硬膜外注射吗啡和胃复安用于胆道系统术后镇痛及胃肠功能影响的观察

目的观察吗啡与胃复安复合液硬膜外腔持续输注行术后镇痛对腹部手术后病人胃肠功能的影响。方法选择ASAI～II级、硬膜外麻醉效果满意的上腹部胆道系统手术病人81例,术毕即开始用经硬膜外麻醉管注入吗啡和胃复安混合液(吗啡3mg+胃复安30mg稀释至10ml),送回病房,按2ml/h持续输注施行硬膜外腔术后镇痛48h。在术后按疼痛视觉模拟评分(VAS)评估镇痛效果;随访记录首次肛门排气时间。结果VAS评分3,首次排气时间分别为62.3±12.7h。结论吗啡和胃复安混合液硬膜外腔持续输注术后镇痛用于上腹部胆道系统手术病人,术后并无首次排气时间延迟的副作用。提示吗啡和胃复安混合液硬膜外腔持续输注术后镇痛有助于促进胃肠功能的恢复。     

蛛网膜下腔吗啡和连续硬膜外芬太尼用于剖宫产术后镇痛效果的比较

目的:比较蛛网膜下腔吗啡和连续硬膜外芬太尼用于剖宫产术后镇痛效果。方法:选择60例在腰麻下行剖宫产的产妇并分为3组,每组各20例。吗啡组以0.5%布比卡因2.5ml加吗啡0.1mg作为蛛网膜下腔麻醉给药,对照组和芬太尼组,只以0.5%布比卡因2.5ml作为蛛网膜下腔麻醉给药,芬太尼组产妇术后通过镇痛泵给于芬太尼0.5mg加0.25%布比卡因80ml以2ml/h持续硬膜外腔给药镇痛。术后48小时,观测所有产妇首次要求追加镇痛药的时间及不良反应。结果:从腰麻开始到首次要求追加镇痛药的时间,芬太尼组(41±14)小时明显长于吗啡组(24±17)小时,吗啡组明显长于对照组(5.8±4.8)小时。未见明显不良反应。结论:腰麻下行剖宫产的产妇在术后镇痛中,持续硬膜外注入芬太尼比蛛网膜下腔注入吗啡产生更长时间的镇痛作用而且不增加不良反应。     

硬膜外腔吗啡对髋关节手术围术期D-二聚体的影响

目的研究髋关节手术中应用硬膜外腔吗啡持续注射对患者围术期D-二聚体的影响。方法选取中山市黄圃人民医院2018年3月至2020年3月接受全髋关节置换手术治疗患者68例,进行回顾性分析,根据不同麻醉药物及方法的不同分为吗啡组(n=34)与对照组(n=34)。术前,吗啡组患者予以硬膜外腔吗啡2 mg+0.9%生理盐水10 ml注射,对照组采用0.9%生理盐水10 ml注射。术后,观察组与对照组均施行硬膜外导管镇痛,吗啡组给予吗啡8 mg,持续48 h;对照组给予0.15%罗哌卡因2.0 ml/h,持续48 h。分别于麻醉前5 min、术毕以及术后24 h、48 h抽取静脉血,分别对两组患者的围术期凝血酶原时间以及出血量、不同时间点白细胞介素-6(IL-6)、D-二聚体含量等临床指标进行监测。结果两组患者围术期凝血酶原时间和出血量指标比较,差异无统计学意义(P 0.05);两组术后各时间点的IL-6、D-二聚体含量高于麻醉前,差异有统计学意义(P 0.05);吗啡组患者手术结束时及术后各时间点IL-6、D-二聚体含量低于对照组,差异有统计学意义(P 0.05)。结论硬膜外腔注射吗啡对凝血系统亢进以及D-二聚体生成均具有良好的抑制作用,可改善围术期高凝状态。     

氯诺昔康用于术后镇痛的临床观察

目的 观察硬膜外氯诺昔康复合吗啡持续注入对术后镇痛的效果.方法 选ASA (Ⅰ-Ⅱ)级择期下腹部或下肢手术的患者46例,行腰麻-硬膜外联合麻醉,术毕24mg氯诺昔康加吗啡4mg溶于100mg生理盐水,按2ml/h的速度硬膜外腔持续注入,观察镇痛效果及副作用,监测血压、心率、呼吸频率及脉搏氧饱合度.结果 术后镇痛效果满意,呼吸血压均平稳,恶心呕吐发生率低.结论 氯诺昔康复合吗啡硬膜外镇痛安全有效.     

氯诺昔康与曲马多联合吗啡用于术后静脉镇痛的疗效对比

目的:评价氯诺昔康与曲马多连续静脉输入联合吗啡预先硬膜外输注应用于术后镇痛的效果和安全性.方法:44例ASA Ⅰ～Ⅲ在硬膜外阻滞麻醉或腰硬联合阻滞麻醉下行腹部、脊柱、下肢手术的患者随机均分为氯诺昔康组和曲马多组,每组22例.两组均于麻醉后,切皮前以吗啡1～2mg注入硬膜外腔,手术结束前半小时采用一次性静脉输注泵持续输注氯诺昔康0.6mg·2mL-1·h-1(氯诺昔康组);曲马多16.6mg·2mL-1·h-1(曲马多组).两组输注泵内加用氟哌利多5mg,用生理氯化钠溶液稀释至96mL(48h用量).观察并记录术后4,8,12,24,48h各组各时点的VAS分值及不良反应.结果:两组镇痛效果均为良好或基本满意,但在术后12h和48h的VAS评分以曲马多组为高(P<0.05、P<0.01).两组恶心呕吐、头晕、嗜睡等并发症以曲马多组为多,差异有显著性(P<0.01),均未出现呼吸循环抑制、皮肤瘙痒等并发症.氯诺昔康与曲马多的总使用量之比为0.04∶1.结论:氯诺昔康能安全、有效应用于术后镇痛,其镇痛效果优于曲马多,联合吗啡硬膜外预先镇痛能提高其镇痛效果,减少各自药物的用量及降低并发症的发生率.     

咪唑安定硬膜外腔术后镇痛效果观察

目的：探讨咪唑安定硬膜外腔注入的镇痛作用。方法：80例妇科盆腔手术病人髓机分成4组,于持续硬膜外麻醉手术结束时,在硬膜外腔分别注入咪唑安定3mg,咪唑安定3mg 布比卡因6mg、吗啡3mg、布比卡因6mg各20例,观察术后镇痛强度,平均镇痛时间及副作用。结果：咪唑安定有较好的术后镇痛效果,联用布比卡因有更好的术后镇痛作用,吗啡虽比咪唑安定或／和布比卡因的术后镇痛时间长。效果可靠,但有恶心、呕吐、呼吸抑制等明显副作用。结论：咪唑安定 布比卡因用于硬膜外术后镇痛效果好,副作用少,且无延迟性呼吸抑制,可采用留管分次追加的方法替代吗啡用于术后镇痛。     

氟比洛芬酯复合吗啡硬膜外腔镇痛对妇科术后镇痛效果的观察

目的：探讨氟比洛芬酯复合吗啡硬膜外腔多模式镇痛对妇科术后镇痛效果的观察。方法：选择ASAⅠ～Ⅱ级、择期全子宫切除患者90例,随机等分为A、B、C组（各30例）。A组：采用硬膜外腔自控镇痛（吗啡5mg＋罗哌卡因125mg＋氟哌利多2.5mg）,术毕时连接PCEA泵;B组：采用吗啡硬膜外腔镇痛,术毕时硬膜外注射吗啡2mg＋氟哌利多1.5mg,18h后硬膜外再追加吗啡2mg,拔出硬膜外导管;C组：采用吗啡单次硬膜外腔镇痛术复合氟比洛芬酯静脉镇痛,术毕硬膜外注射吗啡2mg＋氟哌利多1.5mg后拔出硬膜外导管,18h后静脉注射氟比洛芬酯100mg,8h后重复注射氟比洛芬酯100mg。观察记录3组的镇痛效果（VAS评分）和不良反应。结果：3组均能取得良好的镇痛效果,VAS评分无显著性差异（P〉0.05）。C组恶心、呕吐、皮肤瘙痒和尿潴留等不良反应的发生率组明显少于A、B组（P〈0.05）。结论：3组均取得了良好的镇痛效果,但是氟比洛芬酯复合吗啡硬膜外镇痛方式可明显减少不良反应的发生。     

微量输液泵持续硬膜外输注法用于手术麻醉及疼痛治疗

笔者在日本进修期间及回国后3年中利用微量输液泵往硬膜外腔输注局麻药和镇痛药,进行了手术麻醉、术后镇痛、晚期癌肿镇痛共92例,获得满意效果。现将其结果报道如下。1 资料和方法 手术麻醉32例,术后镇痛43例,晚期癌肿镇痛17例。按所需要的椎间隙作硬膜外腔穿刺,向头侧旋转硬膜外腔导管3～5cm。妥善固定,导管接微量输注泵。药液配制:手术麻醉配1.3％～1.6%利多卡因碳酸氢钠混合液。术后镇痛及癌肿镇痛用     

硬膜外氯胺酮超前镇痛对术后镇痛的影响

目的观察切皮前应用氯胺酮在硬膜外腔中的超前镇痛作用对术后镇痛的影响。方法选择40例择期产科手术病人,随机分为两组,每组20人,氯胺酮组在手术开始前于硬膜外腔注入氯胺酮30mg,对照组注入生理盐水。两组均行PCEA吗啡镇痛。记录疼痛出现时间,术后4、8、12、16、24小时VAS评分,24小时镇痛药液消耗量及不良反应。结果氯胺酮组术后疼痛出现时间明显延长(P<0.05);术后16小时及24小时两组VAS评分有统计学意义(P<0.05);两组24小时内吗啡消耗量有统计学意义(P<0.05);两组不良反应无明显差异。结论切皮前硬膜外腔应用氯胺酮具有超前镇痛作用,可加强吗啡术后镇痛的效果。     

吗啡硬膜外自控镇痛对剖宫产术后母乳分泌和消化道蠕动的影响

目的观察剖宫产术后应用吗啡硬膜外病人自控镇痛对产妇泌乳和消化道蠕动的影响.方法选择80例拟行剖宫产的足月孕初产妇,在硬膜外麻醉下施行剖宫产术,术毕随机分成镇痛组和对照组(各40例),镇痛组术后用0.15%希比卡因和0.005%吗啡以2ml/h经硬膜外导管持续泵注行术后镇痛,对照组常规按需肌注哌替啶进行镇痛.观察镇痛镇静效果,泌乳时间及肛门排气时间(作为肠蠕动恢复的指标).结果镇痛组的镇痛效果明显优于对照组(P＜0.05).镇痛组泌乳时间比对照组提前(P＜0.05).镇痛组肠蠕动恢复时间明显快于对照组(P＜0.01).结论吗啡行术后硬膜外病人自控镇痛能促进产妇泌乳,促进胃肠功能早恢复.     

抗生素后效应

目的：介绍各种抗生素的抗生素后效应，为临床给药间隔提供参考数据。方法：综述各种抗生素的抗生素后效应概况。结果：提供了各类常用抗生素和联合用药后效应的时间。结论：抗生素后效应为临床设计合理的给药方案提供科学依据，指导临床更合理地使用抗生素。     

Parkinson's disease-like effects of S-adenosyl-L-methionine: effects of L-dopa.

The major symptoms of Parkinson's disease (PD) are due to degeneration of the nigrostriatal pathway and depletion of dopamine (DA). Tyrosine hydroxylase (TH), norepinephrine (NE), serotonin (5-HT), and melanin pigments are also decreased and acetylcholinergic activity increased. Biochemically, increased methylation can cause the depletion of DA, NE, 5-HT, and melanin pigments and also an increase of acetylcholine; thus, increased methylation can present a biochemical picture that resembles the biochemical changes that occur in PD. During the therapy of PD with L-dopa, it is well known that L-dopa reacts avidly with S-adenosyl-L-methionine (SAM), the biologic methyl donor, to produce 3-O-methyl-dopa. Correspondingly, L-dopa has been shown to deplete the concentration of SAM, and SAM has been found to induce PD-like motor impairments in rodents; therefore, an excess of SAM-dependent methylation may be associated with Parkinsonism. To further study the effects of methylation, SAM was injected into the lateral ventricle of rats. SAM caused tremors, rigidity, abnormal posture, and dose-related hypokinesia. Doses of 9.38, 50, and 400 nM/rat caused 61.9, 73.4, and 94.8% reduction, respectively, of motor activity. A 200-mg/kg IP dose of L-dopa, given before 50 nM SAM, blocked the SAM-induced hypokinesia. SAM also caused a decrease in TH immunoreactivity, apparent degeneration of TH-containing fibers, loss of neurons, and the accumulation of phagocytic cells in the substantia nigra. These results showed that excess SAM in the brain, probably due to its ability to increase methylation, can induce symptoms that resemble some of the changes that occur in PD.     

Metabolic effects as a cause of myotoxic effects of fluoroquinolones

Objectives:

To investigate if fluoroquinolones (FQs) influence skeletal muscle metabolism of healthy and malignant hyperthermia susceptible (MHS) pigs.

Materials and Methods:

After approval from of the Animal Care Committee, 10 MHS pigs, and 6 MHS pigs were anesthetized with hemodynamic and systemic metabolic monitoring. Microdialysis catheters were placed intramuscularly. After equilibration, levofloxacin and ciprofloxacin were injected as a rapid bolus and continuous infusions. Lactate was measured in the dialysate and statistically analyzed was done (Wilcoxon-test; U-test; P < 0.05).

Results:

There were no differences in age, weight, and baseline lactate levels between the groups. Both applications of levofloxacin- and ciprofloxacin-induced an increase of local lactate levels in healthy and MHS pigs. No difference between the two groups was observed.

Conclusion:

FQs influence skeletal muscle metabolism. Myotoxic effects of FQs can, therefore, be explained by an influence on the cellular energy balance.KEY WORDS: Fluoroquinolones, malignant hyperthermia, metabolism, myotoxicity     

Ventilatory effects of low-dose paraoxon result from central muscarinic effects

Paraoxon induces respiratory toxicity. Atropine completely reversed parathion- and paraoxon-induced respiratory toxicity. The aim of this study was to assess the peripheral or central origin of ventilatory effects of low-dose paraoxon. Male Sprague-Dawley rats were given paraoxon 0.215 mg/kg subcutaneously and treated with either atropine (10 mg/kg sc) or ascending doses of methylatropine of 5.42 (equimolar to that of atropine), 54.2, and 542 mg/kg administered subcutaneously 30 min after paraoxon. Ventilation at rest was assessed using whole-body plethysmography and rat temperature using infra-red telemetry. Results are expressed as mean ± SE. Statistical analysis used two-way ANOVA for repeated measurements. Paraoxon induced a significant decrease in temperature 30 min after injection lasting the 90 min of the study period. This effect was partially corrected by atropine, but not by methylatropine whatever the dose. Paraoxon induced a decrease in respiratory rate resulting from an increase in expiratory time associated with an increase in tidal volume. Atropine completely reversed the ventilatory effects of low-dose paraoxon while the equimolar dose of methylatropine had no significant effects. The 54.2 and 542 mg/kg doses of methylatropine had no significant effects. Atropine crosses the blood-brain barrier and reverses peripheral and central muscarinic effects. In contrast, methylatropine does not cross the blood-brain barrier. Atropine completely reversed the ventilatory effects of low-dose paraoxon, while methylatropine had no significant effects at doses up to 100-fold the equimolar dose of atropine. We conclude that the ventilatory effects of low-dose paraoxon are mediated by disrupted muscarinic signaling in the central nervous system.