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.     

Effects of sevoflurane preconditioning on p-IκBα in a rat model of myocardial ischemia-reperfusion

Objective To observe the effect of sevoflurane preconditioning on the expression of p-IκBα in a rat model of myocardial ischemia-reperfusion (I/R). Methods Eighty -four male SD rats after setting up the model of I/R, randomly were divided into seven groups: ①Control group; ② Simple-Ischemic group received 30 min I/R merely; ③ SEVO group inhaled 1.0 MAC sevoflurane for 30 min and 15 min wash-out followed by a 30 min I/R; ④ SEVO 165' group inhaled 1.0 MAC sevoflurane for 30 min and then stoped for 165 min; ⑤ PTN group received PTN 500 μg/kg(NF-κB inhibitor) intraperitoneally 60 min before I/R; ⑥ PTN±SEVO group and⑦SEVO+PTN group received PTN 500 μg/kg 15 min before and after sevoflurane preconditioning. Myocardium sample of all groups were collected before and after the time of I/R or the corresponding point in time. p- IκBα was determined by Western Blotting. Results The expression of p- IκBαwas significantly up-regulated in SEVO group(22±3)and SEVO 165'group(20±4) than that in Control group (15±3) before I/R(P<0.05); After perfusion the expression of p- IκBαin Simple-Ischemic group(44±6)and SEVO group (30±3) was significantly up-regulated than that in Control group( 15±4,P<0.05);but the up-regulated adjustment of SEVO group was smaller than that in Simple-Ischemic group (P<0.05). Conclusion This study further confirmed NF-κB participates in the I/R injury and it may play an important role in the mechanism of sevoflurane-induced cardioprotection.     

Effects of sevoflurane preconditioning on p-IκBα in a rat model of myocardial ischemia-reperfusion

Objective To observe the effect of sevoflurane preconditioning on the expression of p-IκBα in a rat model of myocardial ischemia-reperfusion (I/R). Methods Eighty -four male SD rats after setting up the model of I/R, randomly were divided into seven groups: ①Control group; ② Simple-Ischemic group received 30 min I/R merely; ③ SEVO group inhaled 1.0 MAC sevoflurane for 30 min and 15 min wash-out followed by a 30 min I/R; ④ SEVO 165' group inhaled 1.0 MAC sevoflurane for 30 min and then stoped for 165 min; ⑤ PTN group received PTN 500 μg/kg(NF-κB inhibitor) intraperitoneally 60 min before I/R; ⑥ PTN±SEVO group and⑦SEVO+PTN group received PTN 500 μg/kg 15 min before and after sevoflurane preconditioning. Myocardium sample of all groups were collected before and after the time of I/R or the corresponding point in time. p- IκBα was determined by Western Blotting. Results The expression of p- IκBαwas significantly up-regulated in SEVO group(22±3)and SEVO 165'group(20±4) than that in Control group (15±3) before I/R(P<0.05); After perfusion the expression of p- IκBαin Simple-Ischemic group(44±6)and SEVO group (30±3) was significantly up-regulated than that in Control group( 15±4,P<0.05);but the up-regulated adjustment of SEVO group was smaller than that in Simple-Ischemic group (P<0.05). Conclusion This study further confirmed NF-κB participates in the I/R injury and it may play an important role in the mechanism of sevoflurane-induced cardioprotection.     

盐酸戊乙奎醚预先给药对新生大鼠内毒素性急性肺损伤时NF-κB活性的影响

Objective To investigate the effects of penehyclidine (PHCD) pretreatment on nuclear factor kappa B ( NF-kB ) activity during lipopolysaccharide ( LPS )-induced acute lung injury ( ALl ) in neonate rats.Methods Thirty 7-day old Wistar rats of both sexes weighing 18-21 g were randomly divided into 3 groups ( n =10 each): group Ⅰ control (group C); group Ⅱ LPS; group Ⅲ PHCD. Group Ⅱ and Ⅲ received intraperitoneal ( group IP) LPS 3 mg/kg. In group Ⅲ PHCD 5 mg/kg was administered IP at 30 min before LPS respectively. The animals were killed at 4 h after LPS administration. The lungs were immediately removed. The W/D lung weight ratio was measured. The TNF-α, IL-1 βand IL-10 content in the lung were detected by ELISA and expression of NF-kB p65 was detected by immuno-histochemical staining.Results LPS significantly increased W/D lung weight ratio, TNF-α, IL-1 β, IL-10 content and NF-kB p65 expression in the lung as compared with control group. PHCD administered before LPS significantly attenuated the LPS-induced changes. Electron microscopy showed that PHCD before LPS significandy ameliorated the LPS-induced histological damages. Conclusion Pretreatment with PHCD can attenuate LPS-induced acute lung injury though inhibition of NF-kB activation and inflammatory response of lung tissue in neonate rats.     

盐酸戊乙奎醚预先给药对新生大鼠内毒素性急性肺损伤时NF-κB活性的影响

Objective To investigate the effects of penehyclidine (PHCD) pretreatment on nuclear factor kappa B ( NF-kB ) activity during lipopolysaccharide ( LPS )-induced acute lung injury ( ALl ) in neonate rats.Methods Thirty 7-day old Wistar rats of both sexes weighing 18-21 g were randomly divided into 3 groups ( n =10 each): group Ⅰ control (group C); group Ⅱ LPS; group Ⅲ PHCD. Group Ⅱ and Ⅲ received intraperitoneal ( group IP) LPS 3 mg/kg. In group Ⅲ PHCD 5 mg/kg was administered IP at 30 min before LPS respectively. The animals were killed at 4 h after LPS administration. The lungs were immediately removed. The W/D lung weight ratio was measured. The TNF-α, IL-1 βand IL-10 content in the lung were detected by ELISA and expression of NF-kB p65 was detected by immuno-histochemical staining.Results LPS significantly increased W/D lung weight ratio, TNF-α, IL-1 β, IL-10 content and NF-kB p65 expression in the lung as compared with control group. PHCD administered before LPS significantly attenuated the LPS-induced changes. Electron microscopy showed that PHCD before LPS significandy ameliorated the LPS-induced histological damages. Conclusion Pretreatment with PHCD can attenuate LPS-induced acute lung injury though inhibition of NF-kB activation and inflammatory response of lung tissue in neonate rats.     

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.     

异丙酚联合缺血预处理对大鼠肺缺血再灌注损伤时细胞凋亡的影响

Objective To investigate the effects of combination of propofol and ischemic preconditioning (IP) on pneumocyte apoptosis and the mechanism involved during lung ischemia-reperfusion (IR) injury in rats.Methods Fifty male SD rats weighing 200-250 g were randomly divided into 5 groups (n = I0 each) : group Ⅰsham operation (group S); group Ⅱ IR; group Ⅲ propoful (group P); group Ⅳ IP and group Ⅴ P+ IP. The animals were anesthetized with intraperitoneul 1% pentobarbital 10 mg/kg, tracheostomized and mechanically ventilated. Lung IR was induced by occlusion of hilum of the right lung for 1 h followed by 2 h of reperfusion.performed by occlusion of hilum of the right lung for 5 min followed by 5 min of reperfusion, repeating 3 times, ischemia. The animals were killed at 2 h of reperfusion. Tissues of inferior lobe of right lung were obtained for observation of histopathulogy with light microscope and the index of quantitative assessment of histologic lung injury (IQA) was calculated. The apoptosis of pneumocytes was detected using TUNEL and apeptosis index (AI) was calculated. The expression of Bcl-2 and Bax protein in lung tissues was detected using immunohistechemical method. Correlation between IQA and AI and between Bcl-2/Bax protein ratio and AI was analyzed. Results Compared with group S, IQA and AI in the other four groups were significantly increased after reperfusion, and the expression of Bcl-2 and Bax protein was significantly increased and Bcl-2/Bax protein ratio significantly decreased in group IR (P < 0.01). Compared with group IR, 1QA and AI were significantly decreased, Bcl-2 protein expression was up-regulated and Bcl-2/Bax protein ratio was significantly increased in group P, IP and P + IP, Bax protein expression was down-regulated in group IP and P + IP (P < 0.01), but there was no significant difference in Bax protein expression between group P and IR (P > 0.05). IQA and AI were significantly lower and Bcl-2/Bax protein ratio was significantly higher in group P + IP than in group P and IP (P < 0.05). IQA was positively correlated with AI (r = 0.951, P < 0.01). AI was negatively correlated with Bcl-2/Bax protein ratio (r = -0.851, P < 0.01). Conclusion The combination of propofol and IP can inhibit pneumocyte apoptosis through regulating the expression of Bcl-2 and Bax protein and ameliorate lung IR injury.     

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.     

异丙酚对急性肺栓塞大鼠肺细胞凋亡的影响

Objective To evaluate the effect of propofol on lung cell apoptosis induced by acute pulmonary thromboembolism (APTE) .Methods Forty male SD rats weighing 280-300 g were randomly divided into 5 groups ( n = 8 each) : group Ⅰ sham operation ( group S) ; group ⅡAPTE and 3 propofol groups ( group P1-3). APTE was produced by iv injection of auto-blood clots. Venous blood 0.2 ml was obtained from rat tail vein and placed in a sterile test tube which was kept in water bath at 37 ℃ overnight. The blood clot was cut into thrombi ( diameter 1 mm, length 5 mm) the next day. Fifteen thrombi in 2 ml of normal saline were injected into immediately after iv injection of auto-bloed clots. The animals were killed at the end of 4 h propofol infusion and lung specimens were obtained for determination of lung cell apoptosis rate by flow eytometry and expression of caspase-3, Bax, Bcl-2, Fas, FasL mRNA and protein by RT-PCR and Western blot.The expression of Bcl-2/Bax mRNA and protein was calculated. Results Compared with group S,APTE significantly increased the lung cell apoptosis rate, and expression of caspase-3, Bax, Fas, FasL and decreased the expression of Bcl-2 and Bcl-2/Bax. Propofol infusion significantly attenuated these APTE-induced changes. Conclusion Propofol can inhibit APTE-induced lung cell apoptosis by down-regulating the caspase-3, Fas and FasL expression and regulating the balance between Bcl-2 and Bax expression.     

膝关节后交叉韧带断裂治疗临床分析

目的 对35例膝关节后交叉韧带断裂治疗进行临床分析,重点探讨了有关交叉韧带断裂的治疗问题。方法 经明确诊断后,分析采用胫骨附着处撕脱骨折复位固定手术治疗26例、早期髌韧带中1／3移植重建3例、单纯长腿石膏固定6例。结果 本组病例全部进行随访,随访时间13个月－5年,胫骨附着处撕脱骨折复位固定及髋韧带中1／3移植重建29例为优良、单纯长腿石膏固定6例为差。结论 后交叉韧带断裂后应该及时给予手术修复;膝后外侧手术入路,操作简单,暴露充分;少于3个月的陈旧性病例仍适应手术治疗。     

不同方法重建指尖离断静脉回流的疗效分析

目的：探讨不同方法重建指尖离断静脉回流的疗效。方法：2008年3月-2013年2月收治指尖离断患者80例,38例吻合指侧方静脉重建回流,术中吻合动静脉比例1：1或1：2或2：2,平均1：2;22例吻合指腹静脉重建回流,术中吻合动静脉比例1：1;20例未吻合静脉,术中仅吻合1条动脉,行侧切口或甲床放血。观察各组治疗效果。结果：吻合指侧方静脉组手指全部成活,无一例发生回流障碍;吻合指腹静脉组19例发生静脉危象,其中4例手指坏死;未吻合静脉组20例均发生回流障碍,其中6例手指坏死。58例获随访,随访时间6~28个月。吻合指侧方静脉组32例,指尖外形佳、指腹饱满;吻合指腹静脉组14例,指体轻度萎缩,指甲生长不平整;未吻合静脉组12例,指体萎缩明显。吻合指侧方静脉组指甲生长近平整,长度长于其他两组[（14.4±3.2）mm比（12.5±2.3）mm和（12.2±2.2）mm],远侧指间关节活动度大于其他两组[（63±5）°比（48±3）°和（45±7）°],两点分辨觉小于其他两组[（4.6±0.4）mm比（7.1±1.2）mm和（7.3±0.6）mm],感觉级别高于其他两组[S（3.45±0.39）级比S（2.57±0.42）级和S（2.55±0.49）级],差异均具有显著性（P〈0.05）。吻合指腹静脉组和未吻合静脉组在指甲长度、运动和感觉方面差异无统计学意义（P〉0.05）。结论：吻合指侧方静脉能有效解决指尖再植静脉回流问题,可避免回流障碍,成活率高,促进指甲生长,可恢复 DIPJ 活动度及感觉。     

胫骨干骨折的手术治疗对策

目的：明确不同固定器械在胫骨干不同骨折类型固定中的特点，以指导临床应用。方法：68例胫骨干骨折，行加压钢板螺钉、交锁髓内钉、单侧外固定架固定后，作临床疗效分析。结果：加压钢板固定组42例，感染5例，骨不连1例，平均愈合时间3．8个月；交锁髓内钉固定组13例，无感染及骨不连，平均愈合时间5．4个月；单侧外固定架组13例，骨不连1例，踝关节背伸受限3例，平均愈合时间4．5个月。结论：胫骨骨折交锁髓内钉固定并发症少，功能恢复好，适用范围广，但要注意及时进行动力加压。加压钢板及外固定架固定应选择各自的最佳适应证，以达到理想的疗效。