基础与临床研究 >文章正文
基础与临床研究 >文章正文
<?xml:namespace prefix = o ns = "urn:schemas-microsoft-com:office:office" /> Experimental Study on the Effects of Thoracic Epidural Anesthesia to Acute Myocardial Ischemia-Reperfusion Injury 王萍 李刚 山东省立医院,山东 济南 250021 Abstract Objective:To observe the protective effects of thoracic epidural anesthesia(TEA)aganist myocardial ischemia-reperfusion injury. |
<?xml:namespace prefix = o ns = "urn:schemas-microsoft-com:office:office" /> Method:Twenty two canines(14-22kg)were divided randomly into three groups:normal saline group(NS group,7)、Bupivacaine group (BP group,8)、Ropivacaine group(RP group,7). Epidural puncturing at T5~T6 after general anesthesia,injected normal saline、Bupivacaine、Ropivacaine into the epidural space respectively 12ml for NS group、BP group、RP group. These dogs were subjected to 40min left anterior descending coronary artery(LAD)Occlusions followed by 320min of reperfusions. Mean Arterial Pressure(MAP)and Heart Rate(HR)were measured continually;Before epidural injection、at start occlusion and opening 60min、120min,blood Samples were taken to measure the concentrations of malonylaldehyde(MDA)and superoxide dismutase(SOD). Result:During experiment HR of three groups did not change significantly and there was no diference among three groups;Before epidural injection,MAP of three groups increased more significantly than that before surgeon(P<0.05). At latter time points,MAP had no significant diference in NS group and decreased significantly in BP group and RP group(P<0.01). Before surgeon and before epidural injection,MAP had no significant diference among three groups,but at start occlusion、end occlusion、opening 60min、120min,MAP in BP group and RP group was significantly lower than that in NS group(P<0.05 or P<0.01),and there was no diference between BP group and RP group.At end occlusion,MDA and SOD of three groups had no significant diference with that before epidural injection. At opening 60min and 120min,in NS group MDA increased significantly and SOD decreased significantly(P<0.05),But in BP group and RP group,MDA and SOD had no significant diference. Among three groups,MDA had no significant diference at all time point. At time point before epidural injection and end occlusion SOD had no significant diference.In opening duration,SOD of BP group and RP group were especially higher than that of NS group(P<0.01 or P<0.05),and SOD of RP group was significantly higher than that of BP group(P<0.05). Conclusion:TEA can protect myocardial aganist ischemia-reperfusion injury,and the protective effects of Ropivacaine is better than that of Bupivacaine. Key words:thoracic epidural anesthesia;ropivacaine;bupivacaine;ischemia-reperfusion;myocardial injury;malondial dehyde;superoxide dismutase |
<?xml:namespace prefix = o ns = "urn:schemas-microsoft-com:office:office" /> 目前已知自由基介导的脂质过氧化反应是心肌缺血再灌注损伤的重要环节[1]。而交感神经系统与心肌缺血的发生、发展密切相关。心脏交感神经传入、传出纤维起源于T1~T5节段,高位胸段硬膜外阻滞(TEA)能选择性阻滞该节段而使病变血管扩张,使冠脉血流发生有利于缺血区的再分配,缺血区/非缺血区血流比显著提高,从而发挥心脏保护效应[2-4]。本研究观察了0.5%罗哌卡因、0.5%布比卡因下TEA对犬急性心肌缺血再灌注后脂质过氧化物丙二醛(MDA)、超氧化物歧化酶(SOD)浓度的变化,旨在探讨不同局麻药TEA对缺血再灌注损伤心肌的保护作用,为其应用于临床寻找依据。
材料与方法 1. 材料 健康杂种家犬22只,雌雄不限,体重14~22kg,根据硬膜外腔注药的不同分为NS组(7只)、BP组(8只)、RP组(7只)。药物与试剂:罗哌卡因[瑞典阿斯特拉(无锡)制药有限公司];布比卡因(上海禾丰制药有限公司);MDA试剂盒(南京建成生物工程研究所);SOD试剂盒(南京聚力生物医学工程研究所)。 2. 方法 实验前禁食12h,入室后肌注吗啡0.25mg/kg、阿托品0.025mg/kg。30min后以1%硫贲妥钠8~10mg/kg静脉诱导,气管内插入内径(ID)为9.0mm气管导管后,立即静注0.1mg/kg的潘库溴铵、10μg/kg的芬太尼,同时接East呼吸机:潮气量300~350ml,通气频率18次/min,氧流量1L/min,以Commander心电监护仪行体表心电图监护,股动脉穿刺测平均动脉压(MAP)。选择T5~T6间隙行硬膜外穿刺,以阻力骤降感及负压现象为成功依据,并在X线下证实,向头侧置管3cm。切开左侧第4、5肋间隙,打开胸腔,暴露心脏,游离左冠状动脉前降支(LAD),于距根部2cm处穿线,并以小Rumel套之,留置以备阻断血管。自右心耳穿一18号长套管针于右心房,以备采血。NS组、BP组、RP组分别于硬膜外腔注入生理盐水、布比卡因、罗哌卡因各12ml,分2次注入,间隔5min。15min后,收紧套管,阻断LAD,40min后开放,再灌注320min。按时追加潘库溴铵和芬太尼。在术前、注药前、阻断时、阻断末,开放60、120min时监测心率(HR)与MAP,硬膜外腔注药前、阻断末、开放60、120min时SOD、MDA水平。 3. 统计学处理 实验结果用表示,多个样本均数比较用单因素方差分析,两均数比较用t检验。 |
<?xml:namespace prefix = o ns = "urn:schemas-microsoft-com:office:office" /> 综上所述,本实验表明TEA对犬急性缺血再灌注心肌具有一定保护作用;罗哌卡因的心肌保护效果优于布比卡因。提示TEA的保护机制不仅仅在于硬膜外阻滞,其更深的确切机制尚待进一步研究。 参考文献 1. Westlin W,Mullane K. Does captopril attenuate reperfusion-induced myocardial dysfunction by scavenging free radical[J]. Circulation. 1988,77:1-6. 2. Blomberg S,Emanuelsson H,Ricksten S.E. Thoracic epidural anesthesia and central hemodynamics in patients with unstable angina pectoris[J]. Anesth Analg. 1989,69:558-562. 3. Klassen GA,Bramwell RS,Bromage PR,et al. Effect of acute sympathectomy by epidural anesthesia on the canine coronary circulation[J]. Anesthesiology. 1980,52:8-15. 4. Davis RF,Deboer LW,Maroko PR. Thoracic epidural anesthesia reduces myocardial infarct size after coronary artery occlusion in dogs[J]. Anesth Analg. 1986,65:711-717. |