离子色谱法测定氯化琥珀胆碱原料及注射液中的氯化胆碱和氯化琥珀酰单胆碱

目的 采用离子色谱法测定氯化琥珀胆碱原料及注射液中的氯化胆碱和氯化琥珀酰单胆碱。方法 采用Dionex RFICTM Ionpac CS17色谱柱（4 mm×250 mm）,以甲烷磺酸溶液为流动相进行梯度洗脱,流速为1.0 mL·min^-1,采用抑制电导检测器进行测定。结果 氯化胆碱、氯化琥珀酰单胆碱浓度分别在18.0~562.8 μg·mL^-1（r=0.999 9）和14.4~449.8 μg·mL^-1（r=0.999 9）内线性关系良好,定量限均为0.01 μg·mL^-1。原料中氯化胆碱、氯化琥珀酰单胆碱回收率分别为103.4%~105.7%和102.4%~107.1%;注射液中氯化胆碱、氯化琥珀酰单胆碱回收率分别为95.6%~100.2%和94.4%~103.5%。结论 该方法专属性强、准确、简便、快速,适用于氯化琥珀胆碱原料及制剂中的有关物质测定。     

阿曲库铵恢复期应用琥珀胆碱对其肌松恢复的影响

目的：观察在阿曲库铵阻滞恢复期应用琥珀胆碱是否影响其肌松恢复时间。方法：４０例择期眼科手术病人随机分为２组,即对照组和试验组分别为１７和２３例。ＴＯＦ监测肌松,两组病人诱导过程中均用琥珀胆碱协助插管（ＴＯＦ＝０）。气管插管后Ｔ１恢复至对照值７５％时两组病人均静注阿曲库铵０．５ｍｇ／ｋｇ维持肌松,组Ⅰ对照,组Ⅱ当Ｔ１恢复至对照的５０％时静注琥珀胆碱１～１．５ｍｇ／ｋｇ,监测起效时间、临床肌松维持时间     

维库溴铵和阿曲库铵预处理对琥珀胆碱的肌震颤及肌松效应的影响

目的 观察维库溴铵和阿曲库铵预处理对琥珀胆碱肌震颤的预防及对其肌松效应的影响。方法 ３０例全麻病人根据不同预处理药分成３组,即０．９％生理盐水（对照组）;０．０１ｍｇ／ｋｇ维库溴铵组和０．０５ｍｇ／ｋｇ阿中铵组,每组１０例。预处理４分后静注琥珀胆囊１．５ｍｇ／ｋｇ。采用ＰａｒａＧｒａｐｈ监测肌松。结果 阿曲库铵预处理能基本消除琥珀胆碱引起的肌震颤,维库溴铵只能减轻或部分消除琥珀胆碱引起的肌震颤。但     

潘库溴铵预处理对琥珀胆碱临床效应的影响

临床上常用亚肌松量的非去极化肌松剂预处理预防去极化肌松剂琥珀胆碱引起的肌颤、术后肌痛等不良反应.已发现小剂量非去极化肌松药预处理后,去极化肌松药的起效减慢,阻滞程度低,几松恢复时间缩短.但不同的非去极化     

琥珀胆碱诱导致心跳骤停复苏成功1例

患者,女,29岁。ASAⅡ级。术前诊断:L_2椎骨折伴截瘫,拟腰椎管探查减压+Dickei钉内固定术。麻醉经过:入手术室后Bp16/10kPa,HR90次/min,余检查正常。手术前24h急查血钾7.02 mmol/L,选气管插管静脉复合全麻,以Innmor4me,硫喷妥钠0.3g,琥珀胆碱0.1g静脉诱导,快速插管,以1.4％PDS复合液（5％GS500ml+普鲁卡因7g+哌替啶200mg+琥珀胆碱400mg）维持麻醉。（以下简称复合液）,置病人俯卧位,5min后脉捕细弱,继之血压测不出,口唇青紫,心音消失。立即停输复合液,恢复平卧位,给予胸外心脏按压,静推肾上脉素2mg,无效,追加2mg,再追加4mg,继续人工控制呼吸。10min后EKG出现室颤,给予胸外电除颤两次400s,转为窦性,HR150次/min,BP20/14kPa。由于血压不稳定,予多巴胺静滴并快速补充血容量,20min时患者出现自主呼吸,1h神志恢复,给予5％SB100ml纠正酸中毒,观察30min,BP、HR较稳定,神志清楚送病房,随访无后遗症。体会 ①本例心跳骤停可能原因;a,患者血钾较高（7.02mmol/L）,加之琥珀胆碱强烈肌颤致大量细胞内K~+转移至细胞外,使血钾升高,心肌受抑制。b,体位变动致血流动力学变化。②复苏过程中,出现室颤应尽早除颤,电除颤是最直接有效方法,在基层如没有电除颤亦可采用利多卡因除颤。③本例患者应避免使用琥珀胆碱。     

卡肌宁与琥珀胆碱静脉滴注对清醒时间的观察：附100例分析

卡肌宁与琥珀胆碱静脉滴注对清醒时间的观察（附１００例分析）三明市第二医院麻醉科魏秀吾卡肌宁是一新型中短效非去极化肌松药，具有起效快、作用时间短、无蓄积特点，适合于全麻快速诱导气管插管，而全麻中持续静脉滴注是否易清醒时间延长，本文与琥珀胆碱进行比较，现...     

小剂量琥珀胆碱致脱敏感阻滞1例

患者、女.64岁。ASAⅡ级,诊断;急性胰腺炎、胰腺脓肿。在静吸复合麻醉下行胰腺脓肿引流,胆囊切除,胆总管探查,T管引流术。以芬太尼0.2 mg、咪唑安定15mg、万可松8mg快速诱导,气管内插管做控制呼吸,吸入安氟醚,辅以羟丁酸钠5g,术中追加万可松4mg维持麻醉,术毕前30min停吸安氟醚,自主呼吸,潮气量350～400ml。因关腹困难,静脉给琥珀胆碱50mg（与万可松间隔约1h）。术毕,患者无自主呼吸,控制呼吸1h后出现自主呼吸,但潮气量仅30～50ml,辅助呼吸2h无明显明显,遂静注新斯的明0.5mg、纳络酮0.4mg,5min后自主呼吸增强,潮气量达300～400ml SPO_2≥95％,带气管导管送ICU,24h后拔管。讨论 脱敏感阻滞为琥珀胆碱之不良反应且伴发生在长时间或大剂量使用该药之后,而本例仅使用小量即发生脱敏感阻滞,与万可松、安氟醚及电介质紊乱有关,因此,遇有上述情况,应避免使用琥珀胆碱。     

右美托咪定对琥珀胆碱肌震颤及术后肌痛的影响

目的观察右美托咪定用于声带息肉摘除术对血流动力学的影响及预防琥珀胆碱肌震颤及术后肌痛的效果。方法选择择期行声带息肉摘除术患者60例,ASAⅠ~Ⅱ级,随机分为对照组(C组)和右美托咪定组(D组),D组麻醉诱导前10 min静脉给予右美托咪定1μg/kg,C组给予等量生理盐水。监测并记录给予右美托咪定前(基础值T0)、给予右美托咪定后5 min(T1)、麻醉诱导后30 s(T2)、给予琥珀胆碱后30 s(T3)、气管插管后1 min(T4)、支撑喉镜置入时(T5)、手术进行5 min(T6)、手术结束(T7)时的MAP、HR。琥珀胆碱注射后,观察肌震颤情况、气管插管条件,术后24 h肌痛指标。结果与T0时比较,C组T4~T7时MAP明显升高,HR明显增快;与C组相比,T4~T7时D组MAP明显降低,HR明显减慢(P<0.05)。两组插管条件比较差异无统计学意义(P>0.05),D组肌震颤发生率与C组比较差异无统计学意义(P>0.05),但发生程度较C组显著降低(P<0.05),术后24 h C组和D组的VAS评分分别为6.54±0.37和3.48±0.45,两组比较差异有统计学意义(P<0.05)。结论术前预注右美托咪定可有效减轻声带息肉摘除术中循环波动及琥珀胆碱所致的肌震颤及术后肌痛。     

重复静脉注射琥珀胆碱致严重心律失常1例分析

目的 探讨手术过程中重复静脉注射琥珀胆碱致严重心律失常临床分析.方法 采用回顾性分析我院接治的1例因需进行右肩关节复位手术的患者,在行手术之前,静脉注射丙泊酚与琥珀胆碱,因第一次手术效果不良因此进行了第二次静脉注射丙泊酚与琥珀胆碱.结果 在第二次静脉注射琥珀胆碱后,患者出现了严重的心律失常表现.结论 在手术中重复使用肌松剂琥珀胆碱易使患者出现心律失常的表现,因此在术前准备工作中对于存在心动过缓的患者,在应用琥珀胆碱以前可先应用阿托品提升心率,待心率提升后再注射琥珀胆碱.     

小剂量顺式阿曲库铵预注法行快诱导气管插管时对琥珀胆碱肌颤搐T1的抑制程度及肌松效应的影响

目的 观察顺式阿曲库铵预注法对琥珀胆碱肌震颤的预防及对其肌松效应的影响.方法 20例择期全麻患者根据不同预处理药分成2组,即0.01 mg/kg顺式阿曲库铵组(A组):0.9%氯化钠水溶液(B组),每组10例.预处理3 min后静脉注射琥珀胆碱1 mg/kg.采用TOF-WATCH SX监测肌松情况,TOF=0时行快诱导气管插管.结果 预处理能基本消除琥珀胆碱引起的肌震颤,效果优于B组(P＜0.05).可使1 mg/kg剂量的琥珀胆碱的起效时间延长,阻滞程度降低,但与B组差异无统计学意义(P＞0.05).结论 顺式阿曲库铵预处理能基本消除琥珀胆碱引起的肌震颤,并对其肌松效应影响较小,不延长肌松恢复时间,是较好的预处理肌松药.     

布比卡因对肌梭的损害作用

用 54只健康成年家兔 ,观察肌注布比卡因对腓肠肌肌梭的作用。组织学结果显示 ,肌注布比卡因后12 h,肌梭即可出现轻度的变性 ;2～ 3d受损最严重 ,可出现肌梭的广泛坏死 ;1周后受损肌梭可自行修复改善 ,至 3周末可完全修复正常。提示布比卡因能引起肌梭发生可逆性的变性及坏死改变。     

基因工程人丁酰胆碱酯酶的纯化及其在体外对琥珀酰胆碱的解毒作用(英文)

目的　开发丰富又安全的人丁酰胆碱酯酶来源 ,并检测其解毒效率。方法　家蚕血淋巴液中重组人丁酰胆碱酯酶 (rhBChE)的纯化采用批量硫酸铵分段分离和普鲁卡因酰胺 脂糖凝胶 4B亲和层析技术。结果　聚丙烯酰胺凝胶电泳纯的rhBChE从血淋巴液中的总收率为 6 6 % ,酶比活性达 715mmol·min- 1·g- 1蛋白。rhBChE在 - 2 0℃含 2 0 %甘油及0 .0 2 %NaN3 的 10mmol·L- 1磷酸盐缓冲液 (pH 7.4 )中存放 1年 ,酶活性无明显变化。 18只小鼠ip事先与rhBChE孵温的 1.5LD的琥珀酰胆碱 ,不出现任何中毒症状和体征 ,全部存活 ;而琥珀酰胆碱对照组 ,18只小鼠均剧烈抽搐并在 2～ 5min内窒息死亡。结论　实验结果说明 ,从感染家蚕幼虫血淋巴液中纯化rhBChE的方法可靠 ,基因工程rhBChE在琥珀酰胆碱中毒危象的治疗中有潜在应用前景。     

Intrathecal orexin A increases sympathetic outflow and respiratory drive, enhances baroreflex sensitivity and blocks the somato-sympathetic reflex

BACKGROUND

Intrathecal (i.t.) injection of orexin A (OX-A) increases blood pressure and heart rate (HR), but the effects of OX-A on sympathetic and phrenic, nerve activity, and the baroreflex(es), somato-sympathetic and hypoxic chemoreflex(es) are unknown.

EXPERIMENTAL APPROACH

Urethane-anaesthetized, vagotomized and artificially ventilated male Sprague-Dawley rats were examined in this study. The effects of i.t. OX-A (20 nmol 10 µL⁻¹) on cardiorespiratory parameters, and responses to stimulation of the sciatic nerve (electrical), arterial baroreceptors (phenylephrine hydrochloride, 0.01 mg kg⁻¹ i.v.) and peripheral (hypoxia) chemoreceptors were also investigated.

KEY RESULTS

i.t. OX-A caused a prolonged dose-dependent sympathoexcitation, pressor response and tachycardia. The peak effect was observed at 20 nmol with increases in mean arterial pressure, HR and splanchnic sympathetic nerve activity (sSNA) of 32 mmHg, 52 beats per minute and 100% from baseline respectively. OX-A also dose-dependently increased respiratory drive, as indicated by a rise in phrenic nerve amplitude and a fall in phrenic nerve frequency, an increase in neural minute ventilation, a lengthening of the expiratory period, and a shortening of the inspiratory period. All effects of OX-A (20 nmol) were attenuated by the orexin receptor 1 antagonist SB 334867. OX-A significantly reduced both sympathoexcitatory peaks of somato-sympathetic reflex while increasing baroreflex sensitivity. OX-A increased the amplitude of the pressor response and markedly amplified the effect of hypoxia on sSNA.

CONCLUSIONS

Thus, activation of OX receptors in rat spinal cord alters cardiorespiratory function and differentially modulates sympathetic reflexes.     

Orexin‐A and respiration in a rat model of smoke‐induced chronic obstructive pulmonary disease

1. Orexins are neuropeptides synthesized in the hypothalamus that regulate many physiological functions, including energy homeostasis, stress responses, sleep/wake states etc. It is now emerging that orexins may also regulate breathing, but little is known as to how they do this, particularly in chronic obstructive pulmonary disease (COPD). In the present study, we used a rat model of cigarette smoke‐induced COPD to investigate orexin‐A expression in the hypothalamus and medulla and its effect on respiration. 2. Sprague‐Dawley rats were exposed to cigarette smoke (1 h twice daily) for 12 weeks. Lung function and pathological changes associated with inflammation and emphysema were determined to confirm the validity of the COPD model. 3. Hypothalamic and medullary orexin‐A levels, as determined by radioimmunoassay, were higher in smoke‐exposed than control rats. Furthermore, the expression of prepro‐orexin (PPO) mRNA in the hypothalamus and orexin OX₁ receptor mRNA in the medulla, as determined by real‐time quantitative polymerase chain reaction, was higher in smoke‐exposed than control rats. 4. The number of orexin‐A‐positive neurons in the hypothalamus and OX₁ and OX₂ receptor‐positive neurons in the ventrolateral medulla was higher in smoke‐exposed than control rats. 5. Microinjection of orexin‐A (1 μmol/L, 0.1 μL) into the pre‐Bötzinger complex enhanced phrenic nerve discharge to a greater extent in smoke‐exposed compared with control rats (61% vs 36%, respectively). 6. The findings of the present study demonstrate that the increased respiratory activity in smoke‐exposed rats is due to an increase in orexin‐A as well as upregulation of orexin receptors in the ventrolateral medulla.     

丙泊酚对布比卡因诱导的PC12细胞毒性和硫氧还蛋白系统的影响

目的：探讨丙泊酚对布比卡因诱导的PC12细胞毒性的保护作用及内源性硫氧还蛋白（Trx）系统在其中的作用。方法：培养的PC12细胞分成四组，正常对照组、丙泊酚组、布比卡因组、丙泊酚＋布比卡因（PB）组，每组6孔。培养6h和24h后，用MTT比色微量分析细胞存活率，测定上清液乳酸脱氢酶（LDH）活性和细胞内硫氧还蛋白还原酶（TrxR）、活性氧（ROS）活性，RT-PCR检测Trx-1 mRNA和TrxR-1 mRNA表达。结果：与正常PC12细胞相比，布比卡因可显著降低细胞存活率（P〈0．01）和细胞内TrxR活性（P〈0．05），增加上清液中LDH活性和细胞内ROS活性（P〈0．05，P〈0．01），明显降低Trx mRAN和Trx mRAN表达（P〈0．05）；丙泊酚对正常PC12细胞无明显影响；与布比卡因组相比，PB组细胞存活率（P〈0．01）和细胞内Trx活性（P〈0．05）明显增加，上清液中LDH活性和细胞内ROS活性显著降低（P〈0．05，P〈0．01），Trx mRAN和Trx mRAN表达明显增加（P〈0．05）。结论：布比卡因对PC12细胞具有毒性作用可能与降低细胞内TrxR活性、增加ROS活性有关，丙泊酚通过保护细胞内Trx系统的活性及清除ROS来减轻布比卡因诱导的PC12细胞毒性。     

脂肪乳剂治疗布比卡因心脏毒性的研究进展

 布比卡因是临床常用的长效酰胺类局部麻醉药,大剂量的布比卡因快速入血容易引起室性心律失常甚至心跳骤停,临床常规的复苏治疗成功率低。而临床作为静脉营养物质的脂肪乳剂却能逆转布比卡因心脏毒性,并在很多临床病例和动物实验中得到证实。目前研究的结果支持脂肪乳剂是通过“脂肪池”假说和改善心肌能量代谢来产生治疗作用的。进一步阐明脂肪乳剂逆转布比卡因心脏毒性的量效关系以及如何将脂肪乳剂的治疗和常规生命支持治疗结合起来,将为临床上布比卡因的应用提供更加可靠的安全保障。      

碘化N-正丁基氟哌啶醇抑制机械损伤诱导的血管平滑肌细胞增殖的作用及机制

目的探讨碘化N-正丁基氟哌啶醇(F2)对机械损伤所致血管平滑肌细胞(VSMCs)增殖的抑制作用及其机制。方法原代培养大鼠胸主动脉VSMCs,体外建立机械划伤致VSMCs增殖模型,采用Cell Counting Kit-8(CCK-8)法检测细胞增殖情况;流式细胞术法测定细胞周期;Western blot法检测p-MEK,p-ERK,Egr-1蛋白表达;Real Time RT-PCR检测MEK和Egr-1 mRNA表达。结果 F2剂量依赖地抑制机械损伤所致VSMCs增殖,降低损伤刺激下VSMCs的生存率和DNA合成,使G0/G1期细胞比例升高,G2/M期细胞百分比下降,并且抑制损伤后VSMCs中MEK/ERK的活化,使p-MEK/ERK蛋白表达降低,同时下调损伤后MEK和Egr-1的高表达。结论 F2对机械损伤所致血管平滑肌细胞增殖有明显抑制作用,其机制可能与影响MEK/ERK/Egr-1信号途径有关。     

Protection by and anti-oxidant mechanism of berberine against rat liver fibrosis induced by multiple hepatotoxic factors

1. The aim of the present study was to investigate the effect and mechanism of berberine, an alkaloid extracted from the traditional Chinese medicine coptis, on rat liver fibrosis induced by multiple hepatotoxic factors. 2. Male Wistar rats were separated into five groups, a normal control group, a fibrotic control group and fibrotic groups treated with three different doses of berberine. The fibrotic models were established by introduction of multiple hepatotoxic factors, including CCl(4), ethanol and high cholesterol. Rats in the treatment groups were administered 50, 100 or 200 mg/kg berberine, intragastrically, daily for 4 weeks. Serum levels of alanine aminotransferase (ALT) and serum aspartate aminotransferase (AST), hepatic activity of superoxide dismutase (SOD) and hepatic malondialdehyde (MDA) and hepatic hydroxyproline (Hyp) content were determined. Liver biopsies were obtained for histological and immunohistochemical studies to detect the expressions of alpha-smooth muscle actin (SMA) and transforming growth factor (TGF)-beta1. 3. The results showed that, compared with the fibrotic control group, serum levels of ALT and AST and hepatic content of MDA and Hyp were markedly decreased, but the activity of hepatic SOD was significantly increased in berberine-treated groups in a dose-dependent manner. In addition, histopathological changes, such as steatosis, necrosis and myofibroblast proliferation, were reduced and the expression of a-SMA and TGF-b1 was significantly downregulated in the berberine-treated groups (P < 0.01). 4. These results suggest that berberine could be used to prevent experimental liver fibrosis through regulation of the anti-oxidant system and lipid peroxidation.     

针刺对注射型坐骨神经损伤肌萎缩的影响

目的研究针刺对注射型坐骨神经损伤肌萎缩的影响。方法选家兔15只,建立双侧注射型坐骨神经损伤模型,左侧为对照侧,右侧为针刺治疗实验侧,术后1、2、4周观察肌肉的大体形态,测量肌湿重、肌纤维直径和横切面积的变化。结果 1周后实验侧肌肉比对照侧色泽红润,肌块丰满,湿重、肌纤维直径和横切面积均有显著差异。结论针刺治疗可以延缓注射型神经损伤肌萎缩,是其治疗的一种方法。     

尼群地平对大鼠野百合碱性肺动脉高压的防治作用

目的：利用野百合碱（ＭＣＴ）引起的大鼠肺动脉高压（ＰＨ）模型，探讨尼群地平（ＮＩＴ）对ＭＣＴ性ＰＨ的防治作用。方法：给ＭＣＴ或ＭＣＴ＋ＮＩＴ（１０ｍｇ·ｋｇ－１ｉｐ，每日一次）４ｗｋ，测定肺血流动力学参数和静脉血浆及肺组织匀浆中内皮素样免疫反应物（ｉｒ－ＥＴ）、一氧化氮（ＮＯ）、超氧化物歧化酶（ＳＯＤ）和丙二醛（ＭＤＡ）的含量。结果：ＮＩＴ能有效地降低ＭＣＴ模型大鼠的肺动脉压（从４．５±０．９降至３．６±０．５ｋＰａ）和肺血管阻力（从１１８±１７降至７９±１８ｋＰａ·ｍｉｎ·Ｌ－１），能抑制ＭＣＴ引起的肺小动脉中膜增厚；ＮＩＴ能显著抑制ＭＣＴ模型大鼠的肺组织匀浆中ＮＯ含量的减少和血浆中ＳＯＤ活性的降低（Ｐ＜０．０５），明显阻止肺匀浆中ＭＤＡ的升高（Ｐ＜０．０１）。结论：长期使用ＮＩＴ可有效防治ＭＣＴ性ＰＨ，其作用可能与其Ｃａ２＋拮抗作用及保护ＳＯＤ活性和增加ＮＯ含量有关。