选择性肺叶隔离对胸科手术患者氧合及细胞因子的影响

Objective To determine the effect on concentrations of interleukin (IL-6) and tumor necrosis factor-α (TNF-α) in bronchoalveolar lavage fluid (BALF) and serum and oxygenation during selective lobar blockade. Methods Thirty patients undergoing esophagectomy or lobectomy were randomly assigned to the total lung collapse (TLC) group (n=15) and the selective lobar blockade (SLB) group( n=15). Anesthesia was induced and maintained with target-controlled infusion of propofol and remifentanil. After intubating with a 8.0 mm internal diameter single -lumen endotraeheal tube, by the guidance of fiberoptic bronchoscope, a 9F coopdech endobronchial blocker was placed into the target lobe in the SLB group, whereas the blocker was placed into the mainstem bronchus in the TLC group. Intermittent arterial blood gas analysis was performed at the following times: 15 min after two lung ventilation in the lateral decubitus position(T1)); 30 min (T2)and 60 min (T3) after TLC or SLB respectively; 15 min after recovering to two lung ventilation (T4), peak inspiratory airway pressure (Ppeak) was also recorded. BALF and blood samples were collected at T, and T4, the concentrations of IL-6 and TNF -α were measured using enzyme -linked immunosorbent assay. Results airway pressure increased significantly after the beginning of one-lung ventilation (F=215.746,P<0.05)in both groups, with more increasing extent in group T (F=53.798, P<0.01).Significant trends were found toward a better improvement in oxygention index with the group S compared with the group T after the beginning of one lung ventilation (F=1 3.747, P<0.05). IL-6 and TNF-αconcentrations of the serum and BALF collected at T4 increased significantly in both groups, but the concentrations of IL-6 and TNF-α in serum and BALF in the group S was lower than those in the TLC group (IL-6:F=1503.734,P<0.01;TNF-α:F=1423.486,P<0.05). The incidence of postoperative complications was comparable between both groups. Conclusion The SLB strategy improves oxygenation and decreases the proinflammatory cytokines during thoracic surgery.     

盐酸戊乙奎醚对内毒素性急性肺损伤大鼠肺组织Toll样受体4mRNA和Toll样受体2mRNA表达的影响

Objective To investigate the effect of penehyclidine (PHCD) on Toll-like receptor 4 (TLR4)mRNA and Toll-like receptor 2 (TLR2) mRNA expression in the lung tissue in rats with acute lung injury induced by lipopolysaccharide (LPS) .Methods Sixty healthy SD rats of both sexes weighing 200-220 g were randomly divided into 5 groups ( n = 12 each) :control group (group C) , LPS group and P1-3 groups. Acute lung injury was induced by intraperitoneal (IP) LPS 8 mg/kg in LPS and P1-3 groups. PHCD 0.3, 1.0 and 3.0 mg/kg were given IP after LPS administration in P1-3 groups. The animals were anesthetized at 6 h after IP LPS. Blood samples were collected for determination of serum TNF-α and IL-6 concentrations ( by ELISA) and then sacrificed, the lungs were immediately removed for determination of TLR4 mRNA and TLR2 mRNA expression (by RT-PCR), and microscopic examination. Results LPS significantly increased TLR4 mRNA and TLR2 mRNA expression in the lung tissue and serum TNF-α and IL-6 concentrations. PHCD 1.0 or 3.0 mg/kg significantly inhibited LPS-induced increase in TLR4 mRNA and TLR2 mRNA expression in the lung tissue and serum TNF-α and ILr6 concentrations.The lung histopathologic damage was significantly ameliorated in P2 and P3 groups as compared with group LPS.Conclusion PHCD can protect the lungs against LPS-induced acute lung injury through inhibiting TLR4 mRNA and TLR2 mRNA expression in the lung tissue and reducing the inflammatory response.     

盐酸戊乙奎醚对内毒素性急性肺损伤大鼠肺组织Toll样受体4mRNA和Toll样受体2mRNA表达的影响

Objective To investigate the effect of penehyclidine (PHCD) on Toll-like receptor 4 (TLR4)mRNA and Toll-like receptor 2 (TLR2) mRNA expression in the lung tissue in rats with acute lung injury induced by lipopolysaccharide (LPS) .Methods Sixty healthy SD rats of both sexes weighing 200-220 g were randomly divided into 5 groups ( n = 12 each) :control group (group C) , LPS group and P1-3 groups. Acute lung injury was induced by intraperitoneal (IP) LPS 8 mg/kg in LPS and P1-3 groups. PHCD 0.3, 1.0 and 3.0 mg/kg were given IP after LPS administration in P1-3 groups. The animals were anesthetized at 6 h after IP LPS. Blood samples were collected for determination of serum TNF-α and IL-6 concentrations ( by ELISA) and then sacrificed, the lungs were immediately removed for determination of TLR4 mRNA and TLR2 mRNA expression (by RT-PCR), and microscopic examination. Results LPS significantly increased TLR4 mRNA and TLR2 mRNA expression in the lung tissue and serum TNF-α and IL-6 concentrations. PHCD 1.0 or 3.0 mg/kg significantly inhibited LPS-induced increase in TLR4 mRNA and TLR2 mRNA expression in the lung tissue and serum TNF-α and ILr6 concentrations.The lung histopathologic damage was significantly ameliorated in P2 and P3 groups as compared with group LPS.Conclusion PHCD can protect the lungs against LPS-induced acute lung injury through inhibiting TLR4 mRNA and TLR2 mRNA expression in the lung tissue and reducing the inflammatory response.     

七氟烷预处理对脂多糖致大鼠急性肺损伤的保护作用

Objective To investigate the effects of sevoflurane pretreatment on Lipopolysaccharide (LPS)-induced acute lung injury (ALI) in rats. Methods Seventy -two Sprague -Dawley rats were randomly divided into 6 groups: NS group, LPS group and sevoflurane pretreatment (S-l h group, S-6 h group, S-12 h group and S-24 h group). The rat model of ALI was established by intratracheal instillation of LPS. Animals were sacrificed at 6 h after LPS or NS administration. Leukocyte count, concentration of TNF-α and IL-β in bronchoalveolar lavage fluid (BALF); pulmonary capillary permeability, myeloperoxidase (MPO) activity of lung tissue; lung histological changes were compared in rats with or without sevoflurane pretreatment (2.4% inspired for 30 min) at different times before LPS instillation. Results Compared with the NS group,severe injury of lung tissues and increase in leukocyte count in BALF, Production of TNF-α and IL-1β in BALF, pulmonary capillary permeability and MPO activity in the lung were significantly increased in rats treated with LPS (P<0.01). MPO activity, leukocyte count and production of IL-1βin BALF were reduced when sevoflurane was given 1 or 24 h before but not at 6 or 12 h before LPS instillation(P<0.01). Sevoflurane pretreatment also attenuated pulmonary capillary permeability and production of TNF-α in BALF (P<0.01). Pulmonary capillary permeability and concentration of TNF-α in S-l h and S-24 h group was lower than S-6 h and S-12 h group (P<0.01). Sevoflurane pretreatment was effective at 1 h and 24 h suggesting sevoflurane has early and late protection against LPS-induced lung injury. Conclusion Sevoflurane pretreatment has protective effects against acute lung injury when given 1 or 12 h before LPS instillation.     

七氟烷预处理对脂多糖致大鼠急性肺损伤的保护作用

Objective To investigate the effects of sevoflurane pretreatment on Lipopolysaccharide (LPS)-induced acute lung injury (ALI) in rats. Methods Seventy -two Sprague -Dawley rats were randomly divided into 6 groups: NS group, LPS group and sevoflurane pretreatment (S-l h group, S-6 h group, S-12 h group and S-24 h group). The rat model of ALI was established by intratracheal instillation of LPS. Animals were sacrificed at 6 h after LPS or NS administration. Leukocyte count, concentration of TNF-α and IL-β in bronchoalveolar lavage fluid (BALF); pulmonary capillary permeability, myeloperoxidase (MPO) activity of lung tissue; lung histological changes were compared in rats with or without sevoflurane pretreatment (2.4% inspired for 30 min) at different times before LPS instillation. Results Compared with the NS group,severe injury of lung tissues and increase in leukocyte count in BALF, Production of TNF-α and IL-1β in BALF, pulmonary capillary permeability and MPO activity in the lung were significantly increased in rats treated with LPS (P<0.01). MPO activity, leukocyte count and production of IL-1βin BALF were reduced when sevoflurane was given 1 or 24 h before but not at 6 or 12 h before LPS instillation(P<0.01). Sevoflurane pretreatment also attenuated pulmonary capillary permeability and production of TNF-α in BALF (P<0.01). Pulmonary capillary permeability and concentration of TNF-α in S-l h and S-24 h group was lower than S-6 h and S-12 h group (P<0.01). Sevoflurane pretreatment was effective at 1 h and 24 h suggesting sevoflurane has early and late protection against LPS-induced lung injury. Conclusion Sevoflurane pretreatment has protective effects against acute lung injury when given 1 or 12 h before LPS instillation.     

c-Jun氨基末端激酶在大鼠内毒素性急性肺损伤中的作用

Objective To evaluate the role of c-Jun N-terminal kinase (JNK) in lipopolysaccharide (LPS)-induced acute lung injury ( ALI) in rats.Methods Eighty male SD rats weighing 250-300 g were randomly divided into 4 groups ( n = 20 each) : control group (group C) ; ALI group; LPS + SP600125 (JNK inhibitor)group (group S) and LPS+ DMSO (the solvent) group (group DMSO) . ALI was induced by intravenous LPS 5mg/kg. In S and DMSO groups, SP600125 30 mg/kg and DMSO 0.2 ml were injected intravenously after LPS administration respectively. Ten animals were sacrificed by exsanguinafions at 4 h after LPS administration in each group. The broncho-alveolar lavage fluid (BALF) was colleted. The TNF-α and IL-1β concentrations in BALF were measured. The lungs were removed for microscopic examination and determination of W/D lung weight ratio. The other 10 animals in each group were observed for 48 h survival rate. Results Intravenous LPS significantly increased TNF-α and IL-1β concentrations in BALF and W/D lung weight ratio, decreased 48 h survival rate and induced histologic damage. Intravenous SP600125 30 mg/kg significantly attenuated the above-mentioned LPS-induced changes. Conclusion Activation of JNK is involved in the development of endotoxin-induced ALI in rats.     

c-Jun氨基末端激酶在大鼠内毒素性急性肺损伤中的作用

Objective To evaluate the role of c-Jun N-terminal kinase (JNK) in lipopolysaccharide (LPS)-induced acute lung injury ( ALI) in rats.Methods Eighty male SD rats weighing 250-300 g were randomly divided into 4 groups ( n = 20 each) : control group (group C) ; ALI group; LPS + SP600125 (JNK inhibitor)group (group S) and LPS+ DMSO (the solvent) group (group DMSO) . ALI was induced by intravenous LPS 5mg/kg. In S and DMSO groups, SP600125 30 mg/kg and DMSO 0.2 ml were injected intravenously after LPS administration respectively. Ten animals were sacrificed by exsanguinafions at 4 h after LPS administration in each group. The broncho-alveolar lavage fluid (BALF) was colleted. The TNF-α and IL-1β concentrations in BALF were measured. The lungs were removed for microscopic examination and determination of W/D lung weight ratio. The other 10 animals in each group were observed for 48 h survival rate. Results Intravenous LPS significantly increased TNF-α and IL-1β concentrations in BALF and W/D lung weight ratio, decreased 48 h survival rate and induced histologic damage. Intravenous SP600125 30 mg/kg significantly attenuated the above-mentioned LPS-induced changes. Conclusion Activation of JNK is involved in the development of endotoxin-induced ALI in rats.     

Moderate hypothermia attenuates lung in flammation inlipopolysaccharide- induced acute lung injury in rats

Objective To investigate the role of moderate h.vpothennia in the lung inflammation of rat acute lung injury induced by lipopolysaccharide(LPS). Methods A rat model of acute lung injury (ALl) was established by in-tin-tracheal instillation of lipopolysaccharide ( 1.5 mg/kg, 0.5 ml) at 16 h after LPS ( 1.0 mg/kg) intraperitoneal adrninis-tmtion. Thirty-four male Sprague Dawley rats were randomly divided into four groups: control group, receiving saline only;LPS group, receiving LPS; hypothennia group, treated with hypothennia without LPS; LPS hypothennia group, treated with LPS and cooled to 32.5℃-33.0℃ as PaO2/FiO2. was below 300 mmHg. Hemodynamics and blood gases were record-ed every hour throughout the study. Rats were killed 4 h after ALl, and lung lavage was performed to measure the tumor ne-crosis factor α(TNF-α), interleukin-6 (IL-6) and interleukin-10 (IL-10) concentrations in bronchoalveolar lavage fluid (BALF) by using enzyme-linked immunosorbent assay (ELISA). Results PaO2/FiO2 was significantly decreased and PaCO2 was increased in the LPS group as compared to their baseline values( P＜0.01). Treatment with hypothermia inhib-ited the increase in PaCO2( P＜0.05) but had no effect on PaO2/FiO2 in the presence of LPS. The administration of LPS significantly increased the concentrations of TNF-α, IL-6 and IL-10 in BALF as compared to the control experiment( P＜0.05, P＜0.01 ). Moderate hypothermia reduced the expressions of TNF-α and IL-6 ( P＜0.01 ) but had no effect on the production of IL-10 ( P＞0.05). Conclusion Moderate hypothermia significantly inhibits proinflammatory cytokine ex-pressions in lipopolysaccharide-induced acute lung injury.     

乌司他丁对心脏瓣膜置换术患者体外循环期间全身炎性反应的影响

Objective To investigate the effects of ulinastatin on the systemic inflammatory response in the patients undergoing cardiac valve replacement with cardiopulmonary bypass (CPB). Methods Forty ASA Ⅱ or Ⅲ patients of both sexes, aged 27-44 yr, weighing 39-72 kg, scheduled for cardiac vavle replacement, were randomly divided into 2 groups (n = 20 each) : control group (group C) and ulinastatin group (group U). Ulinastatin 10 000 U/kg was injected iv 10 min before CPB, and ulinastatin 10 000 U/kg was added to the priming fluid in group U. The equal volume of normal saline was given in stead of ulinastatin in group C. Venous blood samples were taken at 15 min before CPB (T1), 10 min of CPB (T2), and 30 and 60 min after termination of CPB (T3,4)for determination of the plasma concentrations of IL-6, IL-8, IL-10 and TNF-α. Results The plasma concentrations of IL-6, IL-8 and TNF-α were significantly lower and plasma IL-10 concentration was significantly higher during and after CPB in group U than in group C (P <0.05 or 0.01). The plasma concentrations of IL-6,IL-8, IL-10 and TNF-α were significantly higher in beth groups at T2,3 than at T, (P < 0.01). Conclusion Ulinastatin can ameliorate the unbalance between pro- and anti-inflammatory responses during CPB and reduce the systemic inflammatory response in the patients undergoing cardiac valve replacement.     

Effect of isoflurane on expression of IL-1β mRNA,IL-6 mRNA and TNF-α mRNA In the hippocamapus of immature rats

Obiective To investigate the effect ofisoflurane on expression of IL-1β mRNA,IL-6 mRNA and TNF-α mRNA in the hippocampus of immature rats.Methods sixty-four 7-clay-old SD rats were randomly assigned into 2 groups(n=32 each):control group(group C)and isoflurane group(group S).group S was exposed to 1.5% isoflurane for 6 h while group C to air.Fore animals were killed before anesthesia(T0,baseline),at 2,4,6 h(T1-3)of isoflurane anesthesia and 4,6,12 and 24 h after anesthesia(T4-7).The hippocampi were immediately removed for determimation of the expression of IL-1β mRNA,IL-6 mRNA and TNF-α mRNA by RT-PCR.Results Compared with group C,the expression of IL-1β mRNA at T1-5,IL-6 mRNA at T2.3 and TNF-α mRNA at T1-6 in the hippocampus was upregulated in group S.Conclusion The expression of IL-1β mRNA,IL-6 mRNA and TNF-β mRNA was elevated in the hippocampus of immature rats after being exposed to isoflurane.