吗啡后处理对大鼠离体心脏缺血再灌注损伤的影响

目的 评价吗啡后处理对大鼠离体心脏缺血再灌注损伤的影响.方法 雄性SD大鼠,体重180～200 g,应用Langendorff灌流装置,采用全心停灌45 min、再灌注60 min的方法制备大鼠离体心脏缺血再灌注模型.实验一:取模型制备成功的心脏32个,随机分为4组(n=8):Ⅰ组～Ⅳ组,Ⅰ组不予处理,Ⅱ组～Ⅳ组于再灌注即刻分别灌注含0.3、3.0和30 μmol/L吗啡的K-H液10 min,随后灌注正常K-H液50 min;实验二:根据实验一的结果,选择对离体心脏缺血再灌注损伤影响最强的吗啡浓度,另取模型制备成功的心脏32个,随机分为4组(n=8):Ⅰ组～Ⅳ组,Ⅰ组不予处理,Ⅱ组～Ⅳ组于再灌注即刻分别灌注含吗啡的K-H液5、10和20 min,随后灌注正常K-H液50 min;实验三:根据实验二的结果,选取对离体心脏缺血再灌注损伤影响最强的吗啡后处理方法.另取模型制备成功的心脏37个,随机分为5组:Ⅰ组(n=8)不予处理;Ⅱ组(n=8)、Ⅲ组～Ⅴ组(n=7)于再灌注即刻分别灌注含吗啡、10 μmol/L非选择性阿片受体阻断剂纳洛酮和吗啡、5 μmol/L选择性κ受体阻断剂nor-binahorphimine和吗啡、5 μmol/L选择性δ受体阻断剂naltrindole和吗啡的K-H液,各组均再灌注正常K-H液50 min.于再灌注60 min时测定心肌肌酸激酶同工酶(CK-MB)活性,计算心肌缺血危险区/梗塞区(IS/AAR).结果 根据实验一、二的结果于再灌注即刻灌注含3.0 μmol/L吗啡的K-H液10 min行后处理.实验三的结果:与Ⅰ组比较,Ⅱ组和Ⅴ组心肌IS/AAR和CK-MB活性降低,Ⅳ组心肌CK-MB活性降低(P<0.05或0.01),Ⅲ组以上指标差异无统计学意义(P>0.05);与Ⅱ组比较,Ⅲ组和Ⅳ组心肌IS/AAR和CK-MB活性升高(P<0.01),Ⅴ组上述指标差异无统计学意义(P>0.05).结论 吗啡后处理可减轻大鼠离体心脏缺血再灌注损伤,此作用可能与激活心肌κ受体有关.     

不同肺复张模式对ARDS患者呼吸力学及呼出气冷凝液炎症因子的影响

目的：比较控制性肺膨胀（SI）和压力控制（PCV）两种肺复张模式对急性呼吸窘迫综合征（ARDS）患者肺氧合功能、呼吸力学、呼出气冷凝液炎症因子及血流动力学的影响。方法45例ARDS患者随机分为对照组、SI组和PCV组。对照组使用保护性肺通气治疗;S I组在保护性肺通气基础上使用控制性肺膨胀治疗;PC V组联合压控法肺复张治疗。每12 h重复1次RM ,连续3 d。观察各组患者治疗前、治疗12、24、48、72 h各时间点氧合指数（PaO2／FiO2）、气道峰压（PIP ）、气道平台压（Pplat）、静态肺顺应性（Cst）。检测治疗前、治疗24、72 h呼出气冷凝液（EBC）中 TNF‐α、IL‐6、IL‐10水平,监测SI组与PCV组RM前后血流动力学变化。结果①三组患者治疗12、24、48、72 h各时间点PaO2／FiO2、Cst均呈上升趋势,PIP、Pplat呈下降趋势,与治疗前比较均有统计学意义;同时间点RM组（SI组和PCV组）PaO2／FiO2、Cst高于对照组,PIP、Pplat低于对照组,比较有统计学意义,但上述指标SI组与PCV组比较无统计学意义。②SI组与PCV组患者治疗后呼出气冷凝液（EBC ）中TNF‐α、IL‐6、IL‐10水平均呈下降趋势,在治疗后24、72 h与治疗前比较均有统计学意义,但SI组与PCV组比较差异无统计学意义。③SI组与PCV组在肺复张时MAP下降,HR、CVP升高,与复张前比较差异显著,PCV组上述指标波动幅度及持续时间均低于SI组,在肺复张时、复张后60、120、300 s两组上述指标比较差异有统计学意义。结论 SI与 PCV两种肺复张均能改善ARDS患者肺氧合功能、增加肺顺应性,降低平台压,减轻肺部炎症反应;PCV肺复张对血流动力学影响低于SI。     

急性高容血液稀释和控制性低血压在颅内血管手术中的应用

颅内血管手术中,常常需要控制性降压,以便于显露病变部位,防止血管破裂,减少术中出血,同时,手术后又需要改善手术区周围脑组织的血氧供应,最大限度的保护脑组织.急性高容血液稀释(acute hypervolemic hemodilution,AHH)[1]是临床常用于减少术中红细胞和其他血液有形成分丢失,从而达到血液保护目的的方法之一.实施方法通过深麻醉使血管容量得到一定程度的扩张,同时快速补充相当于20%自身血容量的胶体,使血液稀释,减少失血时红细胞的丢失量.我科自2006年应用AHH 联合控制性降压用于颅内血管手术取得了较好的效果.     

异丙酚对瓣膜置换病人颅内血浆氨基酸代谢的影响

本研究观测体外循环(CPB)期间谷氨酸(Glu)、γ-氨基丁酸(GABA)的变化,及异丙酚对Glu、GABA释放的影响。资料与方法选32例心脏瓣膜置换术病人,男17例,女15例,年龄24～72岁,体重45～72kg,心功能Ⅱ～Ⅲ级。随机分为观察组16例,CPB开始时用微量泵按4mg·kg-1·h-1泵入异丙酚,至CPB结束。对照组16例,CPB中不用异丙酚。     

吗啡预处理-后处理对大鼠离体心脏缺血再灌注损伤的影响

Objective To evaluate the effects of morphine preconditioning-postconditioning on ischemia-reperfusion (I/R) injury in isolated rat hearts. Methods Male SD rats weighing 180-200 g were killed after intraperitoneal injection of heparin 500 U/kg. The hearts were immediately removed and perfused in a Langendorff apparatus with K-H solution gassed with 95%O2-5%CO2 .HR and left ventricular systolic pressure (LVSP) were measured from a fluid-filled latex balloon in the left ventricle. Global myocardial ischemia was induced by interrupting perfusion for 45 min followed by 60 min reperfusion. Forty isolated rat hearts were randomly divided into 5 groups (n = 8 each): group 1 (I/R); group II morphine preconditioning (M1 ); group Ⅲ morphine postconditioning (M2); group IV M1 + M2; group V 5-hydroxydecanoate (5-HD) + M2. Group M1 was perfused with K-H solution containing morphine 3.0 μmol/L for 20 min 30 min before ischemia followed by 10 min normal K-H solution perfusion. Group M2 was perfused with K-H solution containing morphine 3.0 μmol/L for 10 min at the beginning of reperfusion followed by 50 min normal K-H solution perfusion. Group 5-HD + M2 was perfused with K-H solution containing morphine 3.0 μmol/L+ 5-HD 10-4 mmol/L for 10 min at the beginning of reperfusion followed by 50 min normal K-H solution perfusion. Myocardial CK-MB activity was measured and myocardial infarct size (IS/AAR) detennined (by 2,3,5-triphenyl tetrazolium staining) at the end of 60 min reperfusion. Results The preconditioning, postconditioning and combination of preconditioning and postconditioning with morphine 3.0 μmol/L perfusion for 10 min all provided cardio-protective effects in terms of IS/AAR and myocardial activation of CK-MB. Conclusion Although the combination of morphine preconditioning and postconditioning can protect the heart against I/R injury, the effects are similar to those of either of them alone, and the reason may be that either of them alone protects the heart against I/R injury via activating mitoKATP .     

吗啡预处理-后处理对大鼠离体心脏缺血再灌注损伤的影响

Objective To evaluate the effects of morphine preconditioning-postconditioning on ischemia-reperfusion (I/R) injury in isolated rat hearts. Methods Male SD rats weighing 180-200 g were killed after intraperitoneal injection of heparin 500 U/kg. The hearts were immediately removed and perfused in a Langendorff apparatus with K-H solution gassed with 95%O2-5%CO2 .HR and left ventricular systolic pressure (LVSP) were measured from a fluid-filled latex balloon in the left ventricle. Global myocardial ischemia was induced by interrupting perfusion for 45 min followed by 60 min reperfusion. Forty isolated rat hearts were randomly divided into 5 groups (n = 8 each): group 1 (I/R); group II morphine preconditioning (M1 ); group Ⅲ morphine postconditioning (M2); group IV M1 + M2; group V 5-hydroxydecanoate (5-HD) + M2. Group M1 was perfused with K-H solution containing morphine 3.0 μmol/L for 20 min 30 min before ischemia followed by 10 min normal K-H solution perfusion. Group M2 was perfused with K-H solution containing morphine 3.0 μmol/L for 10 min at the beginning of reperfusion followed by 50 min normal K-H solution perfusion. Group 5-HD + M2 was perfused with K-H solution containing morphine 3.0 μmol/L+ 5-HD 10-4 mmol/L for 10 min at the beginning of reperfusion followed by 50 min normal K-H solution perfusion. Myocardial CK-MB activity was measured and myocardial infarct size (IS/AAR) detennined (by 2,3,5-triphenyl tetrazolium staining) at the end of 60 min reperfusion. Results The preconditioning, postconditioning and combination of preconditioning and postconditioning with morphine 3.0 μmol/L perfusion for 10 min all provided cardio-protective effects in terms of IS/AAR and myocardial activation of CK-MB. Conclusion Although the combination of morphine preconditioning and postconditioning can protect the heart against I/R injury, the effects are similar to those of either of them alone, and the reason may be that either of them alone protects the heart against I/R injury via activating mitoKATP .     

吗啡预处理-后处理对大鼠离体心脏缺血再灌注损伤的影响

Objective To evaluate the effects of morphine preconditioning-postconditioning on ischemia-reperfusion (I/R) injury in isolated rat hearts. Methods Male SD rats weighing 180-200 g were killed after intraperitoneal injection of heparin 500 U/kg. The hearts were immediately removed and perfused in a Langendorff apparatus with K-H solution gassed with 95%O2-5%CO2 .HR and left ventricular systolic pressure (LVSP) were measured from a fluid-filled latex balloon in the left ventricle. Global myocardial ischemia was induced by interrupting perfusion for 45 min followed by 60 min reperfusion. Forty isolated rat hearts were randomly divided into 5 groups (n = 8 each): group 1 (I/R); group II morphine preconditioning (M1 ); group Ⅲ morphine postconditioning (M2); group IV M1 + M2; group V 5-hydroxydecanoate (5-HD) + M2. Group M1 was perfused with K-H solution containing morphine 3.0 μmol/L for 20 min 30 min before ischemia followed by 10 min normal K-H solution perfusion. Group M2 was perfused with K-H solution containing morphine 3.0 μmol/L for 10 min at the beginning of reperfusion followed by 50 min normal K-H solution perfusion. Group 5-HD + M2 was perfused with K-H solution containing morphine 3.0 μmol/L+ 5-HD 10-4 mmol/L for 10 min at the beginning of reperfusion followed by 50 min normal K-H solution perfusion. Myocardial CK-MB activity was measured and myocardial infarct size (IS/AAR) detennined (by 2,3,5-triphenyl tetrazolium staining) at the end of 60 min reperfusion. Results The preconditioning, postconditioning and combination of preconditioning and postconditioning with morphine 3.0 μmol/L perfusion for 10 min all provided cardio-protective effects in terms of IS/AAR and myocardial activation of CK-MB. Conclusion Although the combination of morphine preconditioning and postconditioning can protect the heart against I/R injury, the effects are similar to those of either of them alone, and the reason may be that either of them alone protects the heart against I/R injury via activating mitoKATP .     

吗啡预处理-后处理对大鼠离体心脏缺血再灌注损伤的影响

Objective To evaluate the effects of morphine preconditioning-postconditioning on ischemia-reperfusion (I/R) injury in isolated rat hearts. Methods Male SD rats weighing 180-200 g were killed after intraperitoneal injection of heparin 500 U/kg. The hearts were immediately removed and perfused in a Langendorff apparatus with K-H solution gassed with 95%O2-5%CO2 .HR and left ventricular systolic pressure (LVSP) were measured from a fluid-filled latex balloon in the left ventricle. Global myocardial ischemia was induced by interrupting perfusion for 45 min followed by 60 min reperfusion. Forty isolated rat hearts were randomly divided into 5 groups (n = 8 each): group 1 (I/R); group II morphine preconditioning (M1 ); group Ⅲ morphine postconditioning (M2); group IV M1 + M2; group V 5-hydroxydecanoate (5-HD) + M2. Group M1 was perfused with K-H solution containing morphine 3.0 μmol/L for 20 min 30 min before ischemia followed by 10 min normal K-H solution perfusion. Group M2 was perfused with K-H solution containing morphine 3.0 μmol/L for 10 min at the beginning of reperfusion followed by 50 min normal K-H solution perfusion. Group 5-HD + M2 was perfused with K-H solution containing morphine 3.0 μmol/L+ 5-HD 10-4 mmol/L for 10 min at the beginning of reperfusion followed by 50 min normal K-H solution perfusion. Myocardial CK-MB activity was measured and myocardial infarct size (IS/AAR) detennined (by 2,3,5-triphenyl tetrazolium staining) at the end of 60 min reperfusion. Results The preconditioning, postconditioning and combination of preconditioning and postconditioning with morphine 3.0 μmol/L perfusion for 10 min all provided cardio-protective effects in terms of IS/AAR and myocardial activation of CK-MB. Conclusion Although the combination of morphine preconditioning and postconditioning can protect the heart against I/R injury, the effects are similar to those of either of them alone, and the reason may be that either of them alone protects the heart against I/R injury via activating mitoKATP .     

右美托咪啶对高血压患者开颅术麻醉的影响

目的 探讨右美托咪啶对高血压患者枕后开颅面神经显微血管减压术麻醉用药以及麻醉苏醒的影响。方法 选择合并高血压病面神经显微减压术患者48例,随机分为两组,每组24例。研究组麻醉诱导前静脉微量泵入右美托咪啶负荷量(1μg/kg), 继以维持0.2～0.7μg /(kg·h);对照组则微量泵入相同剂量的生理盐水。两组术中控制血压,收缩压维持在术前基础值的70%～80%。两组麻醉诱导选用丙泊酚、芬太尼和维库溴铵。以丙泊酚和瑞芬太尼持续泵注维持麻醉,观察两组患者麻醉药泵注速度、麻醉苏醒时间及拔管时间。结果 研究组麻醉药泵注速度［丙泊酚(0.076±0.014)mg/(kg·min) vs (0.092±0.018)mg/(kg· min);瑞芬太尼(0.106±0.032)μg/(kg·min) vs (0.131±0.030)μg/(kg· min)］、麻醉苏醒时间［(5.2±2.1)min vs (9.3±2.4)min］及拔管时间［(5.3±2.4)min vs (10.3±3.2 )min］与对照组相比差异均有统计学意义(P均＜ 0.05)。结论 右美托咪啶用于高血压患者枕后开颅术可明显减少麻醉用药量,缩短麻醉苏醒时间,加快拔管。     

瑞芬太尼和异丙酚靶控输注对脑肿瘤患者术中脑氧代谢的影响

目的：比较瑞芬太尼和异丙酚靶控输注麻醉与异氟烷静吸复合麻醉对脑肿瘤患者术中脑氧代谢的影响。方法：择期颅内肿瘤手术患者36例,ASA Ⅰ～Ⅱ级,随机分为静吸复合组（C组）15例和瑞芬太尼靶控输注组（R组）21例。R组：诱导时设定异丙酚血浆靶浓度3μg/ml,瑞芬太尼血浆靶浓度6ng/ml,术中根据刺激的强弱、心率和血压的变化调整血浆靶控输注的浓度。C组：异丙酚2mg/kg、芬太尼2μg/kg和维库溴铵0.1mg/kg诱导插管,术中吸入1%～2%异氟醚,间断静注维库溴铵维持麻醉。两组患者均连续监测有创血压(MAP)、心率(HR)、心电图(ECG)和脉搏氧饱和度(SpO₂)、呼末二氧化碳(PETCO₂)。记录诱导前(T₁)、插管即刻(T₂)、插管后5min(T₃)、切开硬膜(T₄)、取瘤30min(T₅)、术毕(T₆)、清醒拔管时(T₇)7个时点BP、HR、SpO₂、PETCO₂及苏醒时间。于麻醉诱导前（t₁）、诱导后30min(t₂)、麻醉后1h(t₃)、2h(t₄)、清醒拔管时(t₅) 采集动静脉血进行血气分析,分别测定颈内静脉氧饱和度（SjvO₂）及动静脉氧差（Da-jvO₂）。结果：T₁～T₇各时点BP、HR、SpO₂和PETCO₂两组之间差异均无统计学意义（P＞0.05）;C组和R组患者T₂时MAP分别低于T₁时(P＜0.05)。C组患者苏醒时间长于R组(P＜0.05)。t₂～t₄时间点C组SjvO2均高于R组,而Da-jvO₂均低于R组(P＜0.05)。C组SjvO₂ t₂～t₄时间点均高于同组t₁时,而C组Da-jvO₂ t₂～t₄时间点均高于同组t₁时(P＜0.05)。结论：瑞芬太尼和异丙酚靶控输注与异氟烷静吸复合麻醉用于脑肿瘤患者的手术,均可维持患者平稳的生命体征,靶控输注麻醉患者术毕清醒更迅速,且比静吸复合麻醉能更好的维持脑氧供需平衡。