剖宫产术后硬膜外镇痛产妇血及初乳中吗啡含量的监测

目的　监测剖宫产术后硬膜外镇痛产妇血及初乳中的吗啡含量 ,探讨微量吗啡对新生儿的影响。　方法　选择剖宫产术的产妇 10 0例 ,分为实验组和对照组各 5 0例 ,两组均为连续硬膜外麻醉 ,穿刺点选择 L1 ～ L3,麻醉药为 2 %利多卡因 15～ 2 0 m l,在手术结束时 ,实验组将吗啡缓慢注入硬膜外管 2 mg然后拔管。于术后 1h取产妇的静脉血 3m l,采集产妇术后 3、6 h尿样及术毕 6～ 12 h采集新生儿尿样 3m l;在产后 4 8h内收集产妇的初乳 3～ 5 m l。　结果　观察组 96 % (48/ 5 0 )的镇痛效果较对照 16 % (8/ 5 0 )明显 ,差异有显著性 (P<0 .0 5 ) ,观察组血吗啡浓度 <5～ 118μg/ m l,初乳吗啡浓度 <5～ 30 .4μg/ L ,产妇尿 92 %呈阳性 ,新生儿尿 13.3%呈阳性。两组产妇和新生儿的生命体征比较差异无显著性。　结论　剖宫产术后硬膜外腔应用吗啡镇痛 ,产妇哺乳对新生儿没有影响 ,是安全可行的。     

电针对吗啡成瘾大鼠戒断-复吸行为影响的初步观察

目的 观察针刺对实验动物戒断及复吸期间操作行为的影响。方法 建立大鼠吗啡自身给药模型，随机分模型对照组、绑缚对照组、针刺治疗组。熄灭期(3d)做相应处理，d4吗啡引燃(2mg／kg体重)，观察动物熄灭踏板数(LPE)、复吸踏板数(LPR)。结果 模型对照组观察到典型熄灭-复吸曲线(ERC)；绑缚对照组该曲线发生变异，主要是缩短了熄灭的过程；针刺治疗组彻底改变了熄灭-复吸曲线的形状，使熄灭反跳现象消失，但复吸值变大。以吗啡平台期平均踏板数(ALPP)为基准值，各组间熄灭平均踏板数(ALPE)和复吸踏板数(LPR)无明显差异。结论 相对于自然戒断，针刺及绑缚在熄灭期间均具有较明显的抑制渴求效果，且针刺比绑缚作用更快．效果更明显；短期(3d)的针刺治疗未达到抗短期复吸(d4)效果。更多结果有待后续观察和进一步验证。     

乳腺癌根治术后曲马多PCIA与吗啡PCEA临床对比研究

 目的　观察比较乳腺癌根治术后曲马多PCIA与吗啡PCEA临床镇痛效果及副作用。方法　乳腺癌根治术后病人 12 0例。随机分两组 :T组 (PCIA组 ) ,M组 (PCEA组 )。PCA设备 :2ml/h持续输注 ,单次PCA剂量 0 .5ml,锁定时间 15min。术后 6 ,12 ,2 4 ,4 8小时观察病人药物用量、镇静镇痛评分 ,满意水平及副作用。结果　T组 4 8小时Tramadol用量 (90 8.2± 5 9.7)mg ,按键次数 (6±1.5 )次 ;M组Mor phine(4 .8± 0 )mg ,按键次数 (0 )次。镇痛效果 :VAS及SS评分无显著性差异 ,优良率 >98%。副作用 :T组病人恶心、呕吐发生率明显低于M组 (P <0 .0 1)。结论　曲马多PCIA与吗啡PCEA镇痛效果确切 ,但在副反应方面曲马多PCIA相对较少     

结肠癌术后吗啡罗哌卡因硬膜外镇痛效果的观察

目的:观察吗啡与罗哌卡因配伍用于结肠癌术后硬膜外镇痛的有效性和安全性。方法:选择结肠癌手术患者75例,随机分为三组(n=25):0.1%吗啡组(Ⅰ组)、0.15%吗啡组(Ⅱ组)和0.1%吗啡加0.2%罗哌卡因组(Ⅲ组),持续注入4ml/h,术后镇痛48h。采用视觉模拟评分法(VAS法)估计镇痛效果。结果:Ⅲ组镇痛效果明显好于其它两组(P<0.05),对下肢肌力无影响,排气时间明显提前。结论:0.2%罗哌卡因与0.1%吗啡配伍用于结肠癌术后镇痛效果确切、安全。     

东莨菪碱预防吗啡、布比卡因持续硬膜外镇痛副作用的临床观察

目的:评价东莨菪碱预防上腹部手术后吗啡、布比卡因持续硬膜外镇痛副作用的优越性.方法:前瞻性设计,对上腹部手术ASA评分为Ⅰ～Ⅱ级者分二组,Ⅰ组(吗啡6 mg 布比卡因0.125 g 东莨菪碱2.4 mg),Ⅱ组(吗啡6 mg 布比卡因0.125 g),均在术后持续硬膜外镇痛泵给药.对吗啡、布比卡因镇痛效果及副作用发生率进行统计分析.结果:Ⅰ组VAS值为0.68,满意率为95.78%;Ⅱ组VAS值为1.62,满意率为86.27%,有显著性差异(P＜0.01).恶心呕吐、多汗、尿潴留发生率Ⅰ组明显低于Ⅱ组,有显著性差异(P＜0.05).嗜睡发生率两组相比无显著差别,且两组均未观察到呼吸抑制.结论:东莨菪碱不仅能增强镇痛效果、提高镇痛的满意率,而且能预防镇痛剂的副作用,为临床镇痛治疗提供新方法.     

加味参附汤对吗啡依赖戒断小鼠免疫功能的影响

吗啡依赖小鼠自然戒断后可见脾脏、胸腺萎缩，巨噬细胞Fc受体阳性百分率及吞噬功能、外周血T淋巴细胞总数、T淋巴细胞对PHA的殖反应、脾T淋巴细胞CD4^ 百分率及CD4^ /CD8^ 比值均明显下降；吗啡继续成瘾而未戒断的小鼠的以上指标进一步损伤；加味参附汤（MSFD）治疗小鼠以上指标均有不同程度的恢复；而丁丙诺啡治疗后免疫功能状态仍低于或相当于自然戒断时。提示MSFD能促进吗啡依赖戒断小鼠损伤的免疫功能的恢复，这一作用可能与其对神经内分泌系统的调节有关。     

Effects of histaminergic neuron on the developmental process of conditioned reward induced by morphine

To investigate the effect of histaminergic neuron on morphine - induced conditioned place preference （ CPP）, the model of CPP was used to assess the rewarding effect of morphine. Morphine （2, 5, 10 mg/kg） significantly produced a CPP in a dose-dependent manner. In addition, morphine simultaneously and markedly lessened the histaminergic neurons in the TM,     

氯诺昔康静脉自控镇痛与吗啡硬膜外自控镇痛的临床比较

目的 比较骨科手术后患者氯诺昔康静脉自控镇痛（PICA）与吗啡硬膜外自控镇痛（PCEA）的临床效果和不良反应。方法 100例ASAⅠ～Ⅱ骨科择期手术患者随机分为两组：PICA（n=50）和PCEA组（n=50）。PICA组于手术结束前约30min静注氯诺昔康8mg和恩丹西琼（恩丹西酮）4mg后连接镇痛泵（48mg氯诺昔康＋生理盐水至100m1）；PCEA组于手术结束前约30min硬膜外腔注入吗啡1mg和恩丹西酮4mg加生理盐水至10ml后连接镇痛泵（9mg吗啡＋布比卡因150mg＋生理盐水至100m1）。连续量为2ml／h，自控量为0．5ml／15min。术后连续监测BP、RR、ECG、Sp02，定时观察记录视觉模拟评分法（VAS）及恶心呕吐、嗜睡、多汗、皮肤瘙痒等不良反应的发生情况。结果 两组术后4h、8h、16h、20h、24h、32h和48h各时间点的VAS评分吗啡PCEA组略低于氯诺昔康PICA组，但差异无显著意义（P〉0．05）。恶心、呕吐、嗜睡、多汗、皮肤瘙痒发生率PCEA组明显多于PICA组（P〈0．05）。结论 骨科手术后氯诺昔康PICA与吗啡PCEA均有良好的镇痛效果，但氯诺昔康PICA组不良反应较少，值得临床推广应用。     

Prevention of precipitated withdrawal symptoms by activating central cholinergic systems during a dependence-producing schedule of morphine in rats

Previous studies in this and other laboratories have suggested an important role for central cholinergic neurons in the expression of morphine withdrawal symptoms. This study was designed to determine whether the symptoms of withdrawal could be mitigated by normalization of the effect of morphine on cholinergic neurons. Since this effect is generally inhibitory, we used centrally acting cholinergic agonists to augment central cholinergic tone during chronic morphine infusion. Rats were made dependent following the intra-arterial (i.a.) infusion of increasing concentrations (35-100 mg kg(-1) day(-1)) of morphine over 5 days. I.a. injection of 0.5 mg/kg of naloxone precipitated a profound withdrawal response that included a dramatic increase in mean arterial pressure (MAP) which was maintained over the 60-min observation period, a short duration increase in heart rate (HR), and characteristic opiate withdrawal symptoms. In separate groups of rats, non-toxic doses (50 and 250 microg/kg) of the acetylcholinesterase (AChE) inhibitor, diisopropylflurophosphate (DFP) were administered as single daily injections concomitant with the morphine infusion. DFP treated rats, exhibited significantly reduced expression of the naloxone-evoked pressor response. The apparent anti-withdrawal effect of DFP was not reproduced by the selective peripherally acting AChE inhibitor, echothiophate, although both compounds effectively reduced the expression of certain other withdrawal symptoms. The centrally acting muscarinic cholinergic receptor agonist, arecoline, resulted in an even more impressive suppression of withdrawal symptoms. While not all symptoms associated with morphine withdrawal are mediated via central cholinergic pathways, these results suggest that physical dependence on morphine can be suppressed to a significant degree by the augmentation of central cholinergic activity during morphine administration.     

Morphine-induced suppression of saccharin intake is correlated with elevated corticosterone levels

Rats suppress intake of a saccharin conditioned stimulus (CS) when paired with a drug of abuse. This phenomenon, however, is not uniform across all subjects and is greater following exposure to stress and in animals that more readily self-administer drugs of abuse. The present study was designed to examine these individual differences in intake suppression following seven saccharin-morphine pairings. Plasma corticosterone also was evaluated both before and after conditioning in order to determine whether the magnitude of CS suppression is, or is not, related to circulating corticosterone levels. The findings indicated that, while all rats were exposed to the same number of saccharin-morphine pairings, only half of these animals actually suppressed intake of the saccharin CS. Moreover, the results showed that greater suppression of CS intake was associated with higher corticosterone levels at test (r=-0.84, P<0.0001). Taken together, the results demonstrate that individual differences affect not only the reduction in CS intake following taste-drug pairings, but also the associated cue-induced elevation in circulating corticosterone.