腺苷预处理对大鼠缺血-再灌注心肌NF-κB和TNF-α的影响

目的 通过研究腺苷预处理对大鼠缺血心肌核转录因子（NF）-κB活性和肿瘤坏死因子（TNF）-α水平的影响，探讨腺苷对心肌缺血-再灌注损伤保护的分子机制。方法 18只健康成年SD大鼠(300～350g)随机分为三组，每组6只。C组为对照组；Ⅰ组为缺血心肌组，缺血30min再灌注2h；P组为腺苷预处理组，腺苷预处理加缺血30min再灌注2h。大鼠开胸阻断左冠状动脉前室间支建立心肌缺血模型，取心尖部心肌组织提取胞核蛋白质，用Western blotting法测定胞核中NF-κB的活性并进行灰度扫描；用ELISA法测定TNF-α水平。结果 腺苷预处理后30min再行缺血-再灌注，NF-κB活性和TNF-α的含量与未处理组相比有明显下降；与对照组相比较，仅有少许升高，无显著差异。结论 腺苷可抑制缺血大鼠心肌的NF-κB活性和TNF-α水平，并由此推测腺苷对缺血大鼠心肌NF-κB活性的抑制可能是使TNF-α水平下调的分子机制。     

布托啡诺预先给药对大鼠心肌缺血再灌注损伤的影响

Objective To investigate the effects of butorphanol pretreatment on myocardial ischemia-reperfusion (IR) injury in rats. Methods Forty healthy male SD rats weighing 200-250 g were randomly divided into 5 groups (n = 8 each) : sham operation group (group S); IR group; butorphanol pretreatment group (group B); Nor-BNI group (group N) and glibenclamide group (group G) . In group IR, B, N and G, myocardial IR was produced by occlusion of left anterior descending artery (LAD) for 30 min followed by 120 min reperfusion. In group S and IR, normal saline S ml/kg was injected via femoral vein 10 min before ischemia and then continuously infused at a rate of 5 ml· kg -1· h-1 iv. In group B, butorphanol 25 μg/kg was injected via femoral vein 10 min before ischemia and the rest method was the same as that described in group IR. In group N, Nor-BNI 2 mg/kg (a selective κ-opioid receptor antagonist) was injected via femoral vein 20 min before ischemia and the rest method was the same as that described in group B. In group G, glibenclamide 1 mg/kg (a KATP channel blocker) was injected via femoral vein 10 min before ischemia and the rest method was the same as that described in group B. Blood samples were taken from femoral artery at 120 min of reperfusion for determination of the concentrations of serum TNF-α, IL-6 and IL-10 by ELISA. Myocardial infarct area and ischemic area were measured by TTC staining and myocardial infarct size was calculated. Results The concentrations of serum TNF-a, IL-6 and IL-10 were significantly higher in the other four groups than in group S (P < 0.05) . The concentrations of serum TNF-α andIL-6 were significantly decreased while IL-10 increased, and the myocardial infarct size was significantly decreased in group B, N and G as compared with group IR ( P < 0.05) . The concentrations of serum TNF-α and IL-6 were significantly increased while the concentration of IL-10 decreased) and the myocardial infarct size was significantly increased in group N and G as compared with group B ( P < 0.05). Conclusion Butorphanol pretreatment can protect the myocardium against IR injury in rate via activating κ receptor and KATP channel.     

不同麻醉方式对炎性细胞因子的影响

目的比较雷米芬太尼-丙泊酚全凭静脉麻醉与异氟醚静吸复合全身麻醉用于胆囊切除术对促炎性和抗炎性细胞因子的影响。方法慢性胆囊炎或胆囊结石患者28例,ASAⅠ或Ⅱ级,随机均分为全凭静脉麻醉组(T组)和静吸复合麻醉组(I组),测定两组患者麻醉前、术后4、12h血浆细胞因子白细胞介素-6(IL-6)和白细胞介素-10(IL-10)水平。结果两组血浆IL-6、IL-10水平在术后4h均显著升高(P<0.05)。术后12hT组血浆IL-6水平显著低于I组(P<0.05)。结论雷米芬太尼-丙泊酚全凭静脉麻醉可增强抗炎细胞因子反应,有利于减轻手术应激的炎症反应。     

布托啡诺预先给药对大鼠心肌缺血再灌注损伤的影响

Objective To investigate the effects of butorphanol pretreatment on myocardial ischemia-reperfusion (IR) injury in rats. Methods Forty healthy male SD rats weighing 200-250 g were randomly divided into 5 groups (n = 8 each) : sham operation group (group S); IR group; butorphanol pretreatment group (group B); Nor-BNI group (group N) and glibenclamide group (group G) . In group IR, B, N and G, myocardial IR was produced by occlusion of left anterior descending artery (LAD) for 30 min followed by 120 min reperfusion. In group S and IR, normal saline S ml/kg was injected via femoral vein 10 min before ischemia and then continuously infused at a rate of 5 ml· kg -1· h-1 iv. In group B, butorphanol 25 μg/kg was injected via femoral vein 10 min before ischemia and the rest method was the same as that described in group IR. In group N, Nor-BNI 2 mg/kg (a selective κ-opioid receptor antagonist) was injected via femoral vein 20 min before ischemia and the rest method was the same as that described in group B. In group G, glibenclamide 1 mg/kg (a KATP channel blocker) was injected via femoral vein 10 min before ischemia and the rest method was the same as that described in group B. Blood samples were taken from femoral artery at 120 min of reperfusion for determination of the concentrations of serum TNF-α, IL-6 and IL-10 by ELISA. Myocardial infarct area and ischemic area were measured by TTC staining and myocardial infarct size was calculated. Results The concentrations of serum TNF-a, IL-6 and IL-10 were significantly higher in the other four groups than in group S (P < 0.05) . The concentrations of serum TNF-α andIL-6 were significantly decreased while IL-10 increased, and the myocardial infarct size was significantly decreased in group B, N and G as compared with group IR ( P < 0.05) . The concentrations of serum TNF-α and IL-6 were significantly increased while the concentration of IL-10 decreased) and the myocardial infarct size was significantly increased in group N and G as compared with group B ( P < 0.05). Conclusion Butorphanol pretreatment can protect the myocardium against IR injury in rate via activating κ receptor and KATP channel.     

全麻复苏期使用麻醉气体吸附器的临床观察

为观察全麻复苏期使用回路内麻醉气体吸附器的吸附性能及对麻醉苏醒的影响 ,对 ASA ～ 级全麻行择期胸、腹部手术患者 2 4例 ,随机分为观察组 A和对照组 B。两组均采用安氟醚复合麻醉 ,在手术结束时关闭安氟醚挥发罐。观察组安接回路内麻醉气体吸附器 ,对照组用过度通气的方法排出回路内安氟醚 ,比较两组关闭安氟醚挥发罐后 10 min内回路内麻醉气体浓度及拨管时间。结果显示 ,观察组关闭安氟醚挥发罐 2 min后回路内安氟醚浓度显著下降 ( P<0 .0 5 ) ,4min后显著低于对照组 ( P<0 .0 5 ) ,观察组拔管时间显著低于对照组 ( P<0 .0 5 )     

断指再植术后自控镇痛的临床应用

患者自控镇痛 ( patient controlled analgesia,PCA)是一种微电脑技术与临床相结合的新型的镇痛方法 ,在临床上已得到了广泛的运用。 1 998年～1 999年 ,我科将这一技术用于断指再植术后患者的镇痛取得了满意的临床效果。1　临床资料1.1　一般资料　 1 0例 ASA ～ 级急诊行断指再植手术患者 ,年龄 8～ 50岁 ;男 8例 ,女 2例 ;再植1指者 6例 ,再植 2指者 3例 ,再植 4指者 1例 ;手术持续时间 4～ 1 7h。1.2 　方法　麻醉方法均采用腋路连续臂丛阻滞法 ,置入硬膜外导管 2～ 4cm,阻滞效果完善 ,术中间断注入浓度为 0 .2 5%布比卡因与 1 %利…     

右美托咪定预处理对大鼠心肌缺血再灌注损伤的保护作用及补体3蛋白的影响

目的：探讨右美托咪定预处理对大鼠心肌缺血再灌注损伤的保护作用及对补体3（C3）蛋白的影响。方法：sD雄性大鼠45只,随机分为3组（n=15）：假手术组（Sham组）、缺血再灌注组（I／R组）、右美托咪定预处理组（DEX组）。DEX组自缺血前2h持续静脉输注右美托咪定5mL·kg^-1（用0．9％氯化钠注射液将右美托咪定稀释为1gg·mL^-1）直到结扎心脏冠状动脉左前降支前停止,输注时间为2h;Sham组72．I／R组在相同的时间内按照5mL·kg^-1速率输注等量0．9％氯化钠注射液。再灌注120min时,取心脏组织,测定心肌梗死面积,用蛋白质印迹法（Westernblot）测定心肌组织中c3蛋白的表达。结果：与Sham组比较,I／R组和DEX组的心肌梗死面积、C3蛋白表达明显升高（P〈0．05）;与I／R组比较,DEX组的心肌梗死面积和C3蛋白表达明显降低（P〈0．05）。结论：右美托咪定预处理能够减轻大鼠心肌缺血再灌注损伤,其机制与减少补体3蛋白表达有关。     

氯沙坦对大鼠心肌缺血再灌注损伤的影响

目的:观察血管紧张肽II1型受体阻断剂 氯沙坦对大鼠缺血再灌注心肌的梗死面积、心肌结 构、肿瘤坏死因子α(TNF α)、白细胞介素6(IL 6) 的影响。方法:雄性Sprague Dawley(SD)大鼠42只 随机分为4组:对照组、缺血再灌注组、氯沙坦 5mg·kg-1组和氯沙坦10mg·kg-1组。除对照组 外,余3组建立心肌缺血再灌注模型,2个氯沙坦组 分别于缺血前15min静脉注射氯沙坦5,10mg· kg-1。计算心肌梗死范围,观察心肌细胞超微结构, 检测再灌注后血浆TNF α和IL 6的浓度。结果:与 缺血再灌注组相比,2氯沙坦组梗死面积减小(P< 0.01),心肌超微结构改善。缺血再灌注组TNF α 和IL 6的浓度均明显高于对照组(P<0.01);2个 氯沙坦组TNF α和IL 6的浓度均低于缺血再灌注 组(P<0.01),其中氯沙坦10mg·kg-1组较 5mg·kg-1组的浓度低(P<0.05,P<0.01)。结 论:氯沙坦具有抗大鼠心肌缺血再灌注损伤的作用, 高剂量氯沙坦的效果明显,其机制可能与从受体水 平阻断肾素 血管紧张肽系统,减少炎性因子TNF α和IL 6的产生有关。