阿片受体在异氟醚延迟预处理减轻兔心肌缺血再灌注损伤中的作用

Objective To investigate the role of opioid receptors in the protective effects of isoflurane-induced delayed preconditioning against myocardial ischemia-reperfusion (I/R) injury in rabbits. Methods Forty male New Zealand white rabbits weighing 2.0-2.5 kg were randomly assigned into 4 groups ( n = 10 each) : group I sham operation (S); group II I/R; group Ⅲ isoflurane + I/R (Iso) and group IV Iso + naloxone + I/R (Nal). Myocardial I/R was induced by 40 min occlusion of left anterior descending branch (LAD) of coronary artery followed by 120 min reperfusion. In group Ⅲ (Iso) 2% isoflurane in 100% O2 was inhaled for 2 h and I/R was produced 24 h later. In group IV (Nal) naloxone 6 mg/kg was given iv 10 min before 2 h of 2% isoflurane inhalation and I/R was produced 24 h later. At the end of 120 min reperfusion, infarct size (IS) and area at risk (AAR) were determined by Evan's blue and TTC staining. Myocardial ultrastructure was examined by electron microscopy. The phosphorylated p38MAPK protein expression in myocardium was determined by Western blot. Results The IS was significantly smaller in group Iso ( Ⅲ ) ( 19.7% ± 2.8%) than in I/R group ( II ) (37.8% ±1.7%) (P<0.05). The phosphorylated p38MAPK protein expression in myocardium was significantly lower in group Iso than in group I/R. Microscopic examination showed less myocardial damage in Iso group than in group I/R. The protective effects of delayed preconditioning by isoflurane was prevented by naloxone pretreatment. ConclusionOpioid receptors may be involved in the protective effects of delayed preconditioning by isoflurane against myocardial I/R injury.     

异丙酚麻醉诱导时低血压的预防

为比较三种方法预防异丙酚麻醉诱导时血压下降和心动过缓的效果，观察４０例房间隔缺损（ＡＳＤ）和室间隔缺损（ＶＳＤ）修补术病人；随机分为四组，即麻黄素组，氯胺酮组，扩容组和对照组，每组１０例，均用异丙酚２ｍｇ／ｋｇ诱导。用惠普监测仪每２ｍｉｎ测量血压，心率１次，持续１０ｍｉｎ。结果发现，异丙酚用于麻醉诱导后２ｍｉｎ时４组病人收缩压均有不同程度的下降，但对照组下降程度最大（Ｐ＜０．０５），而且对照组收缩压的变化明显有三个相，即用药后下降，气管插管时上升，插管后逐渐下降到正常范围。３个治疗组没有明显的三相现象。提示与对照组相比治疗的三个组血压稳定，心率不慢，能有效地防止异丙酚注药后的低血压和心率减慢现象。３个治疗组中又以扩容组最为稳定。     

乌司他丁对心脏瓣膜置换术患者围术期心肌缺血再灌注损伤的保护作用

目的　观察乌司他丁对心脏瓣膜置换术患者围术期心肌缺血再灌注损伤的保护作用。方法　选择择期在体外循环下行瓣膜置换术患者 2 6例 ,随机分为乌司他丁组 (W组 )和对照组 (C组 )。乌司他丁组按 1 2万U·kg-1,于麻醉诱导后劈胸骨前经静脉给予半量 ,另半量加入预充液中 ,经转机进入体内。对照组用等量复方氯化钠代替。分别于诱导后切皮前 (T1) ,转流 2 0min(T2 ) ,主动脉开放 3 0min(T3 ) ,术毕 4h(T4) ,术毕 2 4h(T5)抽取动脉血 ,测定HCT ,测定血浆CK -MB、、CK活性及cTnI浓度。记录CPB转流时间 ,主动脉阻断时间 ,手术时间及术后复跳情况。结果　与T1相比 ,两组患者CK、CK -MB、cTnI在T3 、T4、T5均明显升高 (P<0 0 5 ) ,其中CK -MB、cTnI均在T4达最高值 ,T5开始下降。两组患者之间CK、CK -MB、cTnI在T1、T2 时无明显差别 ,C组的CK、CK-MB在T5明显高于W组 (P <0 0 5 ) ,cTnI在T3 、T4、T5明显高于W组 (P <0 0 5 )。结论　围体外循环期间使用乌司他丁对心肌缺血再灌注损伤有保护作用。     

阿片受体在异氟醚延迟预处理减轻兔心肌缺血再灌注损伤中的作用

Objective To investigate the role of opioid receptors in the protective effects of isoflurane-induced delayed preconditioning against myocardial ischemia-reperfusion (I/R) injury in rabbits. Methods Forty male New Zealand white rabbits weighing 2.0-2.5 kg were randomly assigned into 4 groups ( n = 10 each) : group I sham operation (S); group II I/R; group Ⅲ isoflurane + I/R (Iso) and group IV Iso + naloxone + I/R (Nal). Myocardial I/R was induced by 40 min occlusion of left anterior descending branch (LAD) of coronary artery followed by 120 min reperfusion. In group Ⅲ (Iso) 2% isoflurane in 100% O2 was inhaled for 2 h and I/R was produced 24 h later. In group IV (Nal) naloxone 6 mg/kg was given iv 10 min before 2 h of 2% isoflurane inhalation and I/R was produced 24 h later. At the end of 120 min reperfusion, infarct size (IS) and area at risk (AAR) were determined by Evan's blue and TTC staining. Myocardial ultrastructure was examined by electron microscopy. The phosphorylated p38MAPK protein expression in myocardium was determined by Western blot. Results The IS was significantly smaller in group Iso ( Ⅲ ) ( 19.7% ± 2.8%) than in I/R group ( II ) (37.8% ±1.7%) (P<0.05). The phosphorylated p38MAPK protein expression in myocardium was significantly lower in group Iso than in group I/R. Microscopic examination showed less myocardial damage in Iso group than in group I/R. The protective effects of delayed preconditioning by isoflurane was prevented by naloxone pretreatment. ConclusionOpioid receptors may be involved in the protective effects of delayed preconditioning by isoflurane against myocardial I/R injury.     

铜绿假单胞菌注射液治疗甲状腺乳头状癌颈侧区淋巴结清扫术后淋巴漏的临床观察

背景与目的 淋巴漏为颈部淋巴结清扫术后常见并发症,传统治疗方法作用相对有限,而铜绿假单胞菌注射液处理创面可较好促进局部炎症反应以闭合漏点,因此本研究分析铜绿假单胞菌注射液对甲状腺乳头状癌（PTC）颈侧区淋巴结清扫术后淋巴漏患者引流量的影响及安全性,以明确铜绿假单胞菌注射液的应用价值。方法 回顾性分析2019年1月—2020年1月郑州大学第一附属医院甲状腺外科行颈侧区淋巴结清扫术后出现淋巴漏的69例PTC患者资料,依据淋巴漏治疗方式不同将其分为对照组（37例,术中常规双侧留置负压引流）、观察组（32例,在对照组治疗的基础上,术后第4、6天,通过引流管注入2支铜绿假单胞菌注射液）,比较两组术后引流量、体温变化,记录其引流时间及不良反应发生率。结果 两组术后第1、2、3天引流量比较差异无统计学意义（均P>0.05）,观察组术后第4、5、6天引流量低于对照组［（310.79±32.16）mL vs.（338.64±34.55）mL、（157.82±16.43）mL vs.（325.43±33.96）mL、（87.34±8.59）mL vs.（333.68±34.59）mL,均P<0.05］;观察组术后第6、7 天体温高于对照组［（37.78±3.77）℃ vs.（35.96±3.60）℃、（37.65±3.72）℃ vs.（35.79±3.68）℃,均P<0.05］,其他时点两组体温差异均无统计学意义（均P>0.05）;观察组引流时间明显短于对照组［（6.17±0.63）d vs.（7.28±0.75）d,P<0.01］;观察组部分患者术后2周内出现局部发热、寒战不良反应,予以物理降温后均恢复正常,观察组术后不良反应发生率高与对照组（12.50% vs. 8.11%）,但差异无统计学意义（P>0.05）。结论 铜绿假单胞菌注射液治疗PTC患者颈侧区淋巴结清扫术后淋巴漏患者临床效果较好,可降低引流量,缩短引流时间,部分患者可能有体温升高、发热等现象,经对症处理后均可缓解,不影响治疗。     

罗比卡因与布比卡因硬膜外麻醉剖宫产术时心电图及心肌酶的变化

目的　比较硬膜外麻醉剖宫产术时罗比卡因和布比卡因对心电图及心肌酶的影响。方法　择期剖宫产手术病人 30例 ,硬膜外麻醉时Ⅰ组 (15例 )用 0 5 %罗比卡因 ,Ⅱ组 (15例 )用0 5 %布比卡因。观察麻醉手术期间心电图P R、QRS波间期以及肌酸磷酸激酶 (CK)和同工酶 (CK MB)的变化 ,同时观察麻醉镇痛、肌松效果和不良反应。结果　两组病人P R、QRS波间期均在正常范围内 (P >0 0 5 )。两组病人CK术后 2 4h值明显高于术前 (P <0 0 5 ) ,但反映心肌受损特异性较高的CK MB则无明显变化 (P >0 0 5 ) ,两组间亦无差异 (P >0 0 5 )。麻醉效果及不良反应两组间无差异。结论　硬膜外麻醉时罗比卡因与布比卡因对心电图及心肌酶影响无明显差异     

IMP3与CD44v6在甲状腺乳头状癌中的表达及临床意义

目的 探讨IMP3及CD44v6在甲状腺乳头状癌（PTC）中的表达及其临床意义.方法 应用免疫组织化学方法检测30例甲状腺乳头状癌（甲状腺滤泡型乳头状癌10例,非滤泡型乳头状癌20例）,20例甲状腺乳头状癌并颈部淋巴结转移,20例甲状腺良性组织（10例正常组织,10例结节性甲状腺肿）中IMP3和CD44v6表达水平,检测结果用Biosens Digital Imaging System vl.6专业图像分析软件进行定量分析,选择积分光密度（IOD）作为评价参数.结果 IMP3与CD44V6在PTC中的表达高于良性组织中的表达,差异有统计学意义（P ＜0.05）;IMP3与CD44v6在PTC有淋巴结转移中的表达高于无淋巴结转移组织中的表达,差异有统计学意义（P ＜0.05）;IMP3与CD44v6在PTC中的表达呈正相关（r=0.903,P＜0.05）.结论 IMP3与CD44v6在甲状腺乳头状癌中呈高表达,有作为分子标志物协助PTC的诊断及判断PTC的侵袭力及转移力的价值.     

双下肢与心肌缺血后处理对缺血再灌注兔心肌细胞凋亡的影响

目的 探讨双下肢与心肌缺血后处理对缺血再灌注兔心肌凋亡的影响.方法 选择新西兰大白兔32只,建立兔心肌缺血再灌注模型,随机分为4组(每组8只):①S组,即假手术组,开胸后穿线套环,不收紧结扎线.②I/R组,结扎冠状动脉左前降支30 min,再灌注180 min.③缺血后处理组,④双下肢缺血后处理组.分别在实验结束后,用原位化学法(TUNEL)法观察各组心肌细胞凋亡,免疫印迹法(Western blotting)测各组心肌Bcl-2的表达.结果 双下肢与心肌缺血后处理组细胞凋亡均明显小于I/R组,且心肌Bcl-2的表达明显高于I/R组.结论 双下肢与心肌缺血后处理可能通过上调Bcl-2蛋白的表达,抑制心肌细胞的凋亡,对缺血再灌注兔心肌产生保护作用.     

罗格列酮对糖尿病大鼠视网膜神经节细胞凋亡的影响

目的 观察过氧化物酶体增生物激活受体-γ(peroxisome proliferator-activated receptor-γ,PPAR-γ)激动剂罗格列酮对链脲佐菌素诱导的早期糖尿病(diabetes mellitus,DM)大鼠视网膜神经节细胞(retinal ganglion cells,RGCs)凋亡的影响,进而从分子学水平上阐明PPAR-γ激动剂对糖尿病视网膜病变(diabetic retinopathy,DR)的保护作用,为预防及早期治疗DR提供一种新思路.方法 选择90只健康的雄性Wistar大鼠随机分为三组:正常对照组、DM+罗格列酮组和DM组,进一步将每组大鼠分为给药后4周、8周和12周三个时间点进行观察.采用一次性腹腔注射50 mg· kg-链脲佐菌素的方法建立DM大鼠模型.自DM模型成模后第3天起,DM+罗格列酮组大鼠每天给予罗格列酮3 mg·kg-1灌胃,正常对照组和DM组每天给予等体积的生理盐水灌胃.于给药后4周、8周和12周处死各组大鼠,处死前测各组大鼠的血糖和体质量,然后摘除左眼球制成眼杯,采用TUNEL法测定各组大鼠视网膜上RGCs的凋亡指数,并作对比.结果 给药后4周、8周和12周,DM组和DM+罗格列酮组大鼠血糖水平均明显高于正常对照组(均为P＜0.01);DM组和DM+罗格列酮组大鼠的体质量均较正常对照组降低(均为P＜0.05).正常对照组大鼠RGC层上仅见少量的凋亡细胞;各时间点DM+罗格列酮组大鼠RGCs的凋亡指数较DM组明显降低(均为P＜0.01);DM组和DM+罗格列酮组大鼠RGCs的凋亡指数均明显高于正常对照组(均为P＜0.01).结论 外源性PPAR-γ激动剂罗格列酮能够抑制DM大鼠视网膜上RGCs的凋亡、对早期DM大鼠视网膜具有保护作用,有望成为DR新的治疗手段.     

阿片受体在异氟醚延迟预处理减轻兔心肌缺血再灌注损伤中的作用

Objective To investigate the role of opioid receptors in the protective effects of isoflurane-induced delayed preconditioning against myocardial ischemia-reperfusion (I/R) injury in rabbits. Methods Forty male New Zealand white rabbits weighing 2.0-2.5 kg were randomly assigned into 4 groups ( n = 10 each) : group I sham operation (S); group II I/R; group Ⅲ isoflurane + I/R (Iso) and group IV Iso + naloxone + I/R (Nal). Myocardial I/R was induced by 40 min occlusion of left anterior descending branch (LAD) of coronary artery followed by 120 min reperfusion. In group Ⅲ (Iso) 2% isoflurane in 100% O2 was inhaled for 2 h and I/R was produced 24 h later. In group IV (Nal) naloxone 6 mg/kg was given iv 10 min before 2 h of 2% isoflurane inhalation and I/R was produced 24 h later. At the end of 120 min reperfusion, infarct size (IS) and area at risk (AAR) were determined by Evan's blue and TTC staining. Myocardial ultrastructure was examined by electron microscopy. The phosphorylated p38MAPK protein expression in myocardium was determined by Western blot. Results The IS was significantly smaller in group Iso ( Ⅲ ) ( 19.7% ± 2.8%) than in I/R group ( II ) (37.8% ±1.7%) (P<0.05). The phosphorylated p38MAPK protein expression in myocardium was significantly lower in group Iso than in group I/R. Microscopic examination showed less myocardial damage in Iso group than in group I/R. The protective effects of delayed preconditioning by isoflurane was prevented by naloxone pretreatment. ConclusionOpioid receptors may be involved in the protective effects of delayed preconditioning by isoflurane against myocardial I/R injury.