose of morphine consumed, and the occurrence and severity of adverse events were recorded preoperatively and 1 day, 1 week, 1 month, and 2 months after surgery. @*Results@#Compared with the preoperative scores, the NRS scores and daily morphine consumption decreased and the QOL and PSS scores increased at each postoperative time point (P < 0.001). No patients experienced serious complications. @*Conclusions@#SNN via the transdiscal approach under flouroscopic guidance was an effective, safe, and easy operation for epigastric cancer pain, with fewer complications.
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Objective To evaluate the effect of hydrogen preconditioning during cold ischemia phase on the activity of nuclear factor erythroid 2-related factor 2 ( Nrf2) in rat pulmonary microvascular en-dothelial cells ( PMVECs) subjected to hypoxia-reoxygenation ( H/R) . Methods PMVECs were isolated from clean-grade male Sprague-Dawley rats, aged 2-3 weeks, using the tissue block adherence method and divided into 4 groups ( n=25 each) using a random number table method: control group ( group C) , H/R group, oxygen group ( O group) and hydrogen group ( H group) . Cells were incubated for 4 h with 4℃ low potassium dextransolution ( LPD) pre-equilibrated with 95％ oxygen and 5％ carbondioxide to simulate the cold ischemia phase. LPD pre-balanced with 95％ oxygen and 5％ carbon dioxide was replaced with LPD, and then cells were incubated for 1 h at room temperature to simulate the lung transplantation period. LPD was rapidly replaced with 37℃ M199 complete culture solution, and cells were incubated in the mixture of 40％ oxygen-5％ carbondioxide-55％ nitrogen to simulate the reperfusion period. In O and H groups, the cells were exposed to 40％ oxygen-60％ nitrogen and 3％ hydrogen-40％ oxygen-57％ nitrogen during the cold ischemia period, respectively, and the gas mixture was replaced every 20 min. The cell culture fluid was collected 4 h later for determination of interleukin ( IL )-6, IL-10 and tumor necrosis factor-alpha ( TNF-α) concentrations ( by enzyme-linked immunosorbent assay) and malondialdehyde ( MDA) concen-trations ( by thiobarbituric acid method) . The cytoplasm and nucleoproteins were extracted for measurement of Nrf2 expression ( by Western blot) and cell apoptosis ( by flow cytometry and TUNEL assay) . The cell apoptosis rate was calculated. Results Compared with C group, the IL-6, TNF-α and MDA levels were significantly increased, the IL-10 level was decreased, the apoptosis rate was increased, and the expres-sion of Nrf2 in nucleus was up-regulated in H/R group ( P＞0. 05) . Compared with H/R group, the IL-6, TNF-α and MDA levels were significantly decreased, the IL-10 level was increased, the apoptosis rate was decreased, and the Nrf2 expression in cytoplasm was down-regulated in O and H groups (P＜0. 05), the Nrf2 expression was significantly up-regulated in H group ( P＜0. 05) , and no significant change was found in the expression of Nrf2 in nucleus in O group ( P＞0. 05) . Compared with O group, the IL-6, TNF-αand MDA levels were significantly decreased, the IL-10 level was increased, the apoptosis rate was decreased, the expression of Nrf2 in nucleus was up-regulated, and the expression of Nrf2 protein in cytoplasm was down-regulated in H group ( P＜0. 05 ) . Conclusion The mechanism by which hydrogen preconditioning during cold ischemia phase reduces H/R injury to rat PMVECs is related to activating Nrf2 and thus inhibi-ting oxidative stress.
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Objective Using small interfering RNA (siRNA) against p38 and simulated lung transplantation model,we discussed the effect of p38 siRNA on hypoxia/reoxygenation injury of pulmonary microvascular endothelial cells (PMVECs) after lung transplantation.Methods We transfected the PMVECs with p38 siRNA or non-targeting (NT) siRNA.After 48 h,these cells were exposed to simulated ischemia-reperfusion.At 2 h and 4 h of reperfusion,we detected lactate dehydrofenase (LDH) leakage rate,malondialdehyde (MDA) levels,superoxide dismutase (SOD) activity,cell apoptosis,and the serum levels of interleukin (IL)-1,IL-6 and tumor necrosis factor (TNF)-α.Protein levels of p38,NF-κB and AP-1 were detected.Untreated PMVECs served as the negative control.Results As compared with NT siRNA,p38 siRNA reduced LDH leakage rate (22.3 ± 5.7 vs.45.1 ± 6.2 and 46.3 ± 7.3 vs.75.6 ± 12.4),decreased MDA levels (4.1 ± 2.2 vs.7.1 ± 2.1 and 3.9 ± 0.5 vs.6.1 ± 1.2),increased SOD activity (12.8 ± 3.2 vs.9.4 ± 1.1 and 10.8 ± 1.2 vs.7.0 ± 1.1),and inhibited apoptosis (2.8 ± 0.6 vs.4.1 ± 1.4 and 3.1 ± 1.1 vs.5.8 ± 1.3).p38 siRNA reduced the levels of IL-1 (288 ± 89 vs.592 ± 95 and 380 ± 94 vs.775 ± 175) and IL-6 (38 ± 5 vs.70 ± 12 and 80 ± 20 vs.118-± 17),however,had no influence on TNF-α level.Silencing p38 gene decreased phosphorylation of p65 and inhibitor of nuclear factor kappa-B kinase β,and increased inhibitor of nuclear factor kappa-B expression.However,p38 siRNA had no effect on the phosphorylation of c-Jun and c-Fos.Conclusion Through inhibiting the NF-κB classic activation pathway,p38 siRNA reduced oxidative stress,inflammation and apoptosis of rat PMVECs,protected membrane integrity,and reduced hypoxia/reoxygenation injury.
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Objective To investigate the effect of intratracheal injection of c-Jun N-terminal kinase ( JNK) siRNA plasmid on ischemia-reperfusion ( I∕R) injury in a rat model of lung transplantation. Meth-ods ExperimentⅠ Thirty-two male Wistar rats, weighing 250-280 g, were divided into 2 groups ( n=16 each) using a random number table method: control group ( group C) and JNK siRNA group. JNK siR-NA plasmid 2 mg∕kg ( diluted to 0. 2 ml in sterile phosphate buffer solution) was intratracheally injected in JNK siRNA group. Scrambled siRNA plasmid 2 mg∕kg ( diluted to 0. 2 ml in sterile phosphate buffer solu-tion) was intratracheally injected in group C. Six rats in each group were sacrificed at 48 h of administra-tion, and left lung tissues were removed for determination of the expression of JNK and JNK mRNA ( by Western blot and real-time polymerase chain reaction, respectively) . The other 10 rats left in each group were used for left lung transplantation. Experiment Ⅱ Thirty male Wistar rats, weighing 250-280 g, were divided into 3 groups ( n=10 each ) using a random number table method: sham operation group ( group S) , transplanted lung I∕R group ( group I∕R) and transplanted lung I∕R+JNK siRNA group ( group I∕R+JNK siRNA) . In group I∕R and group I∕R+JNK siRNA, the left lung transplantation was performed, and the donor lungs were obtained from the living donors in group C and group JNK siRNA, respectively. At 15 min of mechanical ventilation and 30, 60, 90 and 120 min of reperfusion, arterial blood samples were obtained for blood gas analysis, PaO2 was recorded, and the oxygenation index ( PaO2 ÷ FiO2 ) was calculated. Arterial blood samples were obtained at 120 min of reperfusion in transplanted lungs for determi-nation of concentrations of interleukin-8 (IL-8), tumor necrosis factor-alpha (TNF-α) and interferon-γ( IFN-γ) in serum ( using enzyme-linked immunosorbent assay) , and the rats were sacrificed and left lung tissues were removed for microscopic examination of the pathological changes which were scored and for de-termination of wet∕dry lung weight ratio ( W∕D ratio) , and nuclear factor kappa B ( NF-κB) and activator protein-1 ( AP-1) activities ( using enzyme-linked immunosorbent assay) . Results ExperimentⅠ Com-pared with group C, the expression of JNK and JNK mRNA was significantly down-regulated in group JNK siRNA (P<0. 05). ExperimentⅡ Compared with group S, the oxygenation index was significantly de-creased, and the concentrations of serum IL-8, TNF-α and IFN-γ, W∕D ratio, lung injury score and ac-tivities of NF-κB and AP-1 were increased in I∕R and I∕R+JNK siRNA groups ( P<0. 05) . Compared with group I∕R, the oxygenation index of receptors were significantly increased, and the concentrations of serum IL-8, TNF-α and IFN-γ, W∕D ratio, lung injury score and activities of NF-κB and AP-1 were decreased in group I∕R+JNK siRNA ( P<0. 05) . Conclusion Intratracheal injection of JNK siRNA can reduce trans-planted lung I∕R injury, and the mechanism may be related to inhibiting inflammatory responses of rats.
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Objective To observe the effects and mechanism of lung inflation with carbon monoxide (CO) during the cold ischemia phase on lung ischemia-reperfusion injury (IRI) after rat lung transplantation.Method Twenty-four pairs of SD rats were selected to establish the model of lung transplantation,and random number method was used to divide 24 donors into 3 groups with 8 rats in each group.(1) CO inflation group (CO group):During the cold ischemia phase,500 ppm CO +volume fraction 40％ O2 + N2 was used for lung inflation,and the volume was 5 mL/kg;(2) O2 inflation group (O2 group):During the cold ischemia phase,volume fraction 40％ O2 + volume fraction 60％ N2 was used for lung inflation;(3) Control group:The lung was deflated during the cold ischemia phase.The gas was replaced every 30 min in the CO and O2 groups,and the lung transplantations were performed after 180 min of cold ischemia.The arterial blood gas analysis was performed at baseline,3 min after reperfusion,and 60,120,and 180 min after reperfusion.The recipient serum levels of relative inflammatory factors,lung tissue cell apoptosis and nuclear factor kappa B (NF-κB) protein expression were detected after 180 min of reperfusion.Result As compared with the control group (238 ± 61 mm Hg),the oxygenation index in the O2 group (293 ± 78 mm Hg) and CO group (361 ± 48 mm Hg) was increased (P＜0.05),and as compared with the O2 group,that in the CO group was increased (P＜0.05).Furthermore,as compared with the control group,the interleukin (IL)-8,tumor necrosis factor (TNF)-α,and cell apoptosis in the O2 group and CO group were decreased significantly,and as compared with the O2 group,those in the CO group and NF-κB protein expression were significantly decreased (P＜0.05).Conclusion Lung inflation with CO during the cold ischemia phase ameliorated the rat lung IRI via reducing the inflammatory response and cell apoptosis mediated by the NF-κB pathway.
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Objective To evaluate the relationship between the concentration of pentane in the exhaled air and degree of the lung injury in non-heart-beating (NHB) rabbits.Methods Twenty-four healthy male Japanese white rabbits weighing 2.4-3.0 kg were randomly divided into 4 groups ( n =6 each):A,B,C and D groups.The NHB model was established by exsanguination through the femoral artery.The exhaled gases were collected and lung tissues were removed at 0,30,60 and 120 min after cardiac arrest in A,B,C and D groups respectively.The concentration of pentane in the exhaled gases was detected immediately using the gas chromatography-mass spectrography.The wet to dry (W/D) lung weight ratio and content of malondialdehyde (MDA) in lung tissues were measured.The lung injury score (LIS) was recorded.The maximal volume ( Vmax ) of the lung was recorded when the airway pressure reached 30 cm H2O.Results Compared with groups A and B,the exhaled pentane concentration was significantly increased in group C,and the W/D ratio,content of MDA and LIS were significantly increased,while Vmax was significantly decreased in group D ( P ＜ 0.05).Compared with group C,W/D ratio and LIS were significantly increased in group D ( P ＜ 0.05 ).Conclusion The concentration of exhaled pentane can not reflect the degree of the lung injury in NHB rabbits.
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Objective To investigate the effects of exogenous biliverdin on lung injury induced by brain death (BD) in rats. Methods Twenty-three adult male Wistar rats in which Fogarty balloon catheter was successfully inserted into cranial cavity were randomly divided into 3 groups: group Ⅰ sham operation (group S,n = 7); group Ⅱ brain death (group BD, n = 8) and group Ⅲ biliverdin + BD (group B, n = 8). The animals were anesthetized, intubated and mechanically ventilated. Femoral artery and vein were cannulated for MAP monitoring and drug and fluid administration. Brain death was induced by injecting slowly normal saline into the balloon in group Ⅱ and Ⅲ. BD was confirmed by dilated and fixed pupils, apnea, transient hypertension and EEG changes. In group Ⅲ biliverdin 35 mg/kg was injected intraperitoneally as soon as BD was confirmed. The animals were mechanically ventilated for another 1.5 h during which MAP was maintained at 80-120 mm Hg by iv norepinephrine infusion. Arterial blood samples were obtained before anesthesia, immediately before and at 5, 30,60, 90 min after intraperitoneal biliverdin for blood gas analysis and determination of plasma bilirubin concentration. PaO2/FiO2 was calculated. The animals were sacrificed at 1.5 h after biliverdin administration. The left lung was removed for detection of MDA content, SOD activity, total antioxidant capacity, cell apoptosis and biliverdin reductase expression in lung tissue. Results Brain death significantly decreased PaO2/FiO2, lung SOD activity and total antioxidant capacity and increased lung MDA content and apoptosis as compared with sham operation group. IP biliverdin significantly attenuated BD-induced lung injury in group B as compared with group BD. The plasma bilirubin concentration and biliverdin reductase expression were significantly higher in group B than group BD. Conclusion Exogenous biliverdin can attenuate BD-induced lung injury by inhibiting pulmonary oxidative stress response and apoptosis.
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Objective To investigate the effects of inhalation of different concentrations of carbon monoxide (CO) on brain death (BD)-induced lung injury in rats. Methods Thirty-two pathogen free adult male Wistar rats weighing 250-300 g were randomly divided into 4 groups ( n= 8 each): group Ⅰ sham operation (group S);group Ⅱ brain death (group BD) and group Ⅲ and Ⅳ BD + CO 0.025% and 0.050% (group C1, C2 ). The animals were anesthetized and tracheally intubated. Fogarty catheter was inserted into the skull. BD was induced by inflating the balloon slowly at 20 μl/min until apnea developed. The animals were then mechanically ventilated (VT 10 ml/kg, RR 50 bpm, PEEP 2 cm H2O) with 40% O2 in N2 . In group Ⅲ and Ⅳ CO 0.025% and 0.050%were added to the air mixture respectively. In group S the balloon was not inflated. BD was confirmed by apnea,dilated pupils and flat EEG. In group BD,C1 and C2, MAP was maintained at 80-120 mm Hg by norepinephrine infusion. The arterial blood gas analysis was performed before (baseline) and immediately after BD was confirmed (T1) and at 30, 60, 90 and 120 min (T2-5) of CO inhalation. The animals were then sacrificed. The plasma concentrations of IL-6 and TNF-α and the activity of myeloperoxidase (MPO) in the lungs were measured. The W/D lung weight ratio and lung injury score (LIS) were recorded. Results BD significantly decreased PaO2/FiO2, BE and pH while increased plasma IL-6 and TNF-α concentrations, MPO activity in the lungs, the W/D ratio and lung injury score as compared with group S. CO inhalation ameliorated the deleterious effects induced by BD. The antiinfiammatory effect of 0.050% CO was better than that of 0.025 % CO. Conclusion Inhalation of 0.025 % or 0.050% CO can ameliorate BD-induced lung injury in rats, but there is no significant difference in the efficacy.